ライフサイエンスコーパス: aneurysmal

1 n layers, which allowed the artery to become aneurysmal.

2 n=6) none of the grafts had ruptured or were aneurysmal.

3 eriaortic adipose tissue attenuation in both aneurysmal (-57.85 HU +/- 7; P < .0001) and nonaneurysma

4 Sequential sectioning of aneurysmal abdominal aorta revealed two major characteri

5 PEVAC is an isolated, perifoveal, aneurysmal abnormality, occurring in otherwise healthy p

6 hypothesis by descriptive analyses of 31 non-aneurysmal and 29 aneurysmal ascending thoracic aortic s

7 ored as a site for endovascular treatment of aneurysmal and atherosclerotic disease.

8 d using semiautomated software in periaortic aneurysmal and nonaneurysmal segments of the abdominal a

9 Aneurysmal and occlusive changes are potentially progres

10 Compared with NAA, the aneurysmal aorta (AAA and rAAA) demonstrated significant

11 recipitation performed on cultured VSMCs and aneurysmal aorta demonstrated physical interaction betwe

12 In smooth muscle cells derived from aneurysmal aorta, PGE2 also caused cell death, with gene

13 cle cells over time, eventually resulting in aneurysmal aortas and ectatic esophagi.

14 The remaining aneurysms and all the non-aneurysmal aortas had a similar leukocytic infiltrate th

15 as of AngII-infused mice and human ascending aneurysmal aortas that mimicked the gradient of medial a

16 n of smooth muscle cells (SMCs) characterize aneurysmal aortas.

17 severely reduced in both atherosclerotic and aneurysmal aortic lesions.

18 +) T cells, the most abundant infiltrates in aneurysmal aortic tissue, is uncertain.

19 surgical, with ligation or resection of the aneurysmal arterial segment with or without splenectomy,

20 Moreover, analyses of human atherosclerotic aneurysmal arteries by flow cytometry, gene expression a

21 althy arteries to disturbed flow (D-flow) in aneurysmal arteries, platelets are subjected to external

22 There is debate concerning whether an aneurysmal ascending aorta should be replaced when assoc

23 riptive analyses of 31 non-aneurysmal and 29 aneurysmal ascending thoracic aortic specimens.

24 Seven aneurysmal balloons, 15 sheep (5 with chronic LV aneurys

25 2DE correlated well with actual volumes for aneurysmal balloons.

26 Aneurysmal bone cyst (ABC) is a locally aggressive osseo

27 Aneurysmal bone cyst (ABC) is a locally recurrent bone l

28 Aneurysmal bone cyst (ABC) is a pediatric osseous tumor

29 Aneurysmal bone cyst (ABC) is an aggressive, pediatric b

30 17/USP6 is translocated and overexpressed in aneurysmal bone cyst (ABC), a pediatric tumor characteri

31 slocation in various human tumors, including aneurysmal bone cyst (ABC), and the related benign lesio

32 Hemorrhagic cavities (secondary aneurysmal bone cyst [ABC] regions) were common, seen in

33 f the spine with secondary development of an aneurysmal bone cyst, and none of the patients developed

34 emorrhage, which simulated the appearance of aneurysmal bone cyst.

35 t-tissue mass, which allows distinction from aneurysmal bone cyst.

36 Aneurysmal bone cysts (ABC) are locally aggressive bone

37 Aneurysmal bone cysts are enigmatic lesions of unknown c

38 We have reviewed a series of 150 aneurysmal bone cysts treated over the last 20 years.

39 Bony tumours encompass enchondromas, aneurysmal bone cysts, osteoid osteomas, giant-cell lesi

40 common types of cysts are the unicameral and aneurysmal bone cysts.

41 nal aorta calcium score thereby establishing aneurysmal calcification as a marker for slower aneurysm

42 Significant focal uptake was observed in aneurysmal carotid arteries, peaking at 4 wk after aneur

43 aft thrombectomy, and repeat bypass for late aneurysmal change of a vein conduit.

44 iagnosis, allowing detailed visualization of aneurysmal changes and ischemic progression.

45 A brief overview highlights the aneurysmal changes that can accrue when vessel wall infl

46 nd 2 patients were hospitalized for elective aneurysmal clipping.

47 evere cardiovascular defects with an unusual aneurysmal common arterial trunk.

48 rs, abdominal aortic aneurysm incidence, and aneurysmal death in apolipoprotein E- and interferon-gam

49 dilation by 56% (P = 0.003) and ameliorates aneurysmal degeneration (P = 0.016).

50 x metalloproteinase-9, which is required for aneurysmal degeneration in the murine AAA model.

51 kade of AngII type I receptor AT1R prevented aneurysmal degeneration of TGFBR1 deficient aortas.

52 Elastase-induced aneurysmal degeneration was suppressed by treatment with

53 ve late aorta-related complications, such as aneurysmal degeneration, that increase mortality and oft

54 FBR1 deficiency resulted in rapid and severe aneurysmal degeneration, with 100% penetrance of ascendi

55 ring effects, these agents may help suppress aneurysmal degeneration.

56 ut it is not known if either is necessary in aneurysmal degeneration.

57 ancreatic elastase) under pressure to induce aneurysmal degeneration.

58 GFBR1 deficient aortas at the early stage of aneurysmal degeneration.

59 ity, elastin degradation, calcification, and aneurysmal development in the aorta (269% expansion in c

60 the inflammatory process that culminates in aneurysmal development.

61 Therefore, novel biomarkers, besides aneurysmal diameter, are needed to assess aortic wall in

62 ent-grafts remained patent without increased aneurysmal diameter.

63 , the remaining unruptured grafts (n=6) were aneurysmal (diameter increase > or =100%), whereas in th

64 peripheral vascularization (14 eyes, 100%), aneurysmal dilatation (12 eyes, 85.7%), terminal arboriz

65 isplayed an abnormally thin tunica media and aneurysmal dilatation before rupturing into the amniotic

66 factors may serve as potential predictors of aneurysmal dilatation following surgical repair of TAAD.

67 g of circumaortic left renal vein with gross aneurysmal dilatation of both pre- and retro-aortic part

68 ting multiple vascular pathologies including aneurysmal dilatation of the aorta and patent ductus art

69 te the relationship between the diameter and aneurysmal dilatation of the paraumbilical vein (PUV) an

70 monly associated with focal inflammation and aneurysmal dilatation.

71 Recurrence of symptoms, aortic aneurysmal dilation (>55 mm), or a yearly increase of >4

72 Aneurysmal dilation of intracranial vessels was visualiz

73 An autopsy showed aneurysmal dilation of the stented arterial segments wit

74 t arteries and arterial beds, which leads to aneurysmal dilation, dissection and hemorrhage.

75 esonance imaging demonstrated no evidence of aneurysmal dilation.

76 Characterized by retinal vasculitis, aneurysmal dilations, exudation, and neuroretinitis, IRV

77 Aneurysmal dilations, observed in 57% of eyes, substanti

78 ment for acute limb ischemia (n = 14 642) or aneurysmal disease (n = 3456), unreported symptom status

79 ntion (OR, 5.7 P = 0.006), family history of aneurysmal disease (OR, 9.5; P = 0.075), and renal insuf

80 166 patients underwent root replacement for aneurysmal disease (porcine: 39% [n=65]; mechanical: 61%

81 ese data support both the systemic nature of aneurysmal disease and a primary role of MMP-2 in aneury

82 to address various arch disorders, including aneurysmal disease and aortic dissections.

83 n endovascular treatment of abdominal aortic aneurysmal disease and carotid artery disease, and relev

84 es and blood were examined for parameters of aneurysmal disease and oxidative stress.

85 Aneurysmal disease can affect any segment of the aorta,

86 n, the role of plasminogen activators in the aneurysmal disease is unclear.

87 extraction method can be used to standardize aneurysmal disease management and sets the foundation fo

88 Aneurysmal disease occurred in 60.5% of affected relativ

89 etermine factors that lead to progression of aneurysmal disease that might be amenable to interventio

90 omatic lower extremity arterial occlusive or aneurysmal disease underwent imaging with four-channel m

91 Fusiform aneurysmal disease was present in 21.6% of patients at a

92 In aortic aneurysmal disease, a thrombus adherent to the aortic wa

93 In aortic aneurysmal disease, a thrombus adherent to the aortic wa

94 h arterial thromboembolic disease, nonaortic aneurysmal disease, atrial fibrillation, cardiac conduct

95 g; data on the role for medical therapies in aneurysmal disease, including beta-blockers, angiotensin

96 To correlate our findings to human aortic aneurysmal disease, we examined S100A12 expression in ao

97 s in uPA/Plg-accelerated atherosclerosis and aneurysmal disease.

98 have been proposed to prevent progression of aneurysmal disease.

99 in, and statin therapy in the progression of aneurysmal disease.

100 t of the genetic profile that predisposes to aneurysmal disease.

101 otic coronary, cerebral, or abdominal aortic aneurysmal disease.

102 mited value in preventing the progression of aneurysmal disease.

103 may contribute to the pathogenesis of aortic aneurysmal disease.

104 ciation with BAVM as previously reported for aneurysmal disease.

105 to organ ischaemia or hypertension, and for aneurysmal disease.

106 responsible for Smad2 promoter activation in aneurysmal disease.

107 architecture is a general feature of certain aneurysmal diseases and vasculitides.

108 s thought to play an important role in human aneurysmal diseases as described by an important body of

109 changes may occur in patients with stenotic, aneurysmal, dissection of the carotid artery and its bra

110 h use of MR elastography was associated with aneurysmal events at a 15-month follow-up.

111 tests between participants with and without aneurysmal events.

112 During follow-up, repair of an aneurysmal evolution of the false lumen distal to the as

113 onfirmed a patent covered stent and complete aneurysmal exclusion.

114 GG inhibits elastin degeneration, attenuates aneurysmal expansion, and hinders AAA development in rat

115 en experience disproportionately accelerated aneurysmal expansion, greater risks of rupture or dissec

116 tablished therapy known to alter the rate of aneurysmal expansion.

117 of platinum coils aimed at increasing intra-aneurysmal fibrosis.

118 loped quantitative assessments for disturbed aneurysmal flow.

119 ding the processes that initiate and sustain aneurysmal growth is pivotal for the development of medi

120 generating aortic wall stress and triggering aneurysmal growth, thereby delineating potential underly

121 that properdin-targeting strategies may halt aneurysmal growth.

122 B-94) to the site of an aneurysm and prevent aneurysmal growth.

123 (64)Cu-RYM2 specifically bound to normal and aneurysmal human aortic tissues in correlation with MMP

124 (64)Cu-RYM2 binding to normal and aneurysmal human aortic tissues was assessed by autoradi

125 n short-term outcomes after abdominal aortic aneurysmal intervention, there is a paucity of literatur

126 CT-A showed flow signal correlating with the aneurysmal lesion connecting to retinal capillary plexus

127 clonal expansion in vivo at the site of the aneurysmal lesion, in response to unidentified self- or

128 report in this article that aortic abdominal aneurysmal lesions from 8 of 10 patients with AAA contai

129 alphabeta TCR(+) T lymphocytes infiltrating aneurysmal lesions of patients with AAA have undergone p

130 epertoire of T cells differs in stenotic and aneurysmal lesions, and provide a novel framework for un

131 Although vein of Galen aneurysmal malformations (VGAM) can be diagnosed in the

132 al hemorrhages associated with vein of Galen aneurysmal malformations (VGAMs).

133 Vein of Galen aneurysmal malformations can present with acute intracra

134 A total of 998 aneurysmal men (median age, 69.5 [interquartile range (I

135 (R))) was implanted in the SMA, covering the aneurysmal neck and overlapping the previously implanted

136 the anatomy, which resulted in an incomplete aneurysmal neck covering.

137 data from 258 AAA patients, the lumen of the aneurysmal neck was analysed.

138 Arterial pathology manifests as aneurysmal or obstructive disease depending on changes i

139 The eventual formation of aneurysmal or occlusive lesions appears not to result fr

140 nital heart disease (CHD) may dilate, become aneurysmal, or rupture.

141 lished recently that Ang II infusion induces aneurysmal pathology in the ascending aorta.

142 aphic angiography (CTA) confirmed persistent aneurysmal perfusion due to the incomplete neck coverage

143 Accordingly, the exacerbated aneurysmal phenotype in TB4-null mice was rescued upon t

144 ests that each can independently promote the aneurysmal phenotype.

145 tation of the ascending aortic, with greater aneurysmal progression in Npr2(+/-) mice with bicuspid a

146 NPs may be an attractive strategy to inhibit aneurysmal progression.

147 II physiologic scores on admission, age, and aneurysmal rebleed within 48 hours.

148 y associated with initial neurologic status, aneurysmal rebleeding, amount of blood on CT scan, and i

149 Definitive options include open aneurysmal repair versus endovascular therapy.

150 060 patients were assessed-1692 did not have aneurysmal repair, 1917 had open surgery, and 451 had en

151 Aneurysmal rupture accounts for the majority of nontraum

152 tant role in the inflammatory response after aneurysmal rupture and were identified in the aneurysmal

153 son of the short-term and long-term risks of aneurysmal rupture with the risk associated with the int

154 of micro-ischaemia or infarction after ACoA aneurysmal rupture) or to a disconnection in the ventrom

155 Subsets of the vascular population with aneurysmal rupture, early rupture, or families with more

156 ntly increased systolic blood pressure, with aneurysmal rupture-associated deaths, increased luminal

157 ontraumatic convexity SAH unaccounted for by aneurysmal rupture.

158 Postoperative air was within the aneurysmal sac in 51 (58%) patients and surrounded the f

159 rent to the aortic wall within the expanding aneurysmal sac is present in > 90% of cases.

160 rent to the aortic wall within the expanding aneurysmal sac is present in >90% of cases.

161 A should be preferred over DSA for detecting aneurysmal sac reperfusion.

162 None of the patients experienced aneurysmal sac rupture.

163 Type II endoleaks with a stable or decreased aneurysmal sac size can be followed up with CT angiograp

164 In these patients, the aneurysmal sac size was stable or had decreased when com

165 ks were embolized secondary to an increasing aneurysmal sac size when compared with that at preoperat

166 .5%) have persisted with stable or decreased aneurysmal sac size.

167 type II endoleaks and the maximal orthogonal aneurysmal sac size.

168 peri-graft leak; complete thrombosis of the aneurysmal sac was achieved after coil embolization of t

169 Mottled attenuation within the aneurysmal sac was seen in 50 (57%) patients.

170 Stent-graft placement and thrombosis of the aneurysmal sac were successful in all patients.

171 urysm neck supports the coil mass inside the aneurysmal sac, and furthermore, has an effect on local

172 aving potentially ominous conditions such as aneurysmal SAH (aSAH) or cryptogenic "angiogram-negative

173 Non-aneurysmal SAH cases were excluded.

174 trospectively identified cases of first-ever aneurysmal SAH occurring within the referral networks of

175 fter admission in 609 consecutively admitted aneurysmal SAH patients.

176 Of the 575 patients with aneurysmal SAH, 482 patients (mean [SD] age, 55.0 [14.5]

177 ent inclusion criteria were age >/=18 years, aneurysmal SAH, endotracheal intubation with mechanical

178 ociated with minor complications compared to aneurysmal SAH.

179 n activator (uPA) is highly expressed in the aneurysmal segment of the abdominal aorta (AAA) in apoli

180 In addition, biomechanically stress in the aneurysmal segment reinforces CD36 externalization on RB

181 replacement or endovascular exclusion of the aneurysmal segment with healthy artery proximal and dist

182 Aortic aneurysmal segments that expanded during continuous AngI

183 ugh images were limited in two patients with aneurysmal septa.

184 No change in aneurysmal size or development of de novo aneurysms was

185 ore first degree relative affected (FDRA) by aneurysmal subarachnoid haemorrhage (aSAH) are at a high

186 Aneurysmal subarachnoid haemorrhage (aSAH) presents a ch

187 t modalities, the outcomes for patients with aneurysmal subarachnoid haemorrhage (aSAH) remain poor,

188 After aneurysmal subarachnoid haemorrhage (aSAH), extracellula

189 attenuate cerebral vasospasm (cVSP) in human aneurysmal subarachnoid haemorrhage (aSAH).

190 Relatives of people with aneurysmal subarachnoid haemorrhage (SAH) may be at incr

191 Patients with aneurysmal subarachnoid haemorrhage (SAH) secondary to r

192 tood complication for many patients who have aneurysmal subarachnoid haemorrhage and can lead to dela

193 18-65 years with confirmatory evidence of an aneurysmal subarachnoid haemorrhage and presenting less

194 The management of patients with aneurysmal subarachnoid haemorrhage demands expertise to

195 Aneurysmal subarachnoid haemorrhage is a potentially dev

196 he benefit of statins in patients with acute aneurysmal subarachnoid haemorrhage is unclear.

197 risk, such as those with a family history of aneurysmal subarachnoid haemorrhage or unruptured intrac

198 Focal brain damage after aneurysmal subarachnoid haemorrhage predominantly result

199 s in a retrospective series of patients with aneurysmal subarachnoid haemorrhage with strong temporal

200 s (224 with traumatic brain injury, 139 with aneurysmal subarachnoid haemorrhage, and 151 with intrac

201 cerebral ischaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to

202 sive care unit after traumatic brain injury, aneurysmal subarachnoid haemorrhage, or intracerebral ha

203 ions in the human brain injured by trauma or aneurysmal subarachnoid haemorrhage, we used DC electrod

204 rcts are common in poor-grade patients after aneurysmal subarachnoid haemorrhage.

205 -term or short-term outcome in patients with aneurysmal subarachnoid haemorrhage.

206 ptomatic cerebral vasospasm in patients with aneurysmal subarachnoid haemorrhage; (4) the use in the

207 vasospasm (VSP) is a common phenomenon after aneurysmal subarachnoid hemorrhage (aSAH) and contribute

208 irment in cerebral autoregulation (CA) after aneurysmal subarachnoid hemorrhage (aSAH) is associated

209 Prognosis of patients with high-grade aneurysmal subarachnoid hemorrhage (aSAH) is only insuff

210 dies revealed the prognosis differed between aneurysmal subarachnoid hemorrhage (aSAH) patients with

211 In aneurysmal subarachnoid hemorrhage (aSAH), accurate diag

212 driver of adverse outcomes in patients with aneurysmal subarachnoid hemorrhage (aSAH), defining an u

213 butor to delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage (aSAH), leading to hi

214 Cerebral vasospasm is a dreaded sequelae of aneurysmal subarachnoid hemorrhage (aSAH), requiring tim

215 emia is associated with worse outcomes after aneurysmal subarachnoid hemorrhage (aSAH), there is no c

216 y contributes to a devastating outcome after aneurysmal subarachnoid hemorrhage (aSAH), with limited

217 is crucial in the treatment of patients with aneurysmal subarachnoid hemorrhage (aSAH).

218 microbiome in cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (aSAH).

219 are related to poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH).

220 cantly contribute to poor outcomes following aneurysmal subarachnoid hemorrhage (aSAH).

221 common, treatable condition in patients with aneurysmal subarachnoid hemorrhage (SAH) and has been as

222 Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) has devastating

223 cause ischemic neurological damage following aneurysmal subarachnoid hemorrhage (SAH) have remained e

224 Acute aneurysmal subarachnoid hemorrhage (SAH) is a complex mu

225 Aneurysmal subarachnoid hemorrhage (SAH) is a potentiall

226 thophysiology of early ischemic injury after aneurysmal subarachnoid hemorrhage (SAH) is not understo

227 Mortality and morbidity can be reduced if aneurysmal subarachnoid hemorrhage (SAH) is treated urge

228 In this prospective observational study of aneurysmal subarachnoid hemorrhage (SAH) patients, we ex

229 Aneurysmal subarachnoid hemorrhage (SAH) remains a devas

230 Significance statement: Aneurysmal subarachnoid hemorrhage (SAH)--strokes involv

231 he most severe and pervasive consequences of aneurysmal subarachnoid hemorrhage (SAH).

232 In patients with aneurysmal subarachnoid hemorrhage and anemia, a liberal

233 the epidemiology of types of stroke, such as aneurysmal subarachnoid hemorrhage and cerebral vein thr

234 agnosing cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage and for guiding trans

235 se-wave velocity were improved between acute aneurysmal subarachnoid hemorrhage and stable state (p <

236 Early lactate and glucose levels after aneurysmal subarachnoid hemorrhage are associated with d

237 anal-modified protein levels in humans after aneurysmal subarachnoid hemorrhage correlate with the de

238 model to predict 60-day case fatality after aneurysmal subarachnoid hemorrhage developed from the In

239 Ninety-four percent of participants with aneurysmal subarachnoid hemorrhage experienced augmented

240 Patients with aneurysmal subarachnoid hemorrhage had a higher mean mea

241 The care of patients with aneurysmal subarachnoid hemorrhage has evolved significa

242 diagnosis as primary cerebral vasculitis and aneurysmal subarachnoid hemorrhage is common because of

243 is trial, prophylactic lumbar drainage after aneurysmal subarachnoid hemorrhage lessened the burden o

244 A total of 287 adult patients with acute aneurysmal subarachnoid hemorrhage of all clinical grade

245 Aneurysmal subarachnoid hemorrhage often leads to death

246 A substantial group of patients with aneurysmal subarachnoid hemorrhage or intracerebral hemo

247 Fifty aneurysmal subarachnoid hemorrhage patients and 30 intra

248 ated at two time points: on admission (acute aneurysmal subarachnoid hemorrhage phase) and at least 2

249 ge phase) and at least 21 days later (stable aneurysmal subarachnoid hemorrhage state).

250 Consecutive patients with aneurysmal subarachnoid hemorrhage treated with clipping

251 At baseline, the severity of aneurysmal subarachnoid hemorrhage was assessed clinical

252 rovide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk

253 at risk for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage with hemoglobin 7-13

254 atients in coma with traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial hem

255 n ischemic stroke, intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage, and traumatic brain

256 ay be used to prevent early rebleeding after aneurysmal subarachnoid hemorrhage, but anticoagulation

257 ologies including migraine, ischemic stroke, aneurysmal subarachnoid hemorrhage, intracerebral hemato

258 ligible patients had traumatic brain injury, aneurysmal subarachnoid hemorrhage, or intracerebral hem

259 luences hemorrhage severity in patients with aneurysmal subarachnoid hemorrhage, potentially through

260 After aneurysmal subarachnoid hemorrhage, the use of lumbar dr

261 n is associated with poor outcome, but after aneurysmal subarachnoid hemorrhage, this has not been in

262 d with extent of hemorrhage in patients with aneurysmal subarachnoid hemorrhage.

263 ic stiffness occur during the early phase of aneurysmal subarachnoid hemorrhage.

264 een used to prevent cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

265 mprove the outcome among patients with acute aneurysmal subarachnoid hemorrhage.

266 er craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.

267 arted at a median (IQR) of day 2 (1-2) after aneurysmal subarachnoid hemorrhage.

268 hol use, and family history of aneurysms and aneurysmal subarachnoid hemorrhage.

269 oped as a tool for risk stratification after aneurysmal subarachnoid hemorrhage.

270 ignificant morbidity and mortality following aneurysmal subarachnoid hemorrhage; however, the effect

271 -2), have been identified in thoracic aortic aneurysmal (TAA) tissue, but a cause-effect relationship

272 ic and giant aneurysms with or without intra-aneurysmal thrombosis.

273 In particular, aneurysmal tissue expressed interleukin (IL)-4, IL-5, an

274 ed a dose-response study for effect on intra-aneurysmal tissue healing in a murine carotid aneurysm m

275 ritical role in promoting inflammatory intra-aneurysmal tissue healing in an MIP-1alpha- and MIP-2-de

276 significant decrease in MCP-1-mediated intra-aneurysmal tissue healing.

277 ecur are characterized by inflammatory intra-aneurysmal tissue healing; therefore, we studied the bio

278 Moreover, aneurysmal tissue lacked the receptor for interferon-gam

279 case of Fas, activation of these proteins in aneurysmal tissue.

280 decrease in the proteolytic activity in the aneurysmal tissues and vascular smooth muscle cells (vSM

281 Pathologies in human ascending aortic aneurysmal tissues were predominant in outer medial laye

282 n or fibrinogen-associated epitopes in human aneurysmal tissues.

283 e 2 (T2, n = 505), type 3 (T3, n = 315), and aneurysmal type 1 (A-T1, n = 75), according to the new p

284 Aneurysmal type 1 NV poses a significant exudation risk,

285 2, 27%; mixed type 1 and 2, 3%; type 3, 3%; aneurysmal type 1, 3%.

286 associated with Smad2 mRNA overexpression in aneurysmal vascular smooth muscle cells (VSMCs), which i

287 Aneurysmal vessels were characterized by enhanced VSMC p

288 D2 promoter is dramatically altered in human aneurysmal VSMCs in vitro and in situ with a switch from

289 ociated protein in Smad2 activation in human aneurysmal VSMCs.

290 n confers protection against degeneration of aneurysmal wall by inhibiting inflammatory cascades and

291 magnetic resonance signal enhancement in the aneurysmal wall compared with nonspecific micelles.

292 Positive (18)F-FDG uptake in the aneurysmal wall is associated with an active inflammator

293 se 1/2 signaling pathway was observed in the aneurysmal wall of Fbln4(GKO) and Fbln4(SMKO) mice and b

294 neurysmal rupture and were identified in the aneurysmal wall of unruptured brain aneurysms.

295 entially participate in the weakening of the aneurysmal wall preceding rupture.

296 amellar cells or extracellular matrix during aneurysmal wall remodeling.

297 The sites of the aneurysmal wall with a positive (18)F-FDG uptake were ch

298 uptake and at a distant negative site of the aneurysmal wall.

299 all, suggesting a systemic alteration of the aneurysmal wall.

300 Larger prospective studies in aneurysmal women are warranted.