ライフサイエンスコーパス: atherosclerotic

1 Investigators classified all patients into atherosclerotic and non-atherosclerotic groups for the p

2 plasia (FMD) is a heterogeneous group of non-atherosclerotic and non-inflammatory arterial diseases t

3 contribute to the CD4(+) T-cell pool in the atherosclerotic aorta.

4 (18)F-FDG uptake was evaluated in murine atherosclerotic aortas after stimulation with M-CSF or G

5 Pharmacological targeting of MC1-R in atherosclerotic apolipoprotein E-deficient mice reduced

6 cific PET imaging of CXCR4 expression in the atherosclerotic arterial wall.

7 RATIONALE: Atherosclerotic-arterial occlusions decrease tissue perf

8 esponses and increased regulatory T cells in atherosclerotic arteries and lymphoid organs.

9 ly showed that CSN5 is up-regulated in human atherosclerotic arteries.

10 and predict the growth and remodeling of an atherosclerotic artery is still lacking.

11 S dose was strongly associated with coronary atherosclerotic burden (increase [95% confidence interva

12 We assessed coronary atherosclerotic burden in 3 individuals with complete AN

13 diet, male and female mice were assessed for atherosclerotic burden in the large vessels, and plasma

14 veral cardiovascular disease risk factors on atherosclerotic burden.

15 at is, subclinical atherosclerosis, incident atherosclerotic cardiovascular (ASCV) events, and ASCV m

16 on study on stools from 218 individuals with atherosclerotic cardiovascular disease (ACVD) and 187 he

17 oward reduction in 10-year predicted risk of atherosclerotic cardiovascular disease (ASCVD) by implem

18 oronary artery calcium (CAC) score, incident atherosclerotic cardiovascular disease (ASCVD) events, a

19 Although risk factors for atherosclerotic cardiovascular disease (ASCVD) in famili

20 Atherosclerotic cardiovascular disease (ASCVD) is associ

21 Besides age, other discriminators of atherosclerotic cardiovascular disease (ASCVD) risk are

22 The use of atherosclerotic cardiovascular disease (ASCVD) risk to p

23 individuals with a higher 10-year predicted atherosclerotic cardiovascular disease (ASCVD) risk, cal

24 L)-cholesterol lowering in the management of atherosclerotic cardiovascular disease (ASCVD) risk.

25 heterogeneity among individuals for CHD and atherosclerotic cardiovascular disease (ASCVD) risk.

26 In patients with atherosclerotic cardiovascular disease (ASCVD), guidelin

27 between neighborhood disadvantage and major atherosclerotic cardiovascular disease (ASCVD)-related e

28 mainstay in the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD).

29 an individuals with subclinical and clinical atherosclerotic cardiovascular disease (ASCVD).

30 recommended for the secondary prevention of atherosclerotic cardiovascular disease (ASCVD).

31 length (TL) in leukocytes is associated with atherosclerotic cardiovascular disease (ASCVD).

32 Approximately 97% of patients had atherosclerotic cardiovascular disease (ASCVD).

33 ears to identify those at increased risk for atherosclerotic cardiovascular disease (ASCVD).

34 Although HIV is associated with increased atherosclerotic cardiovascular disease (CVD) risk, it is

35 included age >65 years (P<0.01), history of atherosclerotic cardiovascular disease (P<0.01), prescri

36 senting 18.3 million adults with established atherosclerotic cardiovascular disease (self-reported or

37 volocumab vs placebo in patients with stable atherosclerotic cardiovascular disease and a baseline LD

38 iation study on stools from individuals with atherosclerotic cardiovascular disease and healthy contr

39 Furthermore, as this population ages, atherosclerotic cardiovascular disease and its risk fact

40 trolled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholester

41 (LDL-C) >/=190 mg/dL are at a higher risk of atherosclerotic cardiovascular disease as a result of lo

42 These findings show that patients with atherosclerotic cardiovascular disease benefit from lowe

43 predictor of coronary heart disease and all atherosclerotic cardiovascular disease combined outcomes

44 ments in 2 subgroups of patients with stable atherosclerotic cardiovascular disease currently receivi

45 Primary outcome was an atherosclerotic cardiovascular disease event, and second

46 Over a follow-up of 3 years, 19 atherosclerotic cardiovascular disease events (9 strokes

47 ndently associated with a 3-fold increase in atherosclerotic cardiovascular disease events among PLWH

48 s associated with a 3-fold increased risk of atherosclerotic cardiovascular disease events and a 4-fo

49 standard background therapy in patients with atherosclerotic cardiovascular disease exceeds generally

50 abetes who have, or who are at high risk of, atherosclerotic cardiovascular disease have provided new

51 which was shown to inversely correlate with atherosclerotic cardiovascular disease in populations wi

52 Atherosclerotic cardiovascular disease is a leading caus

53 Atherosclerotic cardiovascular disease patients reportin

54 ardiovascular events in patients with stable atherosclerotic cardiovascular disease regardless of whe

55 cohort risk equations were used to estimate atherosclerotic cardiovascular disease risk score based

56 The median 10-year atherosclerotic cardiovascular disease risk score of the

57 ment, patients who were older, male, and had atherosclerotic cardiovascular disease were more likely

58 effectiveness of evolocumab in patients with atherosclerotic cardiovascular disease when added to sta

59 se, using US clinical practice patients with atherosclerotic cardiovascular disease with low-density

60 0.672 for ADA HbA1c clinical categories for atherosclerotic cardiovascular disease, 0.701 for ADA fa

61 evidence for an association between CHIP and atherosclerotic cardiovascular disease, but the nature o

62 ntative US adult population with established atherosclerotic cardiovascular disease.

63 nd expenditures among those with established atherosclerotic cardiovascular disease.

64 ovascular death in patients with established atherosclerotic cardiovascular disease.

65 associated with incident type 2 diabetes and atherosclerotic cardiovascular disease.

66 ients with type 2 diabetes mellitus who have atherosclerotic cardiovascular disease.

67 s are effective in the primary prevention of atherosclerotic cardiovascular disease.

68 the aging process and may play a key role in atherosclerotic cardiovascular disease.

69 poiesis correlates with an increased risk of atherosclerotic cardiovascular disease.

70 sterol is a well established risk factor for atherosclerotic cardiovascular disease.

71 ry intake plays a role in the development of atherosclerotic cardiovascular disease; however, few stu

72 stablished predictor of future major adverse atherosclerotic cardiovascular events in asymptomatic in

73 olymorphisms that could modulate the risk of atherosclerotic cardiovascular events.

74 ypertension, diabetes mellitus, obesity, and atherosclerotic cardiovascular risk) underlies the relat

75 The endothelial damage in atherosclerotic carotid arteries was assessed by electro

76 d for patients with moyamoya vasculopathy or atherosclerotic cerebrovascular disease who had undergon

77 plasma endothelial cell-derived exosomes in atherosclerotic cerebrovascular disease.

78 and impact age-related tissue stiffening and atherosclerotic changes.

79 as a putative link between hyperglycemia and atherosclerotic complications in diabetes.

80 rge arteries in healthy, hyperlipidemic, and atherosclerotic conditions.

81 ischaemic electrocardiographic changes or an atherosclerotic culprit lesion identified during angiogr

82 s from 1990 to 2011 for all causes, any CVD, atherosclerotic CVD (ACVD), coronary artery disease (CAD

83 timal performance and a narrow focus on only atherosclerotic CVD (ASCVD).

84 Relative to 1990-2001, atherosclerotic CVD and CAD rates began to decline more

85 in 352 HIV-infected adults without clinical atherosclerotic CVD and not on statins.

86 ify HIV-infected adults who are at increased atherosclerotic CVD risk and may be considered for stati

87 testing modalities would improve global and atherosclerotic CVD risk assessment among individuals wi

88 Baseline carotid atherosclerosis but not atherosclerotic CVD risk scores was an independent predi

89 Intracranial atherosclerotic disease (ICAD) is an important cause of

90 iplatelet therapy for patients with coronary atherosclerotic disease and might be more effective than

91 erved in patients with CKD but without overt atherosclerotic disease and with few traditional risk fa

92 Diabetic kidney disease and atherosclerotic disease are major causes of morbidity an

93 loci and identify candidate genes for human atherosclerotic disease based on circular chromosome con

94 c nitrate might prove useful in ameliorating atherosclerotic disease in Apolipoprotein (Apo)E knockou

95 Intracranial atherosclerotic disease is a highly prevalent cause of s

96 data suggest evolocumab use in patients with atherosclerotic disease is efficacious and safe in patie

97 cumab versus placebo in 27 564 patients with atherosclerotic disease on statin therapy followed for a

98 for 37 disease susceptibility loci for human atherosclerotic disease that are of potential interest t

99 onth) versus placebo in 27 564 patients with atherosclerotic disease who were on statin therapy, foll

100 eptibility loci for their underlying disease-atherosclerotic disease-identification of candidate gene

101 l utility in the prophylaxis of inflammatory atherosclerotic disease.

102 ere considered representative of significant atherosclerotic disease.

103 le risk factors associated with intracranial atherosclerotic disease.

104 y heart disease and cerebrovascular or other atherosclerotic diseases.

105 n-mai-jia (XMJ) recouples eNOS to exert anti-atherosclerotic effects.

106 Level Management to Understand its Impact in Atherosclerotic Events), a trial of torcetrapib (a chole

107 Monocyte recruitment from flowing blood to atherosclerotic foci is the key first step in the develo

108 ed all patients into atherosclerotic and non-atherosclerotic groups for the prespecified, exploratory

109 , elevating LDL cholesterol and accelerating atherosclerotic heart disease, making it a promising car

110 nt cohort study of donor-matched healthy and atherosclerotic human aorta tissue (n = 15) and human ca

111 aques was validated by ex vivo imaging of an atherosclerotic human coronary artery at 16 frames per s

112 erior ciliary artery (PCA) occlusion in old, atherosclerotic, hypertensive monkeys to that in young m

113 normal, healthy rhesus monkeys and 8 of old, atherosclerotic, hypertensive monkeys.

114 milar in both the young healthy and the old, atherosclerotic, hypertensive monkeys.

115 ted (68)Ga-DOTATATE PET as a novel marker of atherosclerotic inflammation and confirmed that (68)Ga-D

116 the M2 state are required for resolution of atherosclerotic inflammation and plaque regression.

117 uggest that endothelial EphA2 contributes to atherosclerotic inflammation by promoting monocyte firm

118 ype-2 (SST2)-binding PET tracer, for imaging atherosclerotic inflammation.

119 Myeloid cells are central to atherosclerotic lesion development and vulnerable plaque

120 First, atherosclerotic lesion development in hyperlipidemic apo

121 Atherosclerotic lesion development in response to high-c

122 versed vascular inflammation and accelerated atherosclerotic lesion formation in cholesterol-fed Ldlr

123 =12-15) or SMCs (n=13-24) markedly increased atherosclerotic lesion formation in hyperlipidemic mice.

124 tial to provide a comprehensive insight into atherosclerotic lesion formation, diagnostics and respon

125 of Ldlr-/- Arhgef1-/- with WT BM exacerbated atherosclerotic lesion formation, supporting Arhgef1 act

126 Csn5 in Apoe(-/-) mice markedly exacerbated atherosclerotic lesion formation.

127 METHODS AND No difference in atherosclerotic lesion size was found in Ldlr(-/-) (low-

128 ase is often triggered by a distinct type of atherosclerotic lesion that displays features of impaire

129 In the atherosclerotic lesion, macrophages ingest high levels o

130 t-like structures have also been detected in atherosclerotic lesions and arterial thrombi in humans a

131 AMPKalpha1(-/-) mice showed reduced sizes of atherosclerotic lesions and lesser numbers of macrophage

132 significantly upregulated on macrophages in atherosclerotic lesions and M1 macrophages in vitro.

133 Monocyte-derived macrophages, located in atherosclerotic lesions and presenting heterogeneous phe

134 essed a cleavage-resistant variant of MerTK, atherosclerotic lesions exhibited higher macrophage MerT

135 fter dexamethasone treatment and in advanced atherosclerotic lesions in fat-fed Ldlr(-/-) mice.

136 erotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation

137 type, and decreased the progression of early atherosclerotic lesions in mice.

138 r heterozygous Tet2 knockout mice had larger atherosclerotic lesions in the aortic root and aorta tha

139 pendent reduction of LKB1 levels occurred in atherosclerotic lesions in western diet-fed Ldlr(-/-) an

140 -/-)LKB1(fl/fl)LysM(cre) mice developed more atherosclerotic lesions in whole aorta and aortic root a

141 d that CaMKIIgamma-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIgamma had

142 DOL-induced dyslipidemia caused formation of atherosclerotic lesions of an intermediate stage, which

143 in activated T cells that infiltrate in vivo atherosclerotic lesions of primary APS patients with ath

144 It has been known for some time that atherosclerotic lesions preferentially develop in areas

145 rol diet, P2X7-deficient mice showed smaller atherosclerotic lesions than P2X7-competent mice (0.162

146 ly, structural and biochemical features from atherosclerotic lesions were acquired in ex vivo human c

147 s of inflammation including amyloid plaques, atherosclerotic lesions, and arthritic joints.

148 P2X7 receptor was higher expressed in murine atherosclerotic lesions, particularly by lesional macrop

149 ed more trafficking of Ly6c(hi) monocytes to atherosclerotic lesions, preferential differentiation of

150 e observe increased P2X7 expression in human atherosclerotic lesions, suggesting that our findings in

151 ival, as well as differentiation in advanced atherosclerotic lesions.

152 hancing recruitment of Ly6c(hi) monocytes to atherosclerotic lesions.

153 educe macrophage cholesterol accumulation in atherosclerotic lesions.

154 lls (SMCs), and endothelial cells from mouse atherosclerotic lesions.

155 IRF5 affects the formation and phenotype of atherosclerotic lesions.

156 plasma cholesterol and TG levels and reduced atherosclerotic lesions.

157 ay allow for molecular imaging of vulnerable atherosclerotic lesions.

158 ulation is a key characteristic of advancing atherosclerotic lesions.

159 que inflammation and progression to advanced atherosclerotic lesions.

160 and macrophage-derived foam cells and cause atherosclerotic lesions.

161 f bifurcated vessels that are susceptible to atherosclerotic lesions.

162 ) mice have a significant increase of aortic atherosclerotic lesions.

163 etion in myeloid cells increased the size of atherosclerotic lesions.

164 lipid-laden macrophages that infiltrate the atherosclerotic lesions.

165 lerosis by enhancing monocyte recruitment to atherosclerotic lesions.

166 racy of measurements and characterization of atherosclerotic lesions.

167 Compared with nonatherosclerotic-MSCs, atherosclerotic-MSCs displayed higher levels of both int

168 d at restoring the mitochondrial function of atherosclerotic-MSCs improve their in vitro immunosuppre

169 ochondrial reactive oxygen species levels of atherosclerotic-MSCs promoted a phenotypic switch charac

170 An impaired mitochondrial function of atherosclerotic-MSCs underlies their altered secretome a

171 Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species sc

172 ipose tissue-derived MSCs were isolated from atherosclerotic (n=38) and nonatherosclerotic (n=42) don

173 poE(-/-)) mice on a high fat (HF) diet as an atherosclerotic obesity model, we demonstrated 1) microR

174 es to the management of extracranial carotid atherosclerotic occlusive disease and the basis of these

175 Extracranial internal carotid artery atherosclerotic occlusive disease is a common ischemic s

176 in patients with acute cerebral ischaemia of atherosclerotic origin.

177 Atherosclerotic peripheral artery disease affects 8% to

178 Coronary artery calcified atherosclerotic plaque (CAC) predicts cardiovascular dis

179 iseases; although their contributory role to atherosclerotic plaque and abdominal aortic aneurysm sta

180 ction, both important factors in maintaining atherosclerotic plaque and aneurysm stability.

181 ced endothelial cell activation and elevated atherosclerotic plaque burden compared with Ldlr(-/-) mi

182 ticipated in the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Thera

183 that LOY is associated with the severity of atherosclerotic plaque characteristics and outcome in me

184 Atherosclerotic plaque destabilization is the major dete

185 by plasma cells and determine the impact on atherosclerotic plaque development in mice with and with

186 g lymphatic function to lipid metabolism and atherosclerotic plaque development.

187 inflammation thought to precede and underlie atherosclerotic plaque formation and instability.

188 thelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endotheli

189 Atherosclerotic plaque formation results from chronic in

190 (-/-)Apoe(-/-) knockout mice show diminished atherosclerotic plaque formation, characterized by reduc

191 olesterol diet, Tcad/ApoE-DKO mice increased atherosclerotic plaque formation, despite a 5-fold incre

192 olipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation.

193 to ER stress, is a hallmark of all stages of atherosclerotic plaque formation.

194 ays a protective role against neointimal and atherosclerotic plaque formations.

195 coupled eNOS and reduced the size of carotid atherosclerotic plaque in rats feeding with high fat die

196 cannot distinguish between intima, media, or atherosclerotic plaque in the carotid artery.

197 hletes despite the presence of more coronary atherosclerotic plaque in the most active participants.

198 helial interactions also contribute to early atherosclerotic plaque initiation and growth.

199 LOY was also present in atherosclerotic plaque lesions (n=8/242, 3%).

200 mulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-ca

201 sted LOY for association with (inflammatory) atherosclerotic plaque phenotypes and cytokines and asse

202 Atherosclerotic plaque rupture is accompanied by an acut

203 Inflammation drives atherosclerotic plaque rupture.

204 tilized the apoE(-/-) mouse model to compare atherosclerotic plaque size and composition after inorga

205 -helper type-1 immune responses, and reduced atherosclerotic plaque size without altering the plasma

206 al expansion and led to a marked increase in atherosclerotic plaque size.

207 GAPDH levels were reduced in atherosclerotic plaque SMCs, and this effect correlated

208 eractions may be a novel therapy to increase atherosclerotic plaque stability.

209 ivo histopathologic quantitative measures of atherosclerotic plaque tissue characteristics, as well a

210 attenuated, and local antibody deposition in atherosclerotic plaque was absent.

211 MIs result spontaneously from instability of atherosclerotic plaque, whereas type 2 MIs occur in the

212 dothelium predisposes it toward formation of atherosclerotic plaque, which may be a subsequent risk f

213 ctor-alpha, a macrophage M1 marker, in human atherosclerotic plaque.

214 L3 deficiency showed no evidence of coronary atherosclerotic plaque.

215 e has long been a hallmark of the vulnerable atherosclerotic plaque.

216 in removing lipids and debris present in the atherosclerotic plaque.

217 (inflammatory) from stable (noninflammatory) atherosclerotic plaque.

218 ia other mechanisms than inflammation in the atherosclerotic plaque.

219 -181b was overexpressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms a

220 es was located in macrophage-rich regions of atherosclerotic plaques and correlated with the intensit

221 and extracellular matrix deposition both in atherosclerotic plaques and in vascular smooth muscle ce

222 KB1 expression was examined in human carotid atherosclerotic plaques and in western diet-fed atherosc

223 und that LINC00305 expression is enriched in atherosclerotic plaques and monocytes.

224 inflammatory state and macrophage burden of atherosclerotic plaques and potentially identify vulnera

225 Cholesterol crystals (CC) are abundant in atherosclerotic plaques and promote inflammatory respons

226 Atherosclerotic plaques are one of the primary complicat

227 phages surrounding calcium deposits in human atherosclerotic plaques are phenotypically defective bei

228 nhibitor reduced (125)I-pentixafor uptake in atherosclerotic plaques by approximately 40%.

229 fold induction of (18)F-FDG uptake in murine atherosclerotic plaques by both M-CSF and GM-CSF.

230 Here Htun et al. demonstrate that vulnerable atherosclerotic plaques generate near-infrared autofluor

231 lating CCR2(+) monocytes and the size of the atherosclerotic plaques in both the carotid artery and t

232 h cortistatin reduced the number and size of atherosclerotic plaques in carotid artery, heart, aortic

233 Snail was also expressed in EC overlying atherosclerotic plaques in coronary arteries from patien

234 Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced at

235 on imaging and early detection of high-risk atherosclerotic plaques is important for risk stratifica

236 y GM-CSF and M-CSF in either cell culture or atherosclerotic plaques may not be distinguishable by th

237 expression on inflammatory cells present in atherosclerotic plaques of an experimental rabbit model.

238 Male athletes had a higher prevalence of atherosclerotic plaques of any luminal irregularity (44.

239 evation in smooth muscle accumulation within atherosclerotic plaques of ApoE KO mice, suggesting plaq

240 were detected in vivo with PET/MR imaging in atherosclerotic plaques of the abdominal aorta and right

241 he identification of patients with high-risk atherosclerotic plaques prior to the manifestation of cl

242 ously demonstrated that both human and mouse atherosclerotic plaques show elevated expression of EphA

243 peptide expressed in the vascular system and atherosclerotic plaques that regulates vascular calcific

244 Atherosclerotic plaques transplanted into WT or Ccr5-/-

245 ammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression.

246 ed lipids in endarterectomized human carotid atherosclerotic plaques using three-dimensional (3D) ele

247 Atherosclerotic plaques were induced by endothelial abra

248 -) mice show reduced progression to advanced atherosclerotic plaques with diminished smooth muscle an

249 vel technology that allows identification of atherosclerotic plaques with intraplaque hemorrhage and

250 ly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-14

251 occlusion localized at the site of high-risk atherosclerotic plaques, of which early detection and th

252 lial nitric oxide synthase, the stability of atherosclerotic plaques, the production of proinflammato

253 Because HILPDA is highly expressed in atherosclerotic plaques, we examined its regulation and

254 ey autophagy markers in both mouse and human atherosclerotic plaques.

255 o identify a protein signature for high-risk atherosclerotic plaques.

256 se uptake in cultured macrophages and murine atherosclerotic plaques.

257 se-7 (Mmp-7) reduced VSMC apoptosis in mouse atherosclerotic plaques.

258 esterol fecal excretion and reduces inflamed atherosclerotic plaques.

259 a key factor in the development of necrotic atherosclerotic plaques.

260 e platforms accumulated to similar levels in atherosclerotic plaques.

261 vents, such as thrombosis, is the rupture of atherosclerotic plaques.

262 on of calcium phosphate minerals in advanced atherosclerotic plaques.

263 ound on the surface of inflamed and ruptured atherosclerotic plaques.

264 the assessment of macrophage infiltration in atherosclerotic plaques.

265 oteolytic inactivation by other proteases in atherosclerotic plaques.

266 scular cell adhesion molecule 1 (VCAM-1), in atherosclerotic plaques.

267 as surrounding the calcium deposits in human atherosclerotic plaques.

268 and neutrophils in the perivascular area of atherosclerotic plaques.

269 /wk group had a higher prevalence of CAC and atherosclerotic plaques.

270 cy in reducing macrophage burden in advanced atherosclerotic plaques.

271 both the development and the progression of atherosclerotic plaques.

272 heir efficacy to reduce macrophage burden in atherosclerotic plaques.

273 ng with CXCR4 transcript expression in human atherosclerotic plaques.

274 ivation of platelets at the site of ruptured atherosclerotic plaques.

275 ry major cardiovascular events in a severely atherosclerotic population.

276 sts a role for LOX-1 in various steps of the atherosclerotic process, from initiation to plaque desta

277 dition, blocking studies were performed in 2 atherosclerotic rabbits with preinjection of the CXCR4 i

278 Atherosclerotic renal artery stenosis reduces renal bloo

279 udies were performed in patients with severe atherosclerotic renal artery stenosis scheduled for PTRA

280 ction, oxygenation, and RBF in patients with atherosclerotic renal artery stenosis undergoing PTRA.

281 rove outcomes of revascularization for human atherosclerotic renal artery stenosis.

282 Atherosclerotic renovascular disease (RVD) reduces renal

283 middle-age and older (masters) athletes with atherosclerotic risk factors for coronary artery disease

284 felong masters endurance athletes with a low atherosclerotic risk profile have normal CAC scores.

285 rtery disease in masters athletes with a low atherosclerotic risk profile.

286 ialysis, who have an unexplained increase in atherosclerotic risk, had significantly higher RBC chole

287 Human and mouse atherosclerotic samples and primary mouse macrophages we

288 Intracranial atherosclerotic stenosis (ICAS) is a common cause of isc

289 We found a treatment-by-atherosclerotic stenosis interaction (p=0.017).

290 m was to test for a treatment-by-ipsilateral atherosclerotic stenosis interaction in a subgroup analy

291 Potentially symptomatic ipsilateral atherosclerotic stenosis was reported in 3081 (23%) of 1

292 emic attack when associated with ipsilateral atherosclerotic stenosis.

293 Large artery atherosclerotic stroke (LAS) shows substantial heritabil

294 primary aortic endothelial cells and ex-vivo atherosclerotic tissue with IFN-gamma and TNF-alpha and

295 ich vegetables translates to a lower risk of atherosclerotic vascular disease (ASVD) mortality.The ob

296 Patients with atherosclerotic vascular disease remain at high risk for

297 Among patients with atherosclerotic vascular disease who were receiving inte

298 ontrolled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving inte

299 ive capacity of macrophages as a therapy for atherosclerotic vascular disease.

300 KLF2 could be a novel therapeutic target for atherosclerotic vascular disease.