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 dominantly inherited disorder

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

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

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

7 Marfan syndrome (MFS) is an autosomal dominant disorder

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

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

10 Marfan syndrome (MFS), a heritable connective tissue dis

11 Marfan syndrome has a variable phenotype, even within fa

12 Marfan syndrome is a common inherited disorder of connec

13 Marfan syndrome is a connective tissue disorder caused b

14 Marfan syndrome is an autosomal dominant disorder of con

15 Marfan syndrome is an autosomal dominant disorder of con

16 Marfan syndrome is associated with early death due to ao

17 Marfan syndrome patients were more likely to dissect at

18 Marfan syndrome remains primarily a clinical diagnosis.

19 Marfan syndrome results from mutations in the FBN1 gene,

20 Marfan syndrome was exclusively associated with dissecti

21 Marfan's syndrome is a genetic disorder affecting connec

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

23 /- 1.62, control CH 11.24 +/- 1.21, P = .01; Marfan syndrome CRF 9.77 +/- 1.65, control CRF 11.03 +/-

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

25 Positive aortic controls were from 15 Marfan patients.

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

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

28 es type I and II (12q13.1-q13.3 and 6p21.3), Marfan syndrome (15q21.1), and juvenile glaucoma (chromo

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

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

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

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

33 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).

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

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

36 as Klippel-Feil, familial dysautonomia, and Marfan syndrome demonstrate high rates of scoliotic defo

37 amount of fibrillin expression in normal and Marfan syndrome capsules.

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

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

40 minating connective tissue disorders such as Marfan syndrome in the not-too-distant future.

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

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

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

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

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

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

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

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

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

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

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

52 FBN1 mutations cause Marfan syndrome, whose major cardiovascular complication

53 not previously reported as causing classical Marfan syndrome.

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

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

56 2.8% (35 patients) had genetically confirmed Marfan syndrome and an additional 17.8% (232 patients) h

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

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

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

60 ved ORA variables successfully discriminated Marfan syndrome.

61 lt in the dominant connective tissue disease Marfan syndrome.

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

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

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

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

66 ted individuals meets the Ghent criteria for Marfan syndrome.

67 rs evaluated met the diagnostic criteria for Marfan syndrome.

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

69 ad to alternative therapeutic strategies for Marfan syndrome.

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

71 Allografts were used for Marfan's syndrome patients or those with unusable pulmon

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

73 lly similar to but genetically distinct from Marfan syndrome.

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

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

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

77 Fifty patients had Marfan syndrome.

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

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

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

81 ecapitulates the pulmonary features of human Marfan syndrome.

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

83 ypothesize that the defect in fibrillin-1 in Marfan's syndrome leads to (1) formation of elastin that

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

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

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

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

88 cellular matrix protein that is defective in Marfan syndrome.

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

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

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

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

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

94 ey shifted inferiorly with gaze elevation in Marfan syndrome.

95 - 1.72, P = .01) and corneas were flatter in Marfan syndrome (Marfan syndrome Kmean 41.25 +/- 2.09 di

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

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

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

99 ficiency, the main cardiovascular lesions in Marfan's syndrome, are associated with destruction of co

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

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

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

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

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

105 lium-dependent brachial artery reactivity in Marfan subjects.

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

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

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

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

110 of the reasons why these mutations result in Marfan's syndrome.

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

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

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

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

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

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

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

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

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

120 nents of several genetic diseases, including Marfan syndrome (MFS).

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

122 dissection in multiple disorders, including Marfan syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 The vascular structural defects of Marfan syndrome, Alagille syndrome, neurofibromatosis, a

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

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

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

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

149 ential for noninvasive clinical diagnosis of Marfan syndrome.

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

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

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

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

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

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

156 ces of osteoporosis and a single instance of Marfan syndrome are also the result of mutations at thes

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

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

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

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

161 sponsible for the clinical manifestations of Marfan syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 rt rhythm, peripheral pulses, or stigmata of Marfan syndrome.

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

178 atients) had physical features suggestive of Marfan syndrome.

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

180 sports, family history of heart disease, or Marfan syndrome were included in 0% to 56% of the state

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

182 e arterial tree and phenotypically resembles Marfan syndrome.

183 mes 12q13.1-q13.3 and 6p21.3, respectively), Marfan syndrome (chromosome 15q21.1), and juvenile glauc

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

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

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

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

188 The Marfan syndrome patient undergoes care by many different

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

190 for the Stickler syndrome types 1 and 2, the Marfan syndrome, or the juvenile glaucoma loci.

191 (defective in coagulation factor IX) and the Marfan syndrome (defective in the connective tissue prot

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

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

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

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

196 -two patients (44% of the CVG group) had the Marfan syndrome (MFS).

197 dissections in patients who do not have the Marfan syndrome.

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

199 an fibrillin-1, the 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 rmalities with many clinical features of the Marfan syndrome (MFS), an autosomal dominant disorder of

205 ations in the FBN1 gene are the cause of the Marfan syndrome, an autosomal dominant disorder with ske

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

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

208 sorder that is phenotypically related to the Marfan syndrome.

209 with tricuspid valves unassociated with the Marfan syndrome.

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

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

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

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

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

215 tions lead to clinical features unrelated to Marfan syndrome.

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

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

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

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

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

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

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

228 Recurrent AD is strongly associated with Marfan syndrome.

229 as well as fibrillin defects associated with Marfan's syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 A subset of patients with Marfan syndrome manifested multiple forms of vasculopath

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

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

256 nce (MR) images obtained in 48 patients with Marfan syndrome over a period of 2.3-9.4 years (mean, 5.

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

258 ression in the lens capsule of patients with Marfan syndrome supported a causal relationship to lens

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 l density has been reported in patients with Marfan syndrome.

271 ndings in elastic vessels from patients with Marfan syndrome.

272 ervation was accentuated among patients with Marfan syndrome.

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

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

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

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

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

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

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

280 n reduces aortic dilatation in patients with Marfan syndrome.

281 tection of aortic expansion in patients with Marfan syndrome.

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

283 fter previous aortic repair 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 tegies to block TGF-beta, used in those with Marfan syndrome, are unlikely to be beneficial and could

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

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

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

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

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

300 The treatment of women with Marfan's syndrome who already have aortic root widening