ライフサイエンスコーパス: atheroma

1 eas versus smooth muscle cell regions of the atheroma.

2 ped as sites of apoA1 oxidation within human atheroma.

3 larization is critical to destabilization of atheroma.

4 ramural vasculitic lesions, and the inflamed atheroma.

5 stic and therapeutic biomarkers for advanced atheroma.

6 mage vasa vasorum anatomy in relation to the atheroma.

7 clinical arena for the detection of clinical atheroma.

8 veloped to identify inflammation in coronary atheroma.

9 present different stages in the evolution of atheroma.

10 uptake have been advocated as indicators of atheroma.

11 PO-catalyzed oxidative modification in human atheroma.

12 veral steps involved in the initiation of an atheroma.

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

14 odds of stroke in patients with severe arch atheroma.

15 has been implicated in the development of an atheroma.

16 nsity lipoprotein (LDL) recovered from human atheroma.

17 e fed a high-fat diet for 3 months to induce atheroma.

18 imulated by CD40 ligand, a cytokine found in atheroma.

19 d reactive chlorinating species within human atheroma.

20 progression, and destabilization of vascular atheroma.

21 ctomy and 8 controls without culprit carotid atheroma.

22 may help to identify biologically high-risk atheroma.

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

24 ed monocytes, infarcted myocardium and human atheromas.

25 in the intima was primarily associated with atheromas.

26 ularity in regions of inflammation of active atheromas.

27 sponses in human AAAs compared with stenotic atheromas.

28 in SPC migration and their recruitment into atheromas.

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

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

31 nt mechanisms drive stenosis development and atheroma accumulation.

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

33 Apoptosis is common in advanced human atheroma and contributes to plaque instability.

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

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

46 g, and angiogenesis, and in diseases such as atheroma, arthritis, cancer, and tissue ulceration.

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

48 g (MRDTI) technique demonstrates complicated atheroma as high signal within the carotid arterial wall

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

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

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

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 I Milano/phospholipid complexes (ETC-216) on atheroma burden in patients with acute coronary syndrome

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

58 Changes in atheroma burden monitored by intravascular ultrasound we

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

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

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 Plaque angiogenesis promotes the growth of atheromas, but the functions of plaque capillaries are n

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

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

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

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

69 regressive effects, statins promote coronary atheroma calcification.

70 Atheromas calcify as cells in the lesion undergo apoptos

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

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

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 emonstrate that apolipoprotein C-II in human atheroma co-localizes to regions positive for markers of

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

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

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

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

81 LIPs specifically enhance endothelial injury/atheroma components.

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

83 18a1(+/-) heterozygote mice showed increased atheroma coverage and enhanced lipid accumulation compar

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

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

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

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

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

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

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

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

92 Vascular atheroma excised at endarterectomy and endomyocardial bi

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

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

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

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

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

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

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

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

101 Atheroma formation involves the movement of vascular smo

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

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

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

105 activation is a central initiating event in atheroma formation.

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

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

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

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

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

111 Atheroma imaging has become an integral component of the

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

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

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

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

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

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

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

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

120 xtent of inflammatory cells, not the size of atheromas in apolipoprotein E-deficient mice.

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

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

123 Inflammation in atheroma is associated with large numbers of macrophages

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

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

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

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

128 Atheroma macrophages internalize large quantities of lip

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 approximately 30 times and contribute to the atheroma plaque.

145 Large atheroma, plaque thrombosis, macrophages, and calcificat

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

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

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

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

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

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

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

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

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

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

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

157 AA atheroma progression was associated with composite vascu

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

159 Coronary atheroma progression was evaluated by serial intravascul

160 the effect of medical therapies on coronary atheroma progression.

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

162 bjects who participated in serial studies of atheroma progression.

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

164 with the favorable effect of pioglitazone on atheroma progression.

165 itus is associated with accelerated coronary atheroma progression.

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

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

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

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

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

171 Substantial atheroma regression, compared to progression, was associ

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

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

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

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

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

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

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

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

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

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

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

183 1 (Tyr71), a modified residue found in human atheroma that is critical for HDL binding and PON1 funct

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

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

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

187 in total atheroma volume and average maximal atheroma thickness.

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

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

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

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

192 .38 vs. +0.23 +/- 0.3%, p = 0.009) and total atheroma volume (-0.17 +/- 2.69 mm(3) vs. -2.05 +/- 2.15

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

194 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(

195 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

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

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

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

199 efficacy parameter was the change in percent atheroma volume (follow-up minus baseline) in the combin

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

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

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

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

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

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

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

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

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

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

210 =120 mm Hg) had less progression in percent atheroma volume (PAV) (p < 0.001) and total atheroma vol

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

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

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

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

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

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

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

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

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

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

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

222 .2% vs. 37.8 +/- 10.3%, p < 0.001) and total atheroma volume (TAV) (148.7 +/- 66.6 mm3 vs. 194.7 +/-

223 .9% vs. 37.5 +/- 0.8%, p < 0.0001) and total atheroma volume (TAV) (199.4 +/- 7.9 mm(3) vs. 189.4 +/-

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

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

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

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

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

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

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

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

232 ficacy measures included the change in total atheroma volume and average maximal atheroma thickness.

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

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

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

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

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

238 The mean (SD) percent atheroma volume decreased by -1.06% (3.17%) in the combi

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

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

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

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

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

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

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

246 The absolute reduction in atheroma volume in the combined treatment groups was -14

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

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

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

250 In the placebo group, mean (SD) percent atheroma volume increased by 0.14% (3.09%; median, 0.03%

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

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

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

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

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

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

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

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

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

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

261 Accordingly, atheroma volume statistically significantly decreased at

262 Atheroma volume was determined in serial intravascular u

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

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

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

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

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

268 The primary end point (percentage change in atheroma volume) showed a significantly lower progressio

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

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

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

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

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

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

275 6 mm3 (least-square mean +/- SE) increase in atheroma volume, those with "pre-hypertensive" BP had no

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

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

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

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

280 es in lipoprotein levels and coronary artery atheroma volume.

281 therapy could have influenced the changes in atheroma volume.

282 dure remained strong predictors of increased atheroma volume.

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

284 ior revascularization or stroke with percent atheroma volume.

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

286 late stage of necrosis, or thin-cap fibrous atheromas (vulnerable plaques).

287 AA atheroma was detected on baseline transesophageal echoca

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

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

290 Coronary atheroma was quantified by means of electron beam comput

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

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

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

294 Thus, atheromas were characterized by accumulation of choleste

295 r distinct oxidative pathways upregulated in atheroma, were determined by mass spectrometry.

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

297 h pathologic intimal thickening, fibrous-cap atheromas with cores in an early or late stage of necros

298 pathologic intimal thickening or fibrous-cap atheromas with cores in an early stage of necrosis.

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