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 s article aims to describe the behavior of a cavernous angioma in its natural history, documenting: a

10 Familial cerebral cavernous angioma occurs as an autosomal dominant disord

11 igns can orient the etiological diagnosis of cavernous angioma versus other alternatives: de novo app

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

13 Cavernous angiomas (CA) are common vascular anomalies ca

14 Cavernous angiomas are cerebral vascular malformations t

15 Cerebral cavernous angiomas are collections of closely clustered

16 Two patients had multiple classic cerebral cavernous angiomas.

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

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

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

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

21 to be achieved in the lizard lung due to its cavernous central lumen and honeycomb-shaped wall.

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

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

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

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

26 cts, switching capillaries from branching to cavernous expansion.

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

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

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

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

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

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

33 with subretinal fluid secondary to a carotid cavernous fistula.

34 described as a rare complication of carotid cavernous fistula.

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

36 Carotid-cavernous fistulas are abnormal communications between t

37 Carotid cavernous fistulas are abnormal communications between t

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

39 11 pseudoaneurysms, 17 thromboses, 4 carotid cavernous fistulas, and 1 transected internal carotid ar

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

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

42 measured with a microdialysis approach, and cavernous gene and protein expression assessed by qRT-PC

43 The findings were consistent with diffuse cavernous haemangiomatosis of the rectum (DCHR), an extr

44 The most common diagnosis was cavernous hemangioma (72.7%) followed by orbital sheet m

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

46 Congenital retinal macrovessels and retinal cavernous hemangioma are benign lesions.

47 Our case demonstrates that the conjunctival cavernous hemangioma can mimic malignant conjunctival le

48 Therefore, a diagnosis of conjunctival cavernous hemangioma was made.

49 etinal macrovessel associated with a retinal cavernous hemangioma was made.

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

51 etinal macrovessel associated with a retinal cavernous hemangioma.

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

53 Extra-axial cavernous hemangiomas (ECHs) are complex vascular lesion

54 resulting in gradual regression of cutaneous cavernous hemangiomas and improved motor strength, with

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

56 afish ccm2 resulting in a novel lethal multi-cavernous lesion in the embryonic caudal venous plexus (

57 ntaining adjacent dilated blood-filled multi-cavernous lesions.

58 xplain the formation of characteristic multi-cavernous lesions.

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

60 The loss function of cerebral cavernous malformation (CCM) genes leads to most CCM les

61 integrins in the vascular disease, cerebral cavernous malformation (CCM) has yet to be explored in v

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

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

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

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

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

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

68 Cerebral cavernous malformation (CCM) is a neurovascular disease

69 Cerebral cavernous malformation (CCM) is a rare neurovascular dis

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

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

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

73 The cerebral cavernous malformation (CCM) signaling pathway utilizes

74 D GWAS signals that converge on the cerebral cavernous malformation (CCM) signalling pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

88 The cerebral cavernous malformation disease causing gene KRIT1 partic

89 , suggesting that KRIT1 mutation in cerebral cavernous malformation disease may alter epithelial func

90 etic and molecular underpinnings of cerebral cavernous malformation disease, the mechanisms that lead

91 therapies for clinical treatment of cerebral cavernous malformation disease.

92 and who were first diagnosed with a cerebral cavernous malformation during 1999-2003 or 2006-10.

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

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

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

96 Cerebral cavernous malformation is a common human vascular diseas

97 Cerebral cavernous malformation is a vascular disease of the brai

98 eurological deficit attributable to cerebral cavernous malformation over 24 months.

99 olecular and cellular mechanisms of cerebral cavernous malformation pathologies.

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

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

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

103 or older with symptomatic familial cerebral cavernous malformation were eligible for enrolment.

104 essed 300 of 306 individuals with a cerebral cavernous malformation who were eligible for study.

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

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

107 T1 loss is the most common cause of cerebral cavernous malformation, a neurovascular dysplasia result

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

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

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

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

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

113 0.52%), six pituitary adenomas (0.16%), five cavernous malformations (0.14%), eight vascular stenoses

114 Brainstem cerebral cavernous malformations (CCM) are clinically more aggres

115 Cerebral cavernous malformations (CCM) are congenital vascular an

116 Cerebral cavernous malformations (CCM) are irregularly shaped and

117 Cerebral cavernous malformations (CCM) are vascular lesions causi

118 e that TLNRD1 is a component of the cerebral cavernous malformations (CCM) complex through its direct

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

120 ome following surgical resection of cerebral cavernous malformations (CCM) in pediatric patients.

121 c transporters are mis-expressed in Cerebral Cavernous Malformations (CCM) patient tissues.

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

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

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

125 nduces vascular anomalies including cerebral cavernous malformations (CCM), which are caused by a clo

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

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

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

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

130 ranolol reduces experimental murine cerebral cavernous malformations (CCMs) and prevents embryonic ca

131 Cerebral cavernous malformations (CCMs) and spinal cord cavernous

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

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

134 Cerebral cavernous malformations (CCMs) are common brain vascular

135 Cerebral cavernous malformations (CCMs) are common inherited and

136 Cerebral cavernous malformations (CCMs) are common neurovascular

137 Cerebral cavernous malformations (CCMs) are common sporadic and i

138 Cerebral cavernous malformations (CCMs) are common vascular anoma

139 Cerebral cavernous malformations (CCMs) are congenital vascular a

140 Cerebral cavernous malformations (CCMs) are human vascular malfor

141 Cerebral cavernous malformations (CCMs) are neurovascular lesions

142 Familial cerebral cavernous malformations (CCMs) are predominantly neurova

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

144 Cerebral cavernous malformations (CCMs) are sporadically acquired

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

146 Cerebral cavernous malformations (CCMs) are vascular abnormalitie

147 Cerebral cavernous malformations (CCMs) are vascular abnormalitie

148 Cerebral cavernous malformations (CCMs) are vascular anomalies of

149 Cerebral cavernous malformations (CCMs) are vascular lesions affe

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

151 Cerebral cavernous malformations (CCMs) are vascular lesions with

152 Cerebral Cavernous Malformations (CCMs) are vascular malformation

153 Cerebral cavernous malformations (CCMs) are vascular neoplasms in

154 In the brain, cerebral cavernous malformations (CCMs) arise owing to inactivati

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

156 Cerebral cavernous malformations (CCMs) can cause symptomatic int

157 Cerebral cavernous malformations (CCMs) carry a high risk of rebl

158 activation of CCM2 in humans causes cerebral cavernous malformations (CCMs) containing adjacent dilat

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

160 been anecdotally reported to reduce cerebral cavernous malformations (CCMs) in humans.

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

162 Cerebral cavernous malformations (CCMs) is a microvascular disord

163 al link hemorrhage associated with cerebral cavernous malformations (CCMs) to anticoagulant properti

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

165 ), have been recently discovered in cerebral cavernous malformations (CCMs), raising the possibility

166 t-derived hBBB assembloids to model cerebral cavernous malformations (CCMs), we found that these asse

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

168 ery (GKS) in treating patients with cerebral cavernous malformations (CCMs).

169 scular malformations reminiscent of cerebral cavernous malformations (CCMs).

170 come of conservatively treated patients with cavernous malformations (CM) is poor.

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

172 ourse of patients with spinal intramedullary cavernous malformations (ISCMs).

173 vernous malformations (CCMs) and spinal cord cavernous malformations (SCCMs) are common vascular abno

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

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

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

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

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

179 Cerebral cavernous malformations are acquired vascular anomalies

180 Cavernous malformations are characterized by enlarged va

181 Hemorrhagic arteriovenous malformations and cavernous malformations are surgically excised if access

182 Thus, propranolol ameliorated cavernous malformations by B1 adrenergic antagonism in z

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

184 cal neurological deficit due to the cerebral cavernous malformations during up to 15 years of prospec

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

186 in people with symptomatic familial cerebral cavernous malformations is justified.

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

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

189 or focal neurological deficit from cerebral cavernous malformations than avoidance of antithrombotic

190 PI3K signaling also contributes to cerebral cavernous malformations, a vascular disorder that affect

191 in people with symptomatic familial cerebral cavernous malformations, although this trial was not des

192 Observations in people with cerebral cavernous malformations, and in preclinical models of th

193 , dural arteriovenous fistulas, and cerebral cavernous malformations, and their associated neurologic

194 is withheld from some patients with cerebral cavernous malformations, because of uncertainty around t

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

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

197 erminal center kinase-1) and CCM-3 (cerebral cavernous malformations-3), participate in a negative fe

198 causes autosomal dominant familial cerebral cavernous malformations.

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

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

201 acranial haemorrhage in adults with cerebral cavernous malformations.

202 cal deficit in people with familial cerebral cavernous malformations.

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

204 nctional intra-operative localization of the cavernous nerve (CN) network for nerve-sparing radical p

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

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

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

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

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

210 Erectile responses to both cavernous nerve stimulation and intracavernosal injectio

211 Moreover, cavernous nerve stimulation was associated with a marked

212 Erectile function was assessed by cavernous nerve-stimulated intracavernous pressure measu

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

214 le function on electrical stimulation of the cavernous nerves as well as spontaneous erectile functio

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

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

217 ted in the inner retina corresponding to the cavernous retinal hemangioma.

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

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

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

221 of ICACs was evaluated in the ophthalmic and cavernous segments of each scan.

222 in postmortem human brain samples, meninges, cavernous sinus (cavum trigeminale), and cranial nerves

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

224 ing often showed preferential involvement of cavernous sinus and middle fossa.

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

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

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

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

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

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

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

232 Cavernous sinus invasion was present in the minority of

233 Isolated orbital or cavernous sinus involvement was present in 3 of 7 patien

234 ds; and (3) ocular, orbital, optic nerve, or cavernous sinus involvement.

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

236 hat tumor invasion of the medial wall of the cavernous sinus may explain the relatively low biochemic

237 Removal of the cavernous sinus medial wall was not associated with perm

238 a longitudinal study of patients with benign cavernous sinus meningiomas localized immediately adjace

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

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

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

242 erative inspection of the medial wall of the cavernous sinus, which was surgically removed when invas

243 an extended anterior MLV network around the cavernous sinus, with exit routes through the foramina o

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

245 scular lesions mainly found in the spine and cavernous sinus.

246 uperior ophthalmic vein thrombosis and bulky cavernous sinus.

247 nications between the carotid system and the cavernous sinus.

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

249 The cavernous sinuses were involved in 1 of 7 LCH patients,

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

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

252 essure, elasticity and shrinkage of repaired cavernous tissue prove that the bioengineered corpora sc

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

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

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

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

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

258 h complete occlusion with collateralization (cavernous transformation).

259 In congenital cavernous transformation, AF exceeded cirrhotic levels,

260 s can result in mesenteric ischemia, chronic cavernous transformation, and complications of portal hy

261 Cavernous transformation, calcifications of the venous w

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

263 ation modules which create artery, vein, and cavernous venous sinus (CVS) segmentation masks from unl

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

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