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 Sequential sectioning of aneurysmal abdominal aorta revealed two major characteri

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

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

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

7 Aneurysmal and occlusive changes are potentially progres

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

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

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

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

12 severely reduced in both atherosclerotic and aneurysmal aortic lesions.

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

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

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

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

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

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

19 2DE correlated well with actual volumes for aneurysmal balloons.

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

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

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

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

24 17/USP6 is translocated and overexpressed in aneurysmal bone cyst (ABC), a pediatric tumor characteri

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

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

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

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

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

30 Aneurysmal bone cysts (ABC) are locally aggressive bone

31 Aneurysmal bone cysts are enigmatic lesions of unknown c

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

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

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

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

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

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

38 nd 2 patients were hospitalized for elective aneurysmal clipping.

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

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

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

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

43 Elastase-induced aneurysmal degeneration was suppressed by treatment with

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

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

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

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

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

49 the inflammatory process that culminates in aneurysmal development.

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

51 ent-grafts remained patent without increased aneurysmal diameter.

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

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

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

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

56 monly associated with focal inflammation and aneurysmal dilatation.

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

58 Aneurysmal dilation of intracranial vessels was visualiz

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

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

61 esonance imaging demonstrated no evidence of aneurysmal dilation.

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

63 166 patients underwent root replacement for aneurysmal disease (porcine: 39% [n=65]; mechanical: 61%

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

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

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

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

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

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

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

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

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

73 mited value in preventing the progression of aneurysmal disease.

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

75 have been proposed to prevent progression of aneurysmal disease.

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

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

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

79 may contribute to the pathogenesis of aortic aneurysmal disease.

80 ciation with BAVM as previously reported for aneurysmal disease.

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

82 responsible for Smad2 promoter activation in aneurysmal disease.

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

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

85 onfirmed a patent covered stent and complete aneurysmal exclusion.

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

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

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

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

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

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

92 that properdin-targeting strategies may halt aneurysmal growth.

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

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

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

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

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

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

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

100 Vein of Galen aneurysmal malformations can present with acute intracra

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

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

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

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

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

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

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

108 ests that each can independently promote the aneurysmal phenotype.

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

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

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

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

113 Definitive options include open aneurysmal repair versus endovascular therapy.

114 060 patients were assessed-1692 did not have aneurysmal repair, 1917 had open surgery, and 451 had en

115 Aneurysmal rupture accounts for the majority of nontraum

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

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

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

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

120 ontraumatic convexity SAH unaccounted for by aneurysmal rupture.

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

122 None of the patients experienced aneurysmal sac rupture.

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

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

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

126 .5%) have persisted with stable or decreased aneurysmal sac size.

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

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

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

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

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

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

133 fter admission in 609 consecutively admitted aneurysmal SAH patients.

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

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

136 Aortic aneurysmal segments that expanded during continuous AngI

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

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

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

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

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

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

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

144 18-65 years with confirmatory evidence of an aneurysmal subarachnoid haemorrhage and presenting less

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

146 Aneurysmal subarachnoid haemorrhage is a potentially dev

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

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

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

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

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

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

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

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

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

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

157 Aneurysmal subarachnoid hemorrhage (SAH) is a potentiall

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

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

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

161 Aneurysmal subarachnoid hemorrhage (SAH) remains a devas

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

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

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

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

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

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

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

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

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

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

172 Aneurysmal subarachnoid hemorrhage often leads to death

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

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

175 Consecutive patients with aneurysmal subarachnoid hemorrhage treated with clipping

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 ociated protein in Smad2 activation in human aneurysmal VSMCs.

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

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

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

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

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

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

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

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