ライフサイエンスコーパス: Marfan

1 Marfan patients with haploinsufficient FBN1 mutations se

2 Marfan syndrome (MFS) and other type 1 fibrillinopathies

3 Marfan syndrome (MFS) is a connective tissue disorder ca

4 Marfan syndrome (MFS) is a connective tissue disorder ca

5 Marfan syndrome (MFS) is a connective tissue disorder th

6 Marfan syndrome (MFS) is a dominantly inherited disorder

7 Marfan syndrome (MFS) is a heritable connective tissue d

8 Marfan syndrome (MFS) is a heritable connective tissue d

9 Marfan syndrome (MFS) is a heritable disorder of connect

10 Marfan syndrome (MFS) is a highly variable genetic conne

11 Marfan syndrome (MFS) is a systemic connective tissue di

12 Marfan syndrome (MFS) is a systemic disorder of connecti

13 Marfan syndrome (MFS) is an autosomal dominant disorder

14 Marfan syndrome (MFS) is caused by mutations in the fibr

15 Marfan syndrome (MFS) is known to cause ascending thorac

16 Marfan syndrome has a variable phenotype, even within fa

17 Marfan syndrome is a common inherited disorder of connec

18 Marfan syndrome is a connective tissue disorder caused b

19 Marfan syndrome is an autosomal dominant disorder of con

20 Marfan syndrome is an autosomal dominant disorder of con

21 Marfan syndrome is associated with early death due to ao

22 Marfan syndrome patients were more likely to dissect at

23 Marfan syndrome was exclusively associated with dissecti

24 Marfan's syndrome is a genetic disorder affecting connec

25 Marfan's syndrome is a systemic disorder of connective t

26 /- 1.62, control CH 11.24 +/- 1.21, P = .01; Marfan syndrome CRF 9.77 +/- 1.65, control CRF 11.03 +/-

27 e, measuring right eyes of 24 control and 13 Marfan syndrome subjects.

28 Positive aortic controls were from 15 Marfan patients.

29 In 20 Marfan and 20 control subjects, brachial artery diameter

30 rs for Stickler syndrome types 1, 2, and 2B; Marfan syndrome; Ehlers-Danlos syndrome type 4; and juve

31 Mitral valve prolapse was present in 5.4%, Marfan syndrome in 1.1% and scoliosis in 29%.

32 METHODS AND We evaluated 789 Marfan patients enrolled in the National Heart, Lung, an

33 In 9 Marfan and 6 control subjects, the above parameters were

34 lastic fiber structure and organization in a Marfan mouse aorta using ex vivo small chamber myography

35 One eye of a Marfan patient sustained a retinal detachment 8 months a

36 mutation in the fibrillin-1 (FBN1) gene of a Marfan syndrome (MFS) patient induces in-frame exon skip

37 ear size (HR: 1.1 [1.04-1.16]; P=0.001), and Marfan syndrome (HR: 3.66 [1.65-8.13]; P=0.001).

38 predictors of late death (P< or =0.005), and Marfan syndrome, initial valve-preserving aortic root re

39 Bicuspid aortic valve (BAV) (39%) and Marfan syndrome (MFS) (22%) were the leading diagnoses i

40 Both bicuspid aortic valve (BAV) and Marfan syndrome have been associated with aortic dissect

41 Fibrillin-based human diseases such as Marfan syndrome and congenital contractural arachnodacty

42 AD) occur as part of known syndromes such as Marfan syndrome but can also be inherited in families in

43 an also be subject to abnormalities (such as Marfan syndrome, bicuspid aortic valve, inflammatory vas

44 es of many of the genetic syndromes, such as Marfan syndrome, that predispose persons to thoracic aor

45 ary causes of large-artery aneurysms such as Marfan's syndrome have long been recognized; recent year

46 ted with connective tissue disorders such as Marfan's syndrome or skin fibrosis in the tight skin mou

47 nin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA p

48 mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6.50+/-4

49 Most mutations in fibrillin-1 cause Marfan syndrome with severe cardiovascular and ocular sy

50 of the known mutations in fibrillin-1 cause Marfan syndrome, a number of other mutations lead to cli

51 FBN1 gene, which encodes fibrillin-1, cause Marfan syndrome (MFS) and have been associated with a wi

52 tations in the fibrillin-1 gene (FBN1) cause Marfan syndrome and related connective tissue disorders

53 in the human fibrillin-1 (FBN-1) gene cause Marfan syndrome (MFS), an autosomal dominant disease of

54 FBN1 mutations cause Marfan syndrome (MFS), an autosomal dominant disorder of

55 FBN1 mutations cause Marfan syndrome, whose major cardiovascular complication

56 not previously reported as causing classical Marfan syndrome.

57 In this predefined substudy of COMPARE, Marfan patients were randomized to daily receive losarta

58 sue have major cardiovascular complications, Marfan syndrome and Ehlers-Danlos syndrome type IV.

59 ls aged 6-40 years with clinically confirmed Marfan syndrome were eligible for inclusion.

60 2.8% (35 patients) had genetically confirmed Marfan syndrome and an additional 17.8% (232 patients) h

61 Retrospective analysis of 86 consecutive Marfan syndrome patients fulfilling Ghent criteria that

62 neal resistance factor (CRF) were decreased (Marfan syndrome CH 9.45 +/- 1.62, control CH 11.24 +/- 1

63 Based on the study of different Marfan mouse models and the discovery of several novel t

64 ved ORA variables successfully discriminated Marfan syndrome.

65 lt in the dominant connective tissue disease Marfan syndrome.

66 nts have unique risk factors for dissection: Marfan syndrome, bicuspid aortic valves, and larger aort

67 idia, albinism, anterior segment dysgenesis, Marfan syndrome, ectopia lentis, neurofibromatosis, reti

68 amily met the diagnostic criteria for either Marfan or Ehlers-Danlos syndrome.

69 variants do not meet diagnostic criteria for Marfan syndrome, though variants are associated with tal

70 ted individuals meets the Ghent criteria for Marfan syndrome.

71 rs evaluated met the diagnostic criteria for Marfan syndrome.

72 verlaps a previously mapped second locus for Marfan syndrome, termed the MFS2 locus.

73 ad to alternative therapeutic strategies for Marfan syndrome.

74 f echocardiograms, changing drug therapy for Marfan syndrome, follow-up of infant with complex corona

75 (HLA) provided the best predictive value for Marfan syndrome (AUROC = 0.85).

76 ortic valves should not be extrapolated from Marfan syndrome and support discrete treatment algorithm

77 ry or idiopathic ectopia lentis, 5 (29%) had Marfan syndrome, 2 (12%) were aphakic after pars plana v

78 s, nine had neuromuscular scoliosis, one had Marfan's disease, and one had congenital scoliosis.

79 Fifty patients had Marfan syndrome.

80 families with familial TAAD who did not have Marfan syndrome.

81 s with recurrent AD were more likely to have Marfan syndrome (21.5% versus 3.1%; P<0.001) but not bic

82 r, younger patients were more likely to have Marfan syndrome, bicuspid aortic valve, and prior aortic

83 ecapitulates the pulmonary features of human Marfan syndrome.

84 Ingenuity pathway analysis identified Marfan syndrome, aneurysm formation, LV dilatation, and

85 s of constituents such as fibrillin-1, as in Marfan syndrome, can compromise both elastic fiber integ

86 re more prevalent in adults than children in Marfan syndrome.

87 is the most life-threatening complication in Marfan syndrome (MFS) patients.

88 e in age at surgery, dissection, or death in Marfan syndrome compared with LDS.

89 dissection is the leading cause of death in Marfan's syndrome.

90 luding timing of surgery, remains debated in Marfan syndrome because of a lack of data on aortic risk

91 cellular matrix protein that is defective in Marfan syndrome.

92 a, which does not normally become dilated in Marfan's syndrome, was not affected by ARB therapy.

93 ular junction, which is prone to dilation in Marfan's syndrome as well, also showed a reduced rate of

94 g a common pathogenesis of aortic disease in Marfan syndrome and STAAD.

95 g of the pathogenesis of vascular disease in Marfan syndrome will facilitate the development of thera

96 of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial

97 ey shifted inferiorly with gaze elevation in Marfan syndrome.

98 - 1.72, P = .01) and corneas were flatter in Marfan syndrome (Marfan syndrome Kmean 41.25 +/- 2.09 di

99 rmalities that are similar to those found in Marfan syndrome (MFS), a heritable connective tissue dis

100 hydralazine, both normalize aortic growth in Marfan mice, in association with reduced PKCbeta and ERK

101 The VTI was higher in Marfan syndrome (n=57, median 26; interquartile range 10

102 lective angiotensin-1 receptor inhibitor, in Marfan syndrome might reduce aortic dilatation, which is

103 implying distinct mechanisms of bone loss in Marfan syndrome and congenital contractural arachnodacty

104 fibrils, cause pleiotropic manifestations in Marfan syndrome and congenital contractural arachnodacty

105 dditional treatment strategies are needed in Marfan patients with dominant negative FBN1 mutations.

106 No aortic dissection was observed in Marfan syndrome patients with BAV.

107 where aortic dissection frequently occurs in Marfan's and other syndromes.

108 sudden death is a well-recognized outcome in Marfan syndrome, ventricular arrhythmias are not well de

109 lium-dependent brachial artery reactivity in Marfan subjects.

110 g per unit area was significantly reduced in Marfan capsules compared with normal capsules (16-26% ve

111 features of corneal deformation responses in Marfan syndrome, including increased deformation, decrea

112 the human fibrillin-1 gene, FBN1, result in Marfan syndrome (MFS), a common connective tissue disord

113 Mutations in fibrillin-1 (FBN1) result in Marfan syndrome, demonstrating a critical requirement fo

114 s (SMCs) recapitulated the pathology seen in Marfan aortas, including defects in fibrillin-1 accumula

115 to the pathophysiologic alterations seen in Marfan syndrome are highlighted.

116 , aortic valve function, and aortic shape in Marfan syndrome patients with and without BAV and report

117 ctor (TGF)-beta bioavailability/signaling in Marfan syndrome (MFS) changed the view of the extracellu

118 ept of pharmaceutical aorta stabilization in Marfan syndrome is supported by a wealth of promising st

119 c aneurysms and aortic root stabilization in Marfan syndrome, these claims are not consistently confi

120 iated with thoracic aortic aneurysm (TAA) in Marfan syndrome.

121 er were assessed for discriminative value in Marfan syndrome, measuring right eyes of 24 control and

122 diated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO rel

123 t for nonrepairable abnormalities, including Marfan's syndrome in four, bicuspid aortic valve in four

124 presentations of aortic aneurysm, including Marfan syndrome (MFS) and Loeys-Dietz syndrome (LDS).

125 onnective tissue disorders (CTDs), including Marfan syndrome (MFS), systemic sclerosis (SSc) and Tigh

126 stress contributes to the disease, including Marfan syndrome.

127 progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit this s

128 dissection in multiple disorders, including Marfan syndrome.

129 ated with aneurysm and dissection, including Marfan syndrome and the role of transforming growth fact

130 the context of genetic syndromes, including Marfan syndrome (MFS), an autosomal-dominant connective

131 aneurysms and dissections (TAAD), including Marfan syndrome (MFS), currently lack a cure, and causat

132 tions cause IEL or syndromic ectopia lentis (Marfan syndrome and Weill-Marchesani syndrome).

133 tic wall of a mouse model of neonatal lethal Marfan syndrome.

134 the autosomal dominant microfibrillopathies Marfan syndrome (MFS) and congenital contractural arachn

135 st lone disease predictor was Concavity Min (Marfan syndrome 47.5 +/- 20, control 69 +/- 14, P = .003

136 ing of mechanism based on studies in a mouse Marfan model emphasize the dynamic interplay of differen

137 Mice that harbor both a mutant Marfan syndrome (MFS) allele (Fbn1(C1039G/+)) and Tgfb2

138 drome (MFS) recruited from 2 annual National Marfan Foundation conferences (2012 and 2015).

139 ere forms of the Marfan syndrome ("neonatal" Marfan syndrome).

140 Included were all non-Marfan patients with nonbicuspid aortic valves who had u

141 Even non-Marfan aneurysms have a strong genetic basis.

142 These three syndromes--Noonan, Marfan, and long QT syndrome--span the range of congenit

143 ice with reduced Fbn1 gene expression and of Marfan syndrome (MFS) patients with heterozygous fibrill

144 enes, is increased in the ascending aorta of Marfan (Fbn1(C1039G/+)) mice.

145 nts in the genetic and orthopedic aspects of Marfan syndrome.

146 This report describes a case of Marfan's syndrome, an inherited disorder of connective t

147 three disulfide bonds are frequent causes of Marfan syndrome (MFS).

148 The cardiovascular complications of Marfan syndrome arise due to alterations in the structur

149 s of intact fibrillin-1, the consequences of Marfan syndrome causing mutations, and the ultrastructur

150 a may be more relevant in the development of Marfan syndrome than mechanisms previously proposed in a

151 Patients with the diagnosis of Marfan syndrome and magnetic resonance imaging or comput

152 In multivariate analysis, the diagnosis of Marfan syndrome independently predicted recurrent AD (ha

153 adult females with a confirmed diagnosis of Marfan syndrome was performed.

154 ential for noninvasive clinical diagnosis of Marfan syndrome.

155 s of age and sex with phenotypic features of Marfan syndrome have not been systematically examined in

156 , which recapitulate the most severe form of Marfan syndrome.

157 n a greater understanding of the genetics of Marfan's and other such disorders, including Loeys-Dietz

158 issecting aortic aneurysm is the hallmark of Marfan syndrome (MFS) and the result of mutations in fib

159 opi infection in a patient with a history of Marfan syndrome and recreational feral swine hunting.

160 ; and physical stigmata or family history of Marfan syndrome.

161 neurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in

162 ving or preventing several manifestations of Marfan syndrome in these mice, including aortic aneurysm

163 Cardiac manifestations of Marfan syndrome include aortic root dilation and mitral

164 The major orthopedic manifestations of Marfan syndrome include scoliosis, chest wall deformity,

165 sponsible for the clinical manifestations of Marfan syndrome.

166 and rupture of the aorta in a mouse model of Marfan syndrome (MFS).

167 mal bone growth activity in a mouse model of Marfan syndrome.

168 ration and regurgitation in a mouse model of Marfan syndrome.

169 ficient in fibrillin-1, an accepted model of Marfan syndrome.

170 lerated aneurysm growth in a murine model of Marfan syndrome.

171 w discusses mutant-fibrillin mouse models of Marfan syndrome and SSc (Tsk mice), and studies suggesti

172 ession of aortic aneurysm in mouse models of Marfan syndrome, a systemic disorder of the connective t

173 of promising studies in the murine models of Marfan syndrome-related aortapathy.

174 Recent data from mouse models of Marfan's syndrome suggest that aortic-root enlargement i

175 New insights regarding the pathogenesis of Marfan syndrome have developed from investigation of mur

176 Pathogenesis of Marfan syndrome is currently thought to be driven by mec

177 g is a major contributor to the pathology of Marfan syndrome (MFS) and related diseases.

178 pe B, occurs in an appreciable proportion of Marfan patients, especially in men and after previous pr

179 Patients undergoing AVS had higher rates of Marfan syndrome and lower rates of bicuspid aortic valve

180 p of families exhibits traits reminiscent of Marfan syndrome (MFS).

181 as recently exemplified through the study of Marfan syndrome (MFS), including aortic aneurysm and ske

182 atients) had physical features suggestive of Marfan syndrome.

183 of elastic fibers within the aortic wall of Marfan mice to the levels similar to those observed in c

184 d tested 248 probands with aortic disease or Marfan syndrome.

185 disorders associated with EL, in particular Marfan syndrome (MFS).

186 e arterial tree and phenotypically resembles Marfan syndrome.

187 We have studied Marfan syndrome-causing mutations which affect calcium b

188 and corneas were flatter in Marfan syndrome (Marfan syndrome Kmean 41.25 +/- 2.09 diopter, control Km

189 yndromes, including Birt-Hogg-Dube syndrome, Marfan syndrome, vascular (type IV) Ehlers-Danlos syndro

190 t has been known for more than a decade that Marfan syndrome - a dominantly inherited connective tiss

191 The Marfan syndrome (MFS), initially described just over 100

192 The Marfan syndrome patient undergoes care by many different

193 ng aorta: dissection, 28 patients (19%); the Marfan syndrome or its forme fruste variety, 15 patients

194 hypertension, bicuspid aortic valve, and the Marfan syndrome.

195 has been described in such conditions as the Marfan and Ehlers-Danlos type IV syndromes, due to defec

196 eness of familial aortic disease such as the Marfan syndrome, bicuspid aortic valve disease, and here

197 ons in the fibrillin-1 (FBN1) gene cause the Marfan syndrome (MFS) and related connective tissue diso

198 This distinguishes MSSE from the Marfan syndrome-related disorders in which missense muta

199 llular matrix (ECM) protein defective in the Marfan syndrome (MFS).

200 om fibrillin-1, the defective protein in the Marfan syndrome.

201 erlying connective tissue disorders like the Marfan syndrome.

202 mic presentations of selected aspects of the Marfan phenotype.

203 his region can result in severe forms of the Marfan syndrome ("neonatal" Marfan syndrome).

204 ay underlie one of the major features of the Marfan syndrome: fragmentation of aortic elastic lamella

205 ithin these proteins have been linked to the Marfan syndrome (MFS), CADASIL, protein S deficiency, ha

206 with tricuspid valves unassociated with the Marfan syndrome.

207 In addition to Marfan syndrome and aorta diameter, a large entry tear l

208 tic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number

209 NS-TAA) are incompletely defined compared to Marfan syndrome (MFS) and bicuspid aortic valve (BAV).

210 ents with a history of ectopia lentis due to Marfan syndrome, idiopathic causes, or hereditary causes

211 ween age groups were not entirely related to Marfan syndrome.

212 tions lead to clinical features unrelated to Marfan syndrome.

213 r pulse wave velocity in doxycycline-treated Marfan mice starting at 6 months as compared to their no

214 eart Foundation, the UK Marfan Trust, the UK Marfan Association.

215 British Heart Foundation, the UK Marfan Trust, the UK Marfan Association.

216 in the gene for fibrillin 1 (FBN1) underlie Marfan syndrome (MS), a disorder characterized by lens d

217 Unexpectedly, Marfan mice treated with CCBs show accelerated aneurysm

218 All 9 patients (2 with Marfan syndrome, 1 with Takayasu's disease) with undiagn

219 (2,079 with bicuspid aortic valves, 73 with Marfan syndrome, and 11,053 control patients with acquir

220 ients with aortic dissection type A, 74 with Marfan syndrome (58% men; median age, 37 years [first an

221 dilatation in children and young adults with Marfan syndrome and could reduce the incidence of aortic

222 ortic dilatation in children and adults with Marfan syndrome.

223 Among children and young adults with Marfan's syndrome who were randomly assigned to losartan

224 h atenolol in children and young adults with Marfan's syndrome.

225 pediatric and adult patients afflicted with Marfan syndrome (MFS), a multisystem disorder caused by

226 lysis of 90 patients </=50 years of age with Marfan syndrome, LDS, Ehlers-Danlos syndrome, or nonspec

227 e the most severe phenotypes associated with Marfan syndrome (fibrillin-1) and congenital contractura

228 Fibrillin-1 mutations associated with Marfan syndrome have recently been shown to induce genes

229 ess of the clinical features associated with Marfan syndrome may facilitate earlier diagnosis and opt

230 Recurrent AD is strongly associated with Marfan syndrome.

231 ometric findings of adults and children with Marfan syndrome (MFS) recruited from 2 annual National M

232 isease in Turner syndrome in comparison with Marfan-like syndromes and isolated aortic valve disease.

233 d has been extrapolated from experience with Marfan syndrome, despite the absence of comparative long

234 Many individuals with Marfan syndrome (MFS), caused by a deficiency of extrace

235 A distinct subgroup of individuals with Marfan syndrome have distal airspace enlargement, histor

236 After excluding individuals with Marfan syndrome or bicuspid aortic valve, a family histo

237 on of severe periodontitis in a patient with Marfan's syndrome.

238 diagnosed in late follow-up in patients with Marfan syndrome (10.8 +/- 4.4%) compared with those with

239 on was significantly higher in patients with Marfan syndrome (5.5 +/- 2.7%) compared with those with

240 ic dissections occurred in 600 patients with Marfan syndrome (mean age 36 +/- 14 years, 52% male).

241 Patients with Marfan syndrome (MFS), a multisystem disorder caused by

242 ne lens is a common finding in patients with Marfan syndrome (MFS).

243 rtic dissection remains low in patients with Marfan syndrome and aortic diameter between 45 and 49 mm

244 risk has not been evaluated in patients with Marfan syndrome and documented pathogenic variants in th

245 Furthermore, patients with Marfan syndrome and other forms of inherited thoracic ao

246 In 81 patients with Marfan syndrome and seven healthy control subjects, aort

247 outcomes in a series of young patients with Marfan syndrome and to define the prevalence of ventricu

248 rd type A aortic dissection in patients with Marfan syndrome are limited.

249 ications after AVR observed in patients with Marfan syndrome compared with those with bicuspid aortic

250 Seventy patients with Marfan syndrome diagnosed at birth to 52 years were foll

251 ckers (CCBs) are prescribed to patients with Marfan syndrome for prophylaxis against aortic aneurysm

252 A total of 146 patients with Marfan syndrome had aortic valve-sparing operations.

253 ing technique, but its role in patients with Marfan syndrome has not previously been defined.

254 Type B dissection in patients with Marfan syndrome is associated with a high need for exten

255 rgery for type A dissection in patients with Marfan syndrome is associated with low in-hospital morta

256 action, and five capsules from patients with Marfan syndrome obtained at intracapsular lens extractio

257 All patients with Marfan syndrome operated on for aortic root aneurysm fro

258 omplications are rare in young patients with Marfan syndrome receiving medical therapy and close clin

259 e was significantly greater in patients with Marfan syndrome than in control subjects (104 mL/m(2); 9

260 t data exist describing MVP in patients with Marfan syndrome undergoing aortic root replacement.

261 979, 82 patients (73.2% of all patients with Marfan syndrome undergoing resection of aneurysm of the

262 ic valve-sparing operations in patients with Marfan syndrome were associated with low rates of valve-

263 Seven hundred thirty-two patients with Marfan syndrome were followed up for a mean of 6.6 years

264 Patients with Marfan syndrome were significantly more likely to underg

265 rgery and long-term results in patients with Marfan syndrome who suffered aortic dissection.

266 Although the majority of patients with Marfan syndrome who undergo elective aortic root replace

267 Patients with Marfan syndrome with prior prophylactic aortic surgery a

268 treat aortic root aneurysm in patients with Marfan syndrome, based on relatively short-term outcomes

269 In 22 patients with Marfan syndrome, mean aortic volume was increased at 3 y

270 tection of aortic expansion in patients with Marfan syndrome.

271 calculated in a subgroup of 22 patients with Marfan syndrome.

272 fter previous aortic repair in patients with Marfan syndrome.

273 l density has been reported in patients with Marfan syndrome.

274 ndings in elastic vessels from patients with Marfan syndrome.

275 f outcome of this operation in patients with Marfan syndrome.

276 isrupted in all three zones in patients with Marfan syndrome.

277 ervation was accentuated among patients with Marfan syndrome.

278 ic valve-sparing operations in patients with Marfan syndrome.

279 re a major clinical problem in patients with Marfan syndrome.

280 ly different from that seen in patients with Marfan syndrome.

281 ct type B aortic dissection in patients with Marfan syndrome.

282 risk for type B dissection in patients with Marfan syndrome.

283 n reduces aortic dilatation in patients with Marfan syndrome.

284 perations are feasible in most patients with Marfan syndrome; they are applicable to patients with bo

285 prosthetic graft and valve in patients with Marfan's syndrome may prevent premature death from ruptu

286 udy, the use of ARB therapy in patients with Marfan's syndrome significantly slowed the rate of progr

287 A total of 675 patients with Marfan's syndrome underwent replacement of the aortic ro

288 repair of aortic aneurysms in patients with Marfan's syndrome when the diameter of the aorta is well

289 We identified 18 pediatric patients with Marfan's syndrome who had been followed during 12 to 47

290 response to ARBs in pediatric patients with Marfan's syndrome who had severe aortic-root enlargement

291 in cause of premature death in patients with Marfan's syndrome.

292 d aortic valves (n = 5) from 7 patients with Marfan's syndrome.

293 educed quality of life (QOL) for people with Marfan syndrome (MFS) compared with those without MFS.

294 to describe aortic risk in a population with Marfan syndrome with pathogenic variants in the FBN1 gen

295 tegies to block TGF-beta, used in those with Marfan syndrome, are unlikely to be beneficial and could

296 observed in aneurysms forming in those with Marfan syndrome, inhibition of TGF-beta would worsen inf

297 A 31-year-old woman with Marfan's syndrome presented with amblyopia and a history

298 complications during pregnancy in women with Marfan syndrome and an aortic diameter <4.5 cm.

299 nd long-term clinical outcomes in women with Marfan syndrome who are followed prospectively during pr

300 nd long-term clinical outcomes in women with Marfan syndrome.