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 9 of 15 additional AVM specimens contained mutant MAP2K1 alleles.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 roblasts, but similar in tCardiomyocytes and AVMs.

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

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

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

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

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

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

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

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

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

36 aneurysm-associated loci and sporadic brain AVM.

37 loci are also associated with sporadic brain AVM.

38 enic activity possibly contributory to brain AVM intracranial hemorrhage.

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

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

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

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

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

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

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

46 apeutic intervention for patients with brain AVMs.

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

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

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

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

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

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

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

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

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

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

57 anges in BMP signaling that lead to cerebral AVMs.

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

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

60 tially other LV abnormalities observed in CM-AVM.

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

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

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

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

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

66 ent zebrafish embryos, which develop cranial AVMs.

67 the flow-dependent development of downstream AVMs.

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

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

70 events AVM formation and reverts established AVMs.

71 in MAP2K1 are a common cause of extracranial AVM.

72 tic agents for individuals with extracranial AVM.

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

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

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

76 For AVM characterization, interobserver agreement was very g

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

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

79 nhibitors would be a promising treatment for AVMs.

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

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

82 rteriovenous connections, thereby generating AVMs.

83 Greater AVM size and interventional treatment were associated wi

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

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

86 exogenously supplied acetylcholine improves AVM circumferential axon guidance.

87 In AVM, patients initially presenting with haemorrhage have

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

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

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

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

92 ) complex is also significantly increased in AVM tissues.

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

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

95 the microvasculature and/or veins to induce AVM.

96 est that an impaired flow response initiates AVM development.

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

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

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

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

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

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

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

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

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

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

107 orrhage in brain arteriovenous malformation (AVM) patients.

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

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

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

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

112 ngiectases, and arteriovenous malformations (AVM).

113 sed by cerebral arteriovenous malformations (AVM).

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

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

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

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

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

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

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

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

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

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

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

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

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

127 e appearance of arteriovenous malformations (AVMs).

128 ry pathology of arteriovenous malformations (AVMs).

129 ry for cerebral arteriovenous malformations (AVMs).

130 giogenesis with arteriovenous malformations (AVMs).

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

132 al and cerebral arteriovenous malformations (AVMs).

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

134 phagocytophilum-occupied vacuolar membrane (AVM).

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

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

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

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

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

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

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

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

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

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

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

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

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

148 ations as compared to the natural history of AVM.

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

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

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

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

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

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

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

156 mitations to observing the initial stages of AVM formation.

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

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

159 eve to be a previously unidentified cause of AVMs.

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

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

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

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

164 The pathophysiology of AVMs is not well understood.

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

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

167 significant association was found for age or AVM size.

168 ymphatic malformation than for hemangioma or AVM.

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

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

171 is very important in the diagnosis of pelvic AVM.

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

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

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

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

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

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

178 ssive angiogenesis but does not fully revert AVM formation.

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

180 Spinal AVMs are rare and so is this syndrome.

181 stive myelopathy caused by intradural spinal AVMs.

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

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

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

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

186 The AVM combines the Vertex Model for confluent epithelial t

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

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

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

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

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

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

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

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

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

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

197 APH_1387 accumulates on the AVM throughout infection.

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

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

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

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

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

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

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

205 render arterial characteristics and lead to AVMs.

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

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

208 The mechanisms that underlie AVM formation remain poorly understood.

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

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

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

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

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

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

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

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

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

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

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

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

221 ses of intracranial bleeding associated with AVM.

222 .64-0.98) were significantly associated with AVM.

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

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

225 de polymorphisms (SNPs) were associated with AVMs.

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