ライフサイエンスコーパス: AVM

1 AVM characterization consisted of arterial feeder, nidus

2 AVMs account for between 1 and 2% of all strokes, 3% of

3 AVMs are difficult to control; they often re-expand afte

4 AVMs are far less common causes of first presentations w

5 AVMs are the underlying cause of three major clinical sy

6 AVMs arose from enlargement of preexisting microvessels

7 AVMs can form anywhere in the body and can cause debilit

8 AVMs in the brain, lung, and visceral organs, including

9 AVMs typically progress, causing destruction of surround

10 er assays, miR-18a also reduced the abnormal AVM-BEC invasiveness, which correlated with a decrease i

11 9 of 15 additional AVM specimens contained mutant MAP2K1 alleles.

12 -endothelial cells, and to screen additional AVM specimens.

13 ll vessels, but not arteries alone, affected AVM formation, suggesting that Notch functions in the mi

14 Smad4-deficient mice, either before or after AVMs form, prevents and alleviates AVM formation and nor

15 PET/CT imaging showed enhanced uptake in all AVM lesions (mean SUV(max), 3.0 +/- 1.1; mean SUV(peak),

16 or after AVMs form, prevents and alleviates AVM formation and normalizes vessel diameters.

17 myopathies were significantly enriched in AM-AVM patients compared with healthy individuals (p = 2.22

18 rea may result in a complete occlusion of an AVM.

19 atients with intracranial bleeding due to an AVM who were included in a prospective database in the p

20 , and identify a novel mechanism by which an AVM can form.

21 nt suffering from this rare syndrome with an AVM arising from the artery of Adamkiewicz, which is ano

22 Sixteen patients presented with an AVM, provided informed consent, and were prospectively i

23 blood flow in their development, we analyzed AVM development in zebrafish embryos harboring a mutatio

24 tle touch is sensed by the anterior (ALM and AVM) and posterior (PLM) touch receptor neurons.

25 ected by miR-18a in patient-derived BECs and AVM-BECs were determined by Western blot, RT-qPCR (quant

26 associations between allele frequencies and AVM occurrence, but rs9298506, near SOX-17 approached st

27 f ACE inhibitor/ARB therapy on major GIB and AVM-related GIB, whereas standard Cox regression assesse

28 k of major gastrointestinal bleeds (GIB) and AVM-related GIBs in continuous-flow left ventricular ass

29 /CaM kinase gene showed a defect in SDQR and AVM positioning that resembled that of unc-2 mutants; th

30 s, the migrations of the ALM, BDU, SDQR, and AVM neurons were often foreshortened or misdirected, ind

31 tion and to prevent abnormal AV shunting and AVM pathogenesis.

32 Except nidus structure and AVM size, all single parameters forming the SM, sSM, ICH

33 With recurring symptoms and AVM recanalisation on angiography, another direct punctu

34 are both intracranial vascular diseases and AVMs often have associated aneurysms, we investigated wh

35 ethods of most studies have been flawed, and AVMs tend to be treated once they are discovered.

36 roblasts, but similar in tCardiomyocytes and AVMs.

37 and have a similar length-to-width ratio as AVMs.

38 hemorrhagic telangiectasia symptoms, such as AVMs.

39 t of blood flow, later increases, as well as AVMs, are dependent on flow.

40 rt a novel two-step model for HHT-associated AVM development in which pathological arterial enlargeme

41 ditary hemorrhagic telangiectasia-associated AVM formation are currently unknown.

42 analysis in 1,581 Northern California brain AVM patients (2000-2007).

43 hat the highest IL-6 protein levels in brain AVM tissue were associated with IL-6-174GG genotype (GG:

44 emorrhage modulates IL-6 expression in brain AVM tissue, which is consistent with the hypothesis that

45 We tested if sEng would be elevated in brain AVM tissues relative to epilepsy brain tissues, and also

46 alifornia, San Francisco (UCSF)-Kaiser Brain AVM Study Project and 504 healthy controls to evaluate g

47 amic changes at the earliest stages of brain AVM formation by time-lapse two-photon imaging through c

48 aneurysm-associated loci and sporadic brain AVM.

49 loci are also associated with sporadic brain AVM.

50 enic activity possibly contributory to brain AVM intracranial hemorrhage.

51 for natural history risk in unruptured brain AVM patients, providing greater statistical power.

52 Brain AVMs (n = 33) had higher mean sEng levels (245 +/- 175 v

53 We further analyzed brain AVMs, as they pose particular health risks.

54 y a role in the generation of sporadic brain AVMs.

55 nstitutively active Notch1 also led to brain AVMs in mice.

56 nse, invasive treatment for unruptured brain AVMs may be considered experimental therapy awaiting the

57 from 'A Randomized Trial of Unruptured Brain AVMs' (ARUBA), which is currently underway.

58 apeutic intervention for patients with brain AVMs.

59 etection, at least 15% of people affected by AVMs are asymptomatic, about one-fifth present with seiz

60 Cardiomyocytes (AVM) from male C57Bl/6 mice were treated with fractalkin

61 understand the cellular mis-steps that cause AVMs, we assessed endothelial cell behavior in alk1-defi

62 les is a reliable clinical tool for cerebral AVM characterization, which showed very good to excellen

63 rospectively enrolled patients with cerebral AVM were grouped according to their initial clinical pre

64 erentiation, and the development of cerebral AVMs in MGP null (Mgp(-/-)) mice.

65 ensitive in the characterization of cerebral AVMs measuring less than 3cm, of those located in eloque

66 icient material for embolization of cerebral AVMs, also in cases of intracranial bleeding associated

67 both involved in the development of cerebral AVMs, but the cross-talk between the two signaling pathw

68 elial differentiation, and prevents cerebral AVMs, but not pulmonary or renal AVMs.

69 Curative embolization of small cerebral AVMs is an efficient and safe alternative to neurosurgic

70 anges in BMP signaling that lead to cerebral AVMs.

71 inding indicates that BV abnormalities in CM-AVM develop as a result of loss of an ability of RASA1 t

72 d to the LV leakage defects that occur in CM-AVM is not understood.

73 cells (EC) result in vascular lesions in CM-AVM is unknown.

74 tially other LV abnormalities observed in CM-AVM.

75 malformation-arteriovenous malformation (CM-AVM) is a blood and lymphatic vessel (LV) disorder that

76 malformation-arteriovenous malformation (CM-AVM) is an autosomal dominant blood vascular (BV) disord

77 malformation-arteriovenous malformation (CM-AVM).

78 malformation-arteriovenous malformation (CM-AVM); whether it also functions as a regulator of the ly

79 standing of the molecular pathogenesis of CM-AVM and possible means of treatment.

80 ations of the RASA1 gene are the cause of CM-AVM in most cases.

81 Whether CM-AVM results from loss of an ability of RASA1 to regulate

82 o determine if overgrown cartilage contained AVM-causing mutations.

83 ent zebrafish embryos, which develop cranial AVMs.

84 the flow-dependent development of downstream AVMs.

85 does not have blood vessels, we studied ear AVMs to determine if overgrown cartilage contained AVM-c

86 The objective of endovascular AVM treatment is set individually for each case upon con

87 The ability of acetylcholine to enhance AVM axon guidance only in the presence of either UNC-6 o

88 events AVM formation and reverts established AVMs.

89 in MAP2K1 are a common cause of extracranial AVM.

90 tic agents for individuals with extracranial AVM.

91 f MMP-9 and MMP-2 in aggressive extracranial AVMs.

92 We studied extracranial AVMs in order to identify their biological basis.

93 d flow and vessel diameter and driving focal AVM growth from AV connections with higher blood velocit

94 For AVM characterization, interobserver agreement was very g

95 s peak velocity was significantly higher for AVM than for other vascular malformations and hemangioma

96 hether intervention should be considered for AVMs that have not bled.

97 nhibitors would be a promising treatment for AVMs.

98 own why and how selective blood vessels form AVMs, and there have been technical limitations to obser

99 Genetics of Arteriovenous Malformation (GEN-AVM) consortium.

100 rteriovenous connections, thereby generating AVMs.

101 Greater AVM size and interventional treatment were associated wi

102 tion by down-regulating LIN-41, an important AVM axon regeneration-promoting factor.

103 ogenously supplied acetylcholine can improve AVM axon guidance in mutants when either UNC-6- or SLT-1

104 exogenously supplied acetylcholine improves AVM circumferential axon guidance.

105 of MMP-9, but not MMP-2, is also elevated in AVM patients compared to healthy controls.

106 yrosine phosphatase (RPTP) that functions in AVM to inhibit signaling through the DCC family receptor

107 , but not MMP-2, are significantly higher in AVM tissues compared to normal tissues.

108 IL-6 protein levels were increased in AVM tissue from patients with hemorrhagic presentation c

109 ) complex is also significantly increased in AVM tissues.

110 212 potential biological targets involved in AVM formation, including the EC surface receptor, TEK (T

111 l targets of the TGFbeta pathway involved in AVM formation, we performed RNA- and chromatin immunopre

112 t difference was found between CT and MRI in AVM size, feeding artery and draining vein diameter, and

113 The first step in AVM axon development is a pioneer axonal projection from

114 to quantitatively determine angiogenesis in AVMs.

115 blood and muscle was significantly higher in AVMs than in background tissue (P = 0.0006 and P = 0.001

116 feasibility study showed increased uptake in AVMs with angiogenic activity, compared with surrounding

117 erotonin-deficient mutants as well as induce AVM-like migrations in the normally nonmotile neuron PVM

118 the microvasculature and/or veins to induce AVM.

119 est that an impaired flow response initiates AVM development.

120 Nevertheless, axons of injured AVM neurons regrow to the ventral nerve cord with over 6

121 iffers between adults who had interventional AVM treatment and those who did not.

122 trial data exist on the benefit of invasive AVM treatment, and the most contentious issue at present

123 However, large AVMs developed in the peripheral vasculature intimately

124 0) and was greater in patients with a larger AVM nidus (hazard ratio 1.3, 95% CI 1.1-1.7).

125 r hemangioma and arteriovenous malformation (AVM) but significantly greater compared with the other v

126 unruptured brain arteriovenous malformation (AVM) depends on a comparison of the estimated lifetime r

127 Congenital arteriovenous malformation (AVM) in the pelvic area is uncommon in males.

128 Arteriovenous malformation (AVM) is a fast-flow, congenital vascular anomaly that ma

129 A uterine arteriovenous malformation (AVM) is a rare cause of uterine bleeding.

130 Arteriovenous malformation (AVM) is an abnormal connection between arteries and vein

131 Extracranial arteriovenous malformation (AVM) is most commonly caused by MAP2K1 mutations in the

132 orrhage in brain arteriovenous malformation (AVM) patients.

133 This arteriovenous malformation (AVM), which shunts nearly all blood directly back to the

134 or patients with arteriovenous malformation (AVM)-related intracerebral haemorrhage (ICH) than other

135 Arteriovenous (AV) malformation (AVM) is a devastating condition characterized by focal l

136 As brain arteriovenous malformations (AVM) and intracranial aneurysms are both intracranial va

137 Liver arteriovenous malformations (AVM) in hereditary hemorrhagic telangiectasia (HHT) can

138 and ultimately arteriovenous malformations (AVM), through transforming growth factor (TGF)-beta and

139 ngiectases, and arteriovenous malformations (AVM).

140 /24), pulmonary arteriovenous malformations (AVMs) (n = 5/24), and proximal interruption of pulmonary

141 Brain arteriovenous malformations (AVMs) are abnormal tangles of vessels where arteries and

142 Brain arteriovenous malformations (AVMs) are an important cause of neurological morbidity i

143 Cerebral arteriovenous malformations (AVMs) are common vascular malformations, which may resul

144 Brain arteriovenous malformations (AVMs) are currently being treated in a variety of ways,

145 Arteriovenous malformations (AVMs) are fragile direct connections between arteries an

146 ngenital pelvic arteriovenous malformations (AVMs) are high-flow vascular lesions consisting of abnor

147 Extracranial arteriovenous malformations (AVMs) are rare but dangerous congenital lesions arising

148 Arteriovenous malformations (AVMs) are tortuous vessels characterized by arteriovenou

149 Pelvic arteriovenous malformations (AVMs) are uncommon lesions and only a rare number of mal

150 Arteriovenous malformations (AVMs) are vascular anomalies where arteries and veins ar

151 Spinal arteriovenous malformations (AVMs) can lead to development of congestive myelopathy (

152 Arteriovenous malformations (AVMs) have an inherent capacity to form new blood vessel

153 Arteriovenous malformations (AVMs) in organs, such as the lungs, intestine, and brain

154 nruptured brain arteriovenous malformations (AVMs) in the natural course is essential for assessing r

155 nical course of arteriovenous malformations (AVMs) of the brain in adults because the methods of most

156 ing to systemic arteriovenous malformations (AVMs), is caused by loss-of-function mutations in the AL

157 s in ALK1 cause arteriovenous malformations (AVMs), our findings suggest that an impaired flow respon

158 nd veins called arteriovenous malformations (AVMs), which can hemorrhage leading to stroke, aneurysm,

159 ry for cerebral arteriovenous malformations (AVMs).

160 giogenesis with arteriovenous malformations (AVMs).

161 s and veins, or arteriovenous malformations (AVMs).

162 al and cerebral arteriovenous malformations (AVMs).

163 e appearance of arteriovenous malformations (AVMs).

164 ry pathology of arteriovenous malformations (AVMs).

165 ases and larger arteriovenous malformations (AVMs); but how ENG functions to regulate the adult vascu

166 ersion of the asymmetric vinylogous Mannich (AVM) products to the unprotected amines in high yields.

167 phagocytophilum-occupied vacuolar membrane (AVM).

168 and immunostaining studies in an Mgp(-)(/-) AVM mouse model showed that miR-18a decreased abnormal c

169 tal decline in anterior ventral microtubule (AVM) axon regeneration.

170 We introduce an Active Vertex Model (AVM) for cell-resolution studies of the mechanics of con

171 l observations included uptake in multifocal AVM lesions and enhanced uptake in intraosseous componen

172 op life-threatening acute viral myocarditis (AVM), given that the causal viral infections are common,

173 e transfer of the adult ventricular myocyte (AVM) transcriptome into either a fibroblast or an astroc

174 deficient animals, the touch receptor neuron AVM and its sister cell, the interneuron SDQR, exhibit c

175 hannel gene unc-2, the touch receptor neuron AVM and the interneuron SDQR often migrated inappropriat

176 tly less disabling than in patients with non-AVM related hemorrhage.

177 ; and that microRNA-18a (miR-18a) normalized AVM-BEC function and phenotype, although its mechanism r

178 y correctly classified 15 of the 16 cases of AVM measuring less than 3cm (93.75% sensitivity).

179 ve to be the first time the entire course of AVM formation in subdermal blood vessels by using intrav

180 mptomatic bleeding in the clinical course of AVM in patients with and without an initial haemorrhage.

181 within AVM may include curative exclusion of AVM from circulation, embolization adjuvant to resection

182 The frequency of AVM haemorrhages during the subsequent clinical course (

183 onclude that MIG-10 mediates the guidance of AVM and PVM axons in response to the extracellular UNC-6

184 ment and AV shunting, which are hallmarks of AVM, and led to lethality within weeks of its expression

185 ations as compared to the natural history of AVM.

186 most recent studies suggest the majority of AVM patients are diagnosed without signs of hemorrhage,

187 Vessel enlargement, a manifestation of AVM, occurred in an apparently tissue-specific fashion;

188 an important TGFbeta downstream mediator of AVM formation.

189 is correlated with the simple morphology of AVM and PVM touch neurons.

190 to provide the best possible predictions of AVM radiosurgery outcomes of any method to date, identif

191 ted to create the most accurate predictor of AVM outcomes.

192 riety of causes, rather than the presence of AVM or the associated embolisation procedure per se, may

193 he treatment should consist in prevention of AVM bleeding in a management procedure characterized by

194 l equivalence, possibly due to prevention of AVM formation.

195 = 0.042) and a 63% reduction in the risk of AVM-related GIB (aHR: 0.37; 95% CI: 0.16 to 0.84; p = 0.

196 mitations to observing the initial stages of AVM formation.

197 Dense and plexiform structure of AVM nidus as well as a low number of supplying vessels a

198 Fractalkine treatment of AVM decreased both the speed of contraction and relaxati

199 eve to be a previously unidentified cause of AVMs.

200 ta(3) expression in the endothelial cells of AVMs.

201 dies of the frequency and clinical course of AVMs in well-defined, stable populations, taking account

202 Development of AVMs and associated progression to high-output heart fai

203 To understand the etiology of AVMs and the role of blood flow in their development, we

204 lial Rbpj from birth resulted in features of AVMs by P14, including abnormal AV shunting and tortuous

205 The incidence of AVMs is approximately 1 per 100 000 per year in unselect

206 The pathophysiology of AVMs is not well understood.

207 angiogenic status and treatment response of AVMs.

208 In older AVM axons, let-7 inhibits regeneration by down-regulatin

209 nt in this pathway and assess its effects on AVM development.

210 g (WES) and whole-genome sequencing (WGS) on AVM tissue from affected individuals.

211 Twenty-one AVMs had a feeding artery diameter of greater than 2 mm,

212 ymphatic malformation than for hemangioma or AVM.

213 re was no evidence of hemorrhage, anemia, or AVMs in major organs to explain the reduced aortic press

214 d intracerebral haemorrhage (ICH) than other AVM or ICH scores.

215 maging findings of a giant congenital pelvic AVM that was diagnosed in a 30-year-old male patient eig

216 is very important in the diagnosis of pelvic AVM.

217 m as an outflow vein of a right-sided pelvic AVM.

218 Pelvic AVMs are uncommon lesions and they can present with vari

219 Development of pelvic AVMs in this region of high VEGF expression occurred bec

220 Methods: Ten patients with a peripheral AVM (mean age, 40 y; 4 men and 6 women) and scheduled fo

221 titatively assess angiogenesis in peripheral AVMs.

222 ed on surgical biopsy sections of peripheral AVMs to investigate the expression pattern of integrin a

223 ncreased blood flow through these peripheral AVMs explained the drop in aortic blood pressure and led

224 in part from decreased cell density, precede AVM development, and that AVMs represent enlargement and

225 ains vessel caliber in adult life to prevent AVM formation and thereby protect heart function.

226 logical PI3K inhibition efficiently prevents AVM formation and reverts established AVMs.

227 ratio for ALS was found in relation to prior AVM (2.69; p=0.005), all strokes (1.38; p<0.001), and TI

228 alternative to CT for detection of pulmonary AVM in HHT, while avoiding repeated exposure to radiatio

229 NPs associate with the presence of pulmonary AVM in HHT1 but not HHT2, indicating genetic variation i

230 he presence and characteristics of pulmonary AVMs, image quality, vessel visibility, and artifact gra

231 Ten patients with pulmonary AVMs who had undergone CT of the chest within 12 months

232 ts cerebral AVMs, but not pulmonary or renal AVMs.

233 ad4-iECKO) mouse model that develops retinal AVMs.

234 ally fully block, but also reversed, retinal AVMs to avert retinal bleeding and anemia.

235 venting, reducing, and potentially reversing AVM.

236 ssive angiogenesis but does not fully revert AVM formation.

237 AHR-1 specifies AVM touch neuron fate by elevating MEC-3 while simultane

238 Spinal AVMs are rare and so is this syndrome.

239 stive myelopathy caused by intradural spinal AVMs.

240 esent a brief review of literature on spinal AVMs and elucidate the evolution of the term Foix-Alajou

241 at Mgp gene deletion in mice caused striking AVMs in lungs and kidneys, where overall small organ siz

242 We previously showed that AVM-brain endothelial cells (BECs) secreted higher VEGF

243 l density, precede AVM development, and that AVMs represent enlargement and stabilization of normally

244 The AVM also includes cell alignment, cell-specific mechanic

245 The AVM combines the Vertex Model for confluent epithelial t

246 In addition, the AVM introduces a flexible, dynamically changing boundary

247 However, the AVM neurons in unc-2 mutant animals extended axons in a

248 cell migration and axonal pathfinding in the AVM neurons appear to involve distinct calcium channel s

249 Uptake in the AVM, blood pool, and muscle was quantified as SUV(max) a

250 variables such as the characteristics of the AVM (size, location, presence of deep venous drainage),

251 /slit to direct the ventral migration of the AVM and PVM axons in C. elegans.

252 lcium channel, affected the migration of the AVM and SDQR bodies, as well as the guidance of the AVM

253 We show that regeneration of the AVM axon to the ventral nerve cord lacks the determinist

254 tor neuron axons, which are neighbors of the AVM axon.

255 SDQR bodies, as well as the guidance of the AVM axon.

256 understanding of the vascular anatomy of the AVM is essential in choosing an effective embolisation s

257 affect circumferential axon guidance of the AVM neuron and in these mutants exogenously supplied ace

258 ments as well as multiarterial supply of the AVM, particularly from meningeal arteries, en-passant ar

259 s and thrombin to the venous aneurysm of the AVM.

260 APH_1387 accumulates on the AVM throughout infection.

261 APH_1387 is expressed and localizes to the AVM in neutrophils recovered from A. phagocytophilum-inf

262 s of adult-stage axon regeneration using the AVM mechanosensory neurons.

263 It associates with the AVM in human HL-60, THP-1, and HMEC-1 cells and tick ISE

264 nce of any type of aneurysm related with the AVM was detected in 13 of 15 cases (86.6% sensitivity);

265 received interventional treatment for their AVM (n=63) with those who did not (n=51).

266 d uptake in intraosseous components in those AVM cases affecting bone integrity.

267 Forty-three AVMs were detected, 13 native and 30 recanalized.

268 ion and BMP9/10 ligand blockade both lead to AVM formation in postnatal retinal vessels and internal

269 regions of high VEGF expression, leading to AVM formation and a rapid injurious impact on heart func

270 eased Angpt2 transcription in ECs leading to AVM formation, increased blood vessel calibers, and chan

271 xogenous serotonin could restore motility to AVM neurons in serotonin-deficient mutants as well as in

272 red for Alk1-deficient vessels to develop to AVMs in adult mice.

273 render arterial characteristics and lead to AVMs.

274 wever, how decreased ALK1 signaling leads to AVMs is unknown.

275 Total AVM occlusion was achieved with no recanalisation on fol

276 Twenty-two AVMs had a feeding artery diameter of less than or equal

277 esis that human genetic factors may underlie AVM in previously healthy children.

278 The mechanisms that underlie AVM formation remain poorly understood.

279 t inducer of IFNs, were proposed to underlie AVM.

280 llular and hemodynamic mechanisms underlying AVM pathogenesis elicited by increased Notch signaling i

281 unately, the molecular mechanisms underlying AVM pathogenesis remain poorly understood, and the TGFbe

282 who were first diagnosed with an unruptured AVM during 1999-2003 (n=114) entered our prospective, po

283 occurrence of haemorrhage from an unruptured AVM is approximately 2%, but the risk of recurrent haemo

284 short-term functional outcome for unruptured AVMs, but the longer-term effects of intervention are un

285 For unruptured AVMs, current morbidity data suggest a higher risk for i

286 morrhage itself carries risks, and untreated AVM may in many cases have a good prognosis.

287 For untreated AVMs, the annual risk of developing de novo seizures is

288 ltrasound/colour Doppler evidence of uterine AVM managed by abdominal hysterectomy, describing the im

289 itized for guidance defects disrupts ventral AVM axon guidance in a SAX-3-dependent manner and enhanc

290 ded as having cerebral and peripheral vessel AVMs, stroke (separately for haemorrhagic and ischaemic)

291 , mucocutaneous telangiectases, and visceral AVMs and caused by mutations in one of several genes, in

292 e if local tissue overgrowth associated with AVM is caused by direct or indirect effects of the MAP2K

293 .64-0.98) were significantly associated with AVM.

294 ses of intracranial bleeding associated with AVM.

295 Consistent with AVM pathology, we found cerebral hemorrhage, hypoxia and

296 ut not RBBP8 were strongest in patients with AVM with associated aneurysms.

297 de polymorphisms (SNPs) were associated with AVMs.

298 g intranidal and flow aneurysms related with AVMs.

299 ensitive in detecting aneurysms related with AVMs.

300 Endovascular interventions within AVM may include curative exclusion of AVM from circulati