ライフサイエンスコーパス: atheroma

1 luble drugs and their subsequent delivery to atheroma.

2 ) is cross-linked and dysfunctional in human atheroma.

3 sed by histopathological analysis of excised atheroma.

4 eas versus smooth muscle cell regions of the atheroma.

5 ped as sites of apoA1 oxidation within human atheroma.

6 larization is critical to destabilization of atheroma.

7 ramural vasculitic lesions, and the inflamed atheroma.

8 ously used for assessing inflammation within atheroma.

9 osphorylation is observed in mouse and human atheroma.

10 mage vasa vasorum anatomy in relation to the atheroma.

11 clinical arena for the detection of clinical atheroma.

12 veloped to identify inflammation in coronary atheroma.

13 present different stages in the evolution of atheroma.

14 uptake have been advocated as indicators of atheroma.

15 PO-catalyzed oxidative modification in human atheroma.

16 veral steps involved in the initiation of an atheroma.

17 t for two months to create various stages of atheroma.

18 odds of stroke in patients with severe arch atheroma.

19 ctomy and 8 controls without culprit carotid atheroma.

20 may help to identify biologically high-risk atheroma.

21 stic and therapeutic biomarkers for advanced atheroma.

22 (SPRR3), in vascular smooth muscle cells of atheromas.

23 the col(V)-rich adventitia subjacent to the atheromas.

24 s expressed by VSMCs in both human and mouse atheromas.

25 ed monocytes, infarcted myocardium and human atheromas.

26 in the intima was primarily associated with atheromas.

27 ularity in regions of inflammation of active atheromas.

28 sponses in human AAAs compared with stenotic atheromas.

29 in SPC migration and their recruitment into atheromas.

30 uptake in culprit versus nonculprit carotid atheroma, (2) spatial distributions of uptake, and (3) h

31 can influence the collagen content of mouse atheroma, a critical component of plaque stability.

32 nt mechanisms drive stenosis development and atheroma accumulation.

33 medial thickness and the volume of coronary atheroma also can be reduced by LDL cholesterol reductio

34 ed cells to conditions thought to operate in atheroma and determined rates of glucose uptake.

35 expression of CD44 and variants within human atheroma and in abdominal aortic aneurysm as well as the

36 In the inflamed atheroma and in arteritic lesions, pathogenic T cells co

37 ocalcification is a key feature of high-risk atheroma and is associated with increased morbidity and

38 Statins can regress coronary atheroma and lower clinical events.

39 that recruits monocytes into the developing atheroma and may contribute to atherosclerotic disease d

40 Despite hyperlipidemia, development of atheroma and occlusive, inflammatory arterial neointimal

41 active oral T. denticola infection with both atheroma and periodontal disease.

42 f ApoE(-/-)/MMP8(-/-) mice had fewer SPCs in atheromas and smaller lesions than ApoE(-/-)/MMP8(-/-) m

43 ithin HDL-like particles isolated from human atheroma, and identification of a probable contact site

44 vessel caliber, significant calcification or atheroma, and severe tortuosity may place patients at pr

45 s on the frequencies of three major types of atheroma, and with epidemiological data on the prevalenc

46 lipoprotein A1 (apoA1), recovered from human atheroma are dysfunctional and are extensively oxidized

47 Here we review the evidence for aortic-arch atheroma as an important independent risk factor for str

48 T1 receptor expression and function on other atheroma-associated cell types is unknown.

49 tes of vascular inflammation activates major atheroma-associated cells including endothelial cells, p

50 mpared with regard to the extent of coronary atheroma at baseline and subsequent change in response t

51 dence linking cerebral SVD with large vessel atheroma, atrial fibrillation, heart failure, and heart

52 on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID) assessed whether rosuvastatin

53 te of patients showing substantial change in atheroma burden (at least 5% change in PAV, 70% vs. 53%,

54 on Intravascular Ultrasound-Derived Coronary Atheroma Burden [ASTEROID]) was performed at 53 communit

55 ed IVUS pullback was used to assess coronary atheroma burden at baseline and after 24 months of treat

56 ors with volumetric measurements of coronary atheroma burden in patients with coronary artery disease

57 Changes in atheroma burden monitored by intravascular ultrasound we

58 ly whether the locus contributes to coronary atheroma burden or plaque instability.

59 rtery disease underwent serial evaluation of atheroma burden with intravascular ultrasound imaging.

60 the vulnerable patient has evolved, with the atheroma burden, its metabolic activity, and the disposi

61 s treated with atorvastatin had no change in atheroma burden, whereas patients treated with pravastat

62 etween changes in LDL-C and HDL-C levels and atheroma burden.

63 ERalphaAF-1, which is sufficient to prevent atheroma, but not to accelerate endothelial healing.

64 Finally, cholesterol was imaged in the atheroma by doping the charge labeling reagent betaine a

65 The Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvast

66 decrease in the prevalence of thin cap fibro-atheroma by optical coherence tomography in DM and non-D

67 ins unclear if statins can modulate coronary atheroma calcification in vivo.

68 regressive effects, statins promote coronary atheroma calcification.

69 Atheromas calcify as cells in the lesion undergo apoptos

70 hat periodontal bacteria obtained from human atheromas can cause atherosclerosis in animal models of

71 vivo; and 7) periodontal isolates from human atheromas can cause disease in animal models of infectio

72 ease that included aorta and coronary artery atheroma, cardiac hypertensive disease, myocardial infar

73 nuclear factor-kappaB activation (P<0.05) in atheroma cell cultures.

74 ne and chemokine production in ex vivo human atheroma cell cultures.

75 and associated intraplaque inflammation and atheroma cell proliferation.

76 x expression was markedly increased in human atheroma compared with normal tissue from the same carot

77 irm specific echogenic immunoliposome (ELIP) atheroma component enhancement in vivo.

78 cterization of the type and extent of active atheroma components and may allow more directed therapy.

79 ion of angiogenesis, liposomes for targeting atheroma components, and microbubbles for imaging transp

80 LIPs specifically enhance endothelial injury/atheroma components.

81 the hypothesis that monocyte accumulation in atheroma correlates with the extent of disease by using

82 18a1(+/-) heterozygote mice showed increased atheroma coverage and enhanced lipid accumulation compar

83 We used experimental mouse models, human atheroma cultures, and well-established human biobanks t

84 Moreover, in human atheroma cultures, TLR7 activation selectively suppresse

85 emonstrate that this organism can accelerate atheroma deposition in animal models.

86 chanisms that link all these risk factors to atheroma development and the clinical manifestations of

87 CC appear early in the atheroma development and trigger inflammation by NLRP3 i

88 We assembled a network describing atheroma development from the literature.

89 ntitis impacts inflammatory responses during atheroma development, thrombotic events or myocardial in

90 d mechanism of chromosome 9p21 for promoting atheroma development.

91 ls and underlying mechanism(s) that regulate atheroma-enriched SPRR3 expression in vascular smooth mu

92 The lipid composition can vary among atheroma, even within a single individual, and is also d

93 ic plaques will improve the understanding of atheroma evolution and could facilitate evaluation of th

94 Vascular atheroma excised at endarterectomy and endomyocardial bi

95 In line with this, MKP-1-null atheroma exhibited less macrophage content.

96 Furthermore, macrophages from advanced human atheromas exhibited increased CAPN6 induction and impair

97 We found that SPCs in atheromas expressed MMP8 and that MMP8 knockout signific

98 r metabolically active and those with active atheroma, faster disease progression, and increased risk

99 f healthy aortas (media layer) or with early atheroma (fatty streak and fibrolipidic, media and intim

100 ge) was higher in culprit than in nonculprit atheroma for both FDG (2.08 [0.52] versus 1.89 [0.40]; P

101 athways that regulate their participation in atheroma formation and complication.

102 rate that senescent cells are key drivers of atheroma formation and maturation and suggest that selec

103 levels modulate processes critical for early atheroma formation and suggest that pfn heterozygosity c

104 n human atheromatous tissue, and accelerates atheroma formation in apolipoprotein E-/- mice with conc

105 to determine whether testosterone modulates atheroma formation via its classic signaling pathway inv

106 hat monocytes accumulate continuously during atheroma formation, accumulation increases in proportion

107 The host immune response favors atheroma formation, maturation and exacerbation.

108 activation is a central initiating event in atheroma formation.

109 e present study addressed the role of pfn in atheroma formation.

110 M-/-) BMDMs may have contributed to unstable atheroma formation.

111 s that together potentially reverse advanced atheroma formation.

112 iations for microinfarction were: TAVI (arch atheroma grade: r=0.46; P=0.0001) and SAVR (concomitant

113 The macrophage-rich core of advanced human atheroma has been demonstrated to be hypoxic, which may

114 tive molecular components of endothelium and atheroma have been developed.

115 d its ligand CCL20 are also present in human atheroma; however, their functional roles in atherogenes

116 Atheroma imaging has become an integral component of the

117 odontal disease and the rapid progression of atheroma in ApoE(-/-) mice.

118 We analyzed human coronary atheroma in de novo and restenotic disease to identify t

119 ws assessment of inflammation within carotid atheroma in symptomatic and asymptomatic patients.

120 l lesion size makes it difficult to identify atheroma in the coronaries with conventional imaging equ

121 is capable of transferring cholesterol from atheroma in the vessel wall to the liver.

122 nanoparticles in human coronary artery-sized atheroma in vivo (P<0.05 versus reference segments).

123 ify macrophage infiltration in human carotid atheroma in vivo and hence may be a surrogate marker of

124 d increases (18)F-FDG uptake within inflamed atheroma in vivo.

125 presence of more risk factors, the extent of atheroma in women with angiographic CAD is less than in

126 n macrophages, the induction of CAPN6 in the atheroma interior limited macrophage movements, resultin

127 The optimum MR imaging time for carotid atheroma is 48 hrs after its administration.

128 However, aortic arch atheroma is a common post-mortem finding, and it seems r

129 Inflammation in atheroma is associated with large numbers of macrophages

130 nown whether progression of aortic arch (AA) atheroma is associated with vascular events in patients

131 One desirable characteristic of atheroma is their stability, as the rupture of unstable

132 compared with control ApoE-/- mice, although atheroma lesion size, intimal macrophage accumulation, a

133 highly enriched in Lp-PLA2; and in advanced atheroma, Lp-PLA2 levels are highly upregulated, colocal

134 he expression of cholesterol transporters on atheroma macrophages leading to increased efflux of chol

135 uptake and, probably, FdG uptake signals in atheroma may reflect hypoxia-stimulated macrophages rath

136 Furthermore, ELIP enhanced atheroma MGS by 39 +/- 18% (n = 8).

137 g, and it seems reasonable to speculate that atheroma might give rise to thrombi with distal embolism

138 pDCs were identified in 53% of carotid atheromas (n=30) in which they localized to the shoulder

139 pothesis for the rupture of thin fibrous cap atheroma, namely that minute (10-mum-diameter) cellular-

140 flammation Using Magnetic Resonance Imaging [ATHEROMA]; NCT00368589).

141 tected in macrophage-positive area of aortic atheroma of ApoE-null mice, but not in healthy aorta.

142 n the adventitia, and to a lesser extent the atheroma, of atherosclerotic carotid arteries.

143 iminary study of stroke/TIA patients with AA atheroma on transesophageal echocardiogram, AA atheroma

144 uent embolization of debris from aortic arch atheroma or from the calcified valve itself ranges betwe

145 OxTrp72-apoA1 recovered from human atheroma or plasma is lipid poor, virtually devoid of ch

146 d with cardiovascular risk markers, coronary atheroma, or CHD.

147 -CyAm7 nanoparticles accumulated in areas of atheroma (P<0.05 versus reference areas).

148 ischemic stroke in a setting of intracranial atheroma, patent cardiac foramen ovale, or elevated leve

149 cking CD69 on lymphoid cells developed large atheroma plaque along with an increased Th17/regulatory

150 ecreases their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification

151 approximately 30 times and contribute to the atheroma plaque.

152 Large atheroma, plaque thrombosis, macrophages, and calcificat

153 icant differences in the presence of carotid atheroma plaques and the severity of periodontitis (P =

154 were recorded in relation to the presence of atheroma plaques in the carotid intima.

155 d with the formation, growth, and rupture of atheroma plaques, and the subsequent formation of clots,

156 as seen to influence the presence of carotid atheroma plaques.

157 This pathway may be related to human atheroma progression and destabilization through intrapl

158 the association between apolipoprotein B and atheroma progression highlights the potential importance

159 a-blocker therapy is associated with reduced atheroma progression in adults with known coronary arter

160 lyceride/HDL-C ratio correlated with delayed atheroma progression in diabetic patients.

161 We investigated coronary atheroma progression in patients with low levels of low-

162 The purpose of this study was to determine atheroma progression in patients with spotty calcificati

163 n-Meier curves showed fewer patients with AA atheroma progression remained free of the composite vasc

164 AA atheroma progression was associated with composite vascu

165 heroma on transesophageal echocardiogram, AA atheroma progression was associated with recurrent vascu

166 Coronary atheroma progression was evaluated by serial intravascul

167 with the favorable effect of pioglitazone on atheroma progression.

168 itus is associated with accelerated coronary atheroma progression.

169 the effect of medical therapies on coronary atheroma progression.

170 a profound impact on the natural history of atheroma progression.

171 bjects who participated in serial studies of atheroma progression.

172 nges in HDL-C were inversely correlated with atheroma progression.

173 t promote inflammation and interact with the atheroma, promotion of dyslipidemia with consequent incr

174 romote selective migration from the media of atheroma-prone SMCs characterized by calmodulin overexpr

175 Substantial atheroma regression (> or =5% reduction in atheroma volu

176 dy was to determine the relationship between atheroma regression and arterial wall remodeling.

177 place in the arterial wall that accompanied atheroma regression in this study.

178 Substantial atheroma regression, compared to progression, was associ

179 o -0.10]) remained independent predictors of atheroma regression.

180 TAV) and the percentage of participants with atheroma regression.

181 Optical imaging of atheroma revealed >100% NIRF signal increases in apolipo

182 ells into the atheroma was examined in human atheroma-SCID mouse chimeras.

183 d similarly to the parent antibody in murine atheroma showing promise for future translation.

184 LOY in blood was associated with a larger atheroma size (odds ratio, 2.15; 95% confidence interval

185 rosis by 40% and decreased the prevalence of atheroma SMCs by 35%, suggesting that beta-arrestin2 pro

186 the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression.

187 the expression of CXCL16 in human and mouse atheroma, suggest that CXCL16 plays a role in atheroscle

188 lipids from surgically removed human carotid atheroma, suggesting that they may play a role in human

189 ddition, the hydrophobic core and endogenous atheroma-targeting ability of sHDL allow for encapsulati

190 esterol efflux from macrophages and enhanced atheroma-targeting relative to free drug.

191 Aortic atheroma (TAVI) and concomitant coronary artery bypass g

192 1 (Tyr71), a modified residue found in human atheroma that is critical for HDL binding and PON1 funct

193 holipid (oxPC) molecular species enriched in atheroma that serve as endogenous ligands for the scaven

194 arise from thrombosis of lipid-rich coronary atheromas that have large plaque burden despite angiogra

195 If these events are due to occult atheroma, the risk-factor profile and coronary prognosis

196 entive action on the development of arterial atheroma, their effect on platelet function in vivo rema

197 IFN-alpha transcript concentrations in atheroma tissues correlated strongly with plaque instabi

198 e tissue factor procoagulant activity within atheroma to initiate a positive feedback loop where thro

199 associated with less progression of percent atheroma volume (+0.16 +/- 0.27% vs. +0.76 +/- 0.20%, p

200 demonstrated greater progression of percent atheroma volume (+0.58 +/- 0.38 vs. +0.23 +/- 0.3%, p =

201 .38 vs. +0.23 +/- 0.3%, p = 0.009) and total atheroma volume (-0.17 +/- 2.69 mm(3) vs. -2.05 +/- 2.15

202 ile showed significant regression of percent atheroma volume (-0.69+/-0.27%, P=0.01).

203 4% vs. +0.29 +/- 0.13%, p < 0.001) and total atheroma volume (-3.0 +/- 1.9 mm(3) vs. +1.0 +/- 1.4 mm(

204 7.6% vs. 29.0 +/- 8.5%; p < 0.001) and total atheroma volume (174.6 +/- 71.9 mm(3) vs. 133.9 +/- 64.9

205 STEMI demonstrated greater segmental percent atheroma volume (40.4 +/- 12 versus 27.5 +/- 14%, P<0.00

206 Patients with PAD had a greater percent atheroma volume (40.4 +/- 9.2% vs. 38.5 +/- 9.1%, p = 0.

207 in segmental lumen volume identified percent atheroma volume (beta=-0.18, P=0.0004), high-sensitivity

208 icacy parameter was the percentage change in atheroma volume (follow-up minus baseline).

209 LDL-C <or=70 mg/dl included baseline percent atheroma volume (p = 0.001), presence of diabetes mellit

210 percent atheroma volume (p = 0.03) and total atheroma volume (p = 0.02).

211 DL-C were associated with changes in percent atheroma volume (p = 0.03) and total atheroma volume (p

212 ficacy parameters, including change in total atheroma volume (P =.02), change in percentage atheroma

213 heroma volume (P =.02), change in percentage atheroma volume (P<.001), and change in atheroma volume

214 s, women had less plaque in terms of percent atheroma volume (PAV) (33.9 +/- 10.2% vs. 37.8 +/- 10.3%

215 calcification demonstrated a greater percent atheroma volume (PAV) (36.0 +/- 7.6% vs. 29.0 +/- 8.5%;

216 etic patients demonstrated a greater percent atheroma volume (PAV) (40.2 +/- 0.9% vs. 37.5 +/- 0.8%,

217 These patients had a greater percentage atheroma volume (PAV) (45% vs. 34%, p < 0.001), total at

218 =120 mm Hg) had less progression in percent atheroma volume (PAV) (p < 0.001) and total atheroma vol

219 trasound, serial changes in coronary percent atheroma volume (PAV) and CaI were measured across match

220 nship between baseline and change in percent atheroma volume (PAV) and total atheroma volume with inc

221 Primary outcome was change in percent atheroma volume (PAV) from baseline to 1 year measured b

222 Change in percent atheroma volume (PAV) from baseline to study completion.

223 efficacy parameter was the change in percent atheroma volume (PAV) from baseline to study completion.

224 cy measure was the nominal change in percent atheroma volume (PAV) from baseline to week 78, measured

225 The primary efficacy end point, percent atheroma volume (PAV), decreased by 0.99% (95% confidenc

226 vincing evidence of regression using percent atheroma volume (PAV), the most rigorous IVUS measure of

227 ary efficacy parameter was change in percent atheroma volume (PAV); the secondary efficacy parameter

228 in EEM volume correlated with the decreased atheroma volume (r = 0.62), but there was no correlation

229 ng/min; P=0.001) and correlated with percent atheroma volume (r(s)=0.37, P=0.04).

230 rved between changes in HDL-C and percentage atheroma volume (r=-0.17, P<0.001).

231 .2% vs. 37.8 +/- 10.3%, p < 0.001) and total atheroma volume (TAV) (148.7 +/- 66.6 mm3 vs. 194.7 +/-

232 .9% vs. 37.5 +/- 0.8%, p < 0.0001) and total atheroma volume (TAV) (199.4 +/- 7.9 mm(3) vs. 189.4 +/-

233 volume (PAV) (45% vs. 34%, p < 0.001), total atheroma volume (TAV) (210 vs. 151 mm3, p < 0.001), and

234 atheroma volume (PAV) (p < 0.001) and total atheroma volume (TAV) (p < 0.001), more frequent plaque

235 ures were nominal change in normalized total atheroma volume (TAV) and percentage of patients demonst

236 ters included the change in normalized total atheroma volume (TAV) and the percentage of participants

237 condary efficacy end point, normalized total atheroma volume (TAV), was more favorable with rosuvasta

238 acy parameter was change in normalized total atheroma volume (TAV).

239 The percent atheroma volume (the primary efficacy measure) increased

240 heroma volume averaged 174.5 mm3 and percent atheroma volume 38.9%.

241 This study compared changes in coronary atheroma volume and calcium indices (CaI) in patients re

242 nvestigate mechanistic relationships between atheroma volume and endothelial function in patients wit

243 ons were observed between changes in percent atheroma volume and triglycerides (r = 0.15, p = 0.04),

244 no/phospholipid complexes appeared to reduce atheroma volume as measured by intravascular ultrasound.

245 In 654 subjects, atheroma volume averaged 174.5 mm3 and percent atheroma

246 In contrast, EEM and atheroma volume did not change in the 10-mm segments con

247 fficacy variable, change in normalized total atheroma volume for the entire artery, was also prespeci

248 s no significant difference in the change in atheroma volume for the most diseased vessel segment.

249 companied by a mean (SD) increase in percent atheroma volume from 39.7% (9.8%) to 40.1% (9.7%) (a 0.5

250 ed a significant decrease in coronary artery atheroma volume has sparked great interest in the potent

251 ntravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40

252 the change in PAV and the change in nominal atheroma volume in the 10-mm subsegment with the greates

253 The atheroma volume in the most diseased 10-mm subsegment re

254 The mean (SD) change in atheroma volume in the most diseased 10-mm subsegment wa

255 tage atheroma volume (P<.001), and change in atheroma volume in the most severely diseased 10-mm vess

256 numeric trend toward regression in the total atheroma volume of -12.18 +/- 36.75 mm(3) in the delipid

257 P = .001) and a mean (SD) decrease in total atheroma volume of 2.4 (23.6) mm3 (P<.001).

258 elipidated group versus an increase of total atheroma volume of 2.80 +/- 21.25 mm(3) in the control g

259 antly in the change from baseline of percent atheroma volume on intravascular ultrasound, CRP-modulat

260 with the greatest plaque burden at baseline, atheroma volume regressed by 10.9% with a similar reduct

261 independently associate with greater percent atheroma volume regression (P=0.01).

262 Intravascular ultrasound showed atheroma volume regression in a single coronary artery w

263 dothelium-dependent vasomotor reactivity and atheroma volume remains constant irrespective of the nat

264 Change in total atheroma volume showed a 6.8% median reduction; with a m

265 d with baseline values, the normalized total atheroma volume showed significant regression in the pla

266 Accordingly, atheroma volume statistically significantly decreased at

267 Atheroma volume was determined in serial intravascular u

268 rameters, percent atheroma volume, and total atheroma volume was investigated.

269 The estimated annual change in atheroma volume was statistically significantly less in

270 Quantitative changes in atheroma volume were measured on unenhanced T1-weighted

271 e in percent atheroma volume (PAV) and total atheroma volume with incident major adverse cardiovascul

272 prove the primary efficacy variable (percent atheroma volume) and adversely affected two major second

273 l atheroma regression (> or =5% reduction in atheroma volume) was observed in patients with levels of

274 ascular ultrasound-derived measures (percent atheroma volume), arterial remodeling index, and segment

275 tion, angina, and hypertension (mean [+/-SE] atheroma volume, -2.4 +/- 0.5 mm3/y in treated patients

276 n changes in biochemical parameters, percent atheroma volume, and total atheroma volume was investiga

277 Changes in atheroma volume, as determined by IVUS after adjustment

278 secondary measure, the change in normalized atheroma volume, showed a small favorable effect for tor

279 6 mm3 (least-square mean +/- SE) increase in atheroma volume, those with "pre-hypertensive" BP had no

280 ular ultrasound end point, change in percent atheroma volume, was investigated.

281 hs), greater increases in PAV, but not total atheroma volume, were observed in subjects who experienc

282 on of atherosclerosis--the change in percent atheroma volume--was similar in the pactimibe and placeb

283 o effect was found of torcetrapib on percent atheroma volume.

284 es in lipoprotein levels and coronary artery atheroma volume.

285 therapy could have influenced the changes in atheroma volume.

286 dure remained strong predictors of increased atheroma volume.

287 s were measured at 1-mm intervals to compute atheroma volume.

288 ior revascularization or stroke with percent atheroma volume.

289 The IVUS end point was change in percent atheroma volume.

290 AA atheroma was detected on baseline transesophageal echoca

291 recruitment of (CD4+)CD28- T cells into the atheroma was examined in human atheroma-SCID mouse chime

292 Progression of AA atheroma was observed in 33 patients (28%) on 12-month f

293 ther understand the pathophysiology of human atheroma, we characterized local Ig production and funct

294 chains has previously been reported in human atheromas, we postulated involvement of col(V) autoimmun

295 >or=1 nonobstructive native coronary artery atheroma were randomized to either 7 weekly HDL selectiv

296 Thus, atheromas were characterized by accumulation of choleste

297 s secreted by macrophages in human and mouse atheroma, where it inactivated the migration of macropha

298 easibility of ferumoxytol in imaging carotid atheroma (with histological assessment); and the optimum

299 ration, innate immune marker expression, and atheroma without elevated systemic inflammatory mediator

300 the IL-27 subunit Ebi3 is elevated in human atheromas, yet its function in atherosclerosis remains u