ライフサイエンスコーパス: plaque

1 erfluorescent plaque in the late frame (late plaque).

2 th carotid artery intima-media thickness and plaque.

3 sms than inflammation in the atherosclerotic plaque.

4 and Gal-3 were not associated with increased plaque.

5 old promise for identification of vulnerable plaque.

6 re on antiretroviral medication, and 50% had plaque.

7 e can identify culprit and high-risk carotid plaque.

8 higher (95% CI, 2.2-17.8) burden of carotid plaque.

9 owed no evidence of coronary atherosclerotic plaque.

10 patients with stable versus unstable carotid plaque.

11 ted microglia that surround the beta-amyloid plaques.

12 sion molecule 1 (VCAM-1), in atherosclerotic plaques.

13 he calcium deposits in human atherosclerotic plaques.

14 in the perivascular area of atherosclerotic plaques.

15 mediated by an accumulation of amyloid beta plaques.

16 higher prevalence of CAC and atherosclerotic plaques.

17 mixed plaques and more often only calcified plaques.

18 acrophage burden in advanced atherosclerotic plaques.

19 nificantly different between NRS and non-NRS plaques.

20 pment and the progression of atherosclerotic plaques.

21 reduce macrophage burden in atherosclerotic plaques.

22 d 8.7% for white women; P < .01) of multiple plaques.

23 lets at the site of ruptured atherosclerotic plaques.

24 E binding in macrophages and excised carotid plaques.

25 analysis improves the identification of NRS plaques.

26 anscript expression in human atherosclerotic plaques.

27 kers in both mouse and human atherosclerotic plaques.

28 wellings at Alzheimer's disease (AD) amyloid plaques.

29 on the structural or molecular properties of plaques.

30 males showed predominantly mixed morphology plaques (61.5%).

31 We prospectively evaluated carotid plaque (68)Ga-DOTATATE uptake in patients with recent ca

32 athletes demonstrated predominantly calcific plaques (72.7%), whereas sedentary males showed predomin

33 ; 95% confidence interval [CI], 1.6-6.6) and plaque (77%; ORadjusted=3.3; 95% CI, 1.6-7.1) compared w

34 tive detection and staining of toxic amyloid plaques, a potential biomarker present in the Alzheimer'

35 However, after plaque accumulation, significantly better results for al

36 roduct use, and subsequently after 5 days of plaque accumulation.

37 inflammation and in response to experimental plaque accumulation.

38 ed to resemble the substrate of human eroded plaques, acute flow perturbation promoted downstream end

39 ial clustering around plaques, and decreased plaque-adjacent neuronal dystrophy in TREM2-deficient mi

40 depending on Braak stage, when adjusting for plaques, age of death, sex, education, and APOE genotype

41 he titanium dioxide (TiO2) layer, and scanty plaque aggregates, whereas the Er:YAG laser (38.2 J/cm(2

42 In addition to protein fibrils, amyloid plaques also contain non-proteinaceous components, inclu

43 h their contributory role to atherosclerotic plaque and abdominal aortic aneurysm stability are poorl

44 rediabetes had an increased risk for carotid plaque and adverse functional cardiac parameters, includ

45 ri-implantitis are evaluated in terms of: 1) plaque and biocorroded titanium oxide coating removal; 2

46 nderlying molecular mechanisms that regulate plaque and CAA deposition in the vast majority of sporad

47 While plaque and tangle accumulation likely contributes to neu

48 However, the mineral composition of Fe plaque and thus its potential to sorb metal(loid)s is af

49 (38.2 J/cm(2)) completely stripped away the plaque and TiO2 layer, leaving a micropitted surface.

50 Implants, however, accumulated less plaque and underwent more heterogeneous shifts in microb

51 pressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms and correlated wi

52 n macrophage-rich regions of atherosclerotic plaques and correlated with the intensity of CXCR4 expre

53 as examined in human carotid atherosclerotic plaques and in western diet-fed atherosclerosis-prone Ld

54 erized by extracellular amyloid-beta (Abeta) plaques and intracellular tau inclusions.

55 ign composition of plaques, with fewer mixed plaques and more often only calcified plaques.

56 C, V181M, R183C and L239I) form gap junction plaques and produce levels of junctional coupling simila

57 rystals (CC) are abundant in atherosclerotic plaques and promote inflammatory responses via the compl

58 pe of a mouse model of AD that develops both plaques and tangles (3xTg).

59 ggregated beta-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer di

60 However, besides plaques and tangles, other biochemical and morphological

61 se of the disease before the accumulation of plaques and tangles.

62 explored by 3DVUS to determine the number of plaques and territories affected, and to quantify global

63 HFD significantly increased amyloid plaques and worsened cognitive performance compared to m

64 its containing by the Abeta peptide (amyloid plaques) and the tau protein (neurofibrillary tangles) i

65 linical research for imaging coronary artery plaque, and ongoing clinical studies are testing whether

66 phagy, restored microglial clustering around plaques, and decreased plaque-adjacent neuronal dystroph

67 Amyloid-beta (Abeta) plaques are a key histopathological hallmark of Alzheime

68 ATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key lesions in Alzheimer's disease (AD) but

69 ial activation, also takes place outside the plaque areas, that is, in areas of normal-appearing whit

70 ssolved titanium were detected in submucosal plaque around implants with peri-implantitis compared wi

71 ore implantation of a radioactive iodine 125 plaque as treatment for the tumor.

72 he biodistribution, nanomedicines' uptake by plaque-associated macrophages/monocytes, and their effic

73 ease in Abeta plaque size and a reduction in plaque-associated neuritic dystrophy with no change in o

74 Plaque bacterial communities showed temporal stability,

75 irin had no significant effect on individual plaque bacterial counts in unadjusted models or those ad

76 derived pathological tau (AD-tau) into Abeta plaque-bearing mouse models that do not overexpress tau,

77 h heavy infection of Streptococcus mutans in plaque-biofilms from children affected with early-childh

78 n in patients treated with repeat episcleral plaque brachytherapy (EPBT) for locally recurrent poster

79 Palladium-103 plaque brachytherapy.

80 with psoriasis had increased total coronary plaque burden (1.22+/-0.31 versus 1.04+/-0.22, P=0.001),

81 ssociated with improvement in total coronary plaque burden (beta=0.45, 0.23-0.67; P<0.001) and NCB (b

82 ry calcification (CARDIA) and carotid artery plaque burden (BioImage).

83 nary plaque burden and noncalcified coronary plaque burden (NCB) and high-risk plaque (HRP) prevalenc

84 eatures (remodeling index [r=0.53, P=0.003], plaque burden [r=0.51, P=0.004]), and predicted cardiova

85 Tracer uptake was compared with calcified plaque burden and cardiovascular risk factors.

86 As such, we sought to compare total coronary plaque burden and noncalcified coronary plaque burden (N

87 of AAV1-mIL-6 + dox treatment lowered total plaque burden by >60% versus untreated controls.

88 territories affected, and to quantify global plaque burden defined as the sum of all plaque volumes.

89 eficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed

90 Plaque burden was directly associated with estimated car

91 ts of bexarotene were accompanied by reduced plaque burden, decreased astrogliosis, and suppression o

92 ovides accurate volumetric quantification of plaque burden.

93 alcification and low attenuation) of carotid plaque by computerized tomography among PLWHIV without k

94 (125)I-pentixafor uptake in atherosclerotic plaques by approximately 40%.

95 f (18)F-FDG uptake in murine atherosclerotic plaques by both M-CSF and GM-CSF.

96 Higher prevalence of plaque calcification was noted in RA, despite similar pl

97 ve specimens of Neanderthal calcified dental plaque (calculus) and the characterization of regional d

98 The incidence of carotid artery stenosis and plaques, cardiac embolic source, TIA/stroke and myocardi

99 presence of parenchymal amyloid-beta (Abeta) plaques, cerebral amyloid angiopathy (CAA) and neurofibr

100 sive method for direct assessment of CAD and plaque characterization with high diagnostic accuracy co

101 h concurrent Abeta suppression could enhance plaque clearance and could improve pathologic outcomes i

102 Subgingival plaque-coated titanium disks with a moderately rough sur

103 ineffective plaque encapsulation and reduced plaque compaction, which is associated with worsened axo

104 ole of vascular CXCR4 in atherosclerosis and plaque composition by inducing an endothelial cell (BmxC

105 nous estradiol and testosterone with carotid plaque composition in elderly men and postmenopausal wom

106 Aggregates of tau and beta amyloid (Abeta) plaques constitute the histopathological hallmarks of Al

107 d carotid, iliofemoral, and abdominal aortic plaques; coronary artery calcification; serum biomarkers

108 ta peptide, which is dominant in the amyloid plaques deposited in the brains of AD patients.

109 t age-related increases in Abeta production, plaque deposition, as well as contextual fear and spatia

110 cosanoids are thought to contribute to Abeta plaque deposition, these 1,5-diarylimidazoles provide to

111 nd tau fragmentation and facilitates amyloid plaque deposits and neurofibrillary tangle (NFT) formati

112 more effective reductions of brain Abeta and plaque deposits, gliosis, and behavioral memory deficits

113 atherosclerotic process, from initiation to plaque destabilization.

114 and determine the impact on atherosclerotic plaque development in mice with and without CD4+ T cells

115 eria and individual species counts in dental plaque did not differ significantly between baseline and

116 surements, and explored the mechanism of any plaque DOTATATE activity with immunohistochemistry in re

117 d amyloid deposits, resulting in ineffective plaque encapsulation and reduced plaque compaction, whic

118 we can reverse the autophagy dysfunction of plaques, enhance aggrephagy of p62-enriched protein aggr

119 ompanied by an acute decrease in the carotid plaque expression of micro-RNAs (miRs)-221 and miR-222.

120 )F-Fluoride uptake correlated with high-risk plaque features (remodeling index [r=0.53, P=0.003], pla

121 rease in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence i

122 K-null phenotype characterized by very small plaque formation and drastic reduction in infectious vir

123 ns, but the specific contributions of KCs to plaque formation are not fully understood.

124 ic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, se

125 ction, pseudorevertant alleles that restored plaque formation for lysis-defective mutants of Rz and R

126 different pathophysiological mechanisms for plaque formation in athletic versus sedentary men.

127 sCD163 was associated with plaque formation in virally suppressed HIV+ men (RR 1.52

128 ces colonization and contributions to dental plaque formation, as well as their potential roles in th

129 nockout mice show diminished atherosclerotic plaque formation, characterized by reduced proinflammato

130 rastically impairs viral RNA replication and plaque formation.

131 osclerotic lesion development and vulnerable plaque formation.

132 e model of shear stress-modulated vulnerable plaque formation.

133 y oxidative stress promoting atherosclerotic plaque formation.

134 4 followed by intramuscular injection of 108 plaque forming units of MVA-CMDR at weeks 12 and 24.

135 e doses of the rVSV-ZEBOV vaccine (3 million plaque-forming units [PFU], 20 million PFU, or 100 milli

136 1 of 3 lots of rVSVDeltaG- ZEBOV-GP (2 x 107 plaque-forming units [pfu], n = 797; combined-lots group

137 ng units/mL; after 3 weeks, </= 4 mL x 10(8) plaque-forming units/mL every 2 weeks).

138 egan in week 1 (first dose, </= 4 mL x 10(6) plaque-forming units/mL; after 3 weeks, </= 4 mL x 10(8)

139 st M2FA demonstrated that M2FA is present in plaque found on the aortic valve of ApoE (-/-) mice.

140 anium surfaces contaminated with subgingival plaque from patients with peri-implantitis are evaluated

141 using gentle sonication to sample intact Fe plaque from the root system and concentrate it for subse

142 h prostatic secretion and subgingival dental plaque from the same individual.

143 gamma-tubulin receptor Spc110 to the central plaque from within the nucleus is important for NE inser

144 cause mortality risk were raised with dental plaque, gingival inflammation, >10 missing teeth and fun

145 If complete examinations (plaque/gingival index, probing depth [PD], vertical clin

146 d coronary plaque burden (NCB) and high-risk plaque (HRP) prevalence between patients with psoriasis

147 sh between intima, media, or atherosclerotic plaque in the carotid artery.

148 ntermediate frames and as a hyperfluorescent plaque in the late frame (late plaque).

149 relates with their associations with amyloid plaques in Alzheimer's brains: RTN3, but not RTN1, is ab

150 the predominantly calcific morphology of the plaques in athletes indicates potentially different path

151 Remarkably, IAPP colocalized with amyloid plaques in brain parenchymal deposits, suggesting that t

152 CYnLIP efficaciously treated psoriatic-like plaques in C57BL/6 mice (PASI score of 1) compared to im

153 so expressed in EC overlying atherosclerotic plaques in coronary arteries from patients with ischemic

154 the number of viral particles that can form plaques in culture is much lower in human neurons than o

155 T were not associated with calcified carotid plaques in either sex.

156 in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic le

157 of amyloid beta (Abeta) peptides into senile plaques in the brain.

158 's disease through their presence in amyloid plaques in the nervous systems of affected individuals.

159 Presence and characteristics (high-risk plaque, including spotty calcification and low attenuati

160 egression, the presence of nonobstructive LM plaque increased the risk for the composite outcome in w

161 Outcome measures were plaque index (PI), gingival index (GI), bleeding on prob

162 They included plaque index (PI), modified sulcus bleeding index (mSBI)

163 luded modified sulcus bleeding index (mSBI), plaque index (PI), probing depth (PD), and clinical atta

164 compare peri-implant soft tissue parameters (plaque index [PI], bleeding on probing [BOP], and probin

165 Clinical data (probing depth [PD], plaque index [PI], gingival index [GI], bleeding on prob

166 del wherein Abeta production is amplified by plaque-induced axonal lysosome transport defects.

167 robiologic status of individuals affected by plaque-induced gingivitis (pGI).

168 P2X7 deficiency resolved plaque inflammation by inhibition of lesional inflammaso

169 ons also contribute to early atherosclerotic plaque initiation and growth.

170 preclinical technology to assess and monitor plaque instability and thereby test potential plaque-sta

171 l Th1 inflammatory response, with subsequent plaque instability that eventually favors atherothrombos

172 Dental plaque is a complex multispecies biofilm, and is a direc

173 ndividual isolates of PIV5-RSV-G (HN-L), but plaque isolates of PIV5-RSV-F (HN-L) had no mutations.

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

175 onectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-cadherin associati

176 stase, and sialidase) in GCF and subgingival plaque levels of Porphyromonas gingivalis, Tannerella fo

177 These data illustrate that calcified plaque limited intravascular drug delivery, and controll

178 (Reduction in Coronary Yellow Plaque, Lipids and Vascular Inflammation by Aggressive L

179 neuritic dystrophy with no change in overall plaque load.

180 luble amyloid-beta (Abeta) species and Abeta plaque load].

181 Finally, we confirm that plaque-localised microglia and astrocytes are reduced in

182 reduced proinflammatory gene expression and plaque macrophage content.

183 In human carotid plaques, MerTK cleavage correlated with plaque necrosis

184 en with S-ECC have a significantly different plaque microbiome than their caries-free counterparts, w

185 in individual species levels in subgingival plaque microbiota were not detectable; however, a small

186 d was effective at concentrating As-bound Fe plaque minerals in a uniform coating onto membranes that

187 The "plaque model" has been successfully implemented in patie

188 er she noticed a periareolar ulcerating skin plaque, more noticeable nipple retraction, and new onset

189 stitutions show in vitro growth kinetics and plaque morphologies similar to those of the wild-type (W

190 an increase in CEC and beneficial changes in plaque morphology including increase in fibrous cap thic

191 gard to their growth kinetics, antigenicity, plaque morphology, genetic stability, and temperature, i

192 imaging-based definitions of the "vulnerable plaque," necessitating an improved approach for predicti

193 e (MerTK) reduces efferocytosis and promotes plaque necrosis and defective resolution.

194 otid plaques, MerTK cleavage correlated with plaque necrosis and the presence of ischemic symptoms.

195 A key cause of plaque necrosis is defective clearance of apoptotic cell

196 that contributes to defective efferocytosis, plaque necrosis, and impaired resolution during the prog

197 nanoparticle deposition occurred in areas of plaque neovascularization.

198 's disease (AD) include amyloid-beta (Abeta) plaques, neurofibrillary tangles, and reactive gliosis.

199 categorical measures for certain non-amyloid-plaque, non-neurofibrillary-tangle neuropathologies.

200 tes in dystrophic neurites surrounding Abeta plaques (NP tau), AD-like neurofibrillary tangles (NFTs)

201 ue presence), negative binominal regression (plaque number), and linear regression (plaque size), and

202 cyclodextrin from 2 to 9 h postentry reduced plaque numbers.

203 elf-described red, itchy skin within a large plaque of FDH on her left posterior thigh and calf.

204 :background ratio were higher in the carotid plaque of symptomatic patients (P=0.021 and P=0.05, resp

205 2 and Spc29 and in this way link the central plaque of the SPB to the nuclear envelope.

206 reduced necrosis and macrophage apoptosis in plaques of these mice was a manifestation of the selecti

207 zed at the site of high-risk atherosclerotic plaques, of which early detection and therapeutic stabil

208 for cardiovascular risk factors and carotid plaque on ultrasound.

209 Subclinical atherosclerosis (plaque or coronary artery calcification) was present in

210 ients with regard to the increased number of plaques or abnormal arterial wall thickness.

211 vascular risk independently of the number of plaques or territories affected (p < 0.01).

212 Y) either form no morphological gap junction plaques or, if they do, produce little or no detectable

213 cation of the culprit lesion; or whether the plaque (or patient) is at high risk of future adverse ev

214 ion was observed for number of teeth, dental plaque, or detectable oral mucosal lesions and PD risk,

215 Am7 accumulation compared with nonthrombosed plaques (P<0.05).

216 was revealed by the worsening of the amyloid plaque pathology arising from JIP3 haploinsufficiency in

217 ot capable of accurate detection of critical plaque pathophysiology in the coronary arteries.

218 IVUS data for a comprehensive assessment of plaques pathophysiology.

219 to exclude confounding by varying amounts of plaque per site.

220 The questions remained (a) whether the plaque phenotype in transplanted mice resulted from a ge

221 he hypothesis that patients have a high-risk plaque phenotype.

222 tions were determined by Poisson regression (plaque presence), negative binominal regression (plaque

223 However, plaque progression renders macrophages unable to degrade

224 8 years or older, had a diagnosis of chronic plaque psoriasis for at least 6 months before baseline,

225 atients (aged >/=4 to <18 years) with severe plaque psoriasis who had not responded to topical therap

226 ts an evolving treatment strategy in chronic plaque psoriasis.

227 o and etanercept in the treatment of chronic plaque psoriasis.

228 ere sequentially passaged in BALB/c mice and plaque-purified from lung samples.

229 A plaque-purified MERSMA clone caused weight loss and fata

230 We also tested maternal serum with plaque reduction neutralisation assays for Zika and deng

231 We assessed the utility of the plaque reduction neutralization test (PRNT) to confirm r

232 A) for screening, followed by a confirmatory plaque reduction neutralization test (PRNT).

233 We measured antibody titers (50% plaque reduction neutralization test) using a panel of W

234 stic strategy in developing countries, where plaque reduction neutralization testing is impractical.

235 122 controls from northeastern Brazil using plaque reduction neutralization tests.

236 nction were assessed in in vitro cultures of plaque-resident cells.

237 ry, and controlled OAS treatment of calcific plaques resulted in greater drug permeability and improv

238 Atherosclerotic plaque rupture is accompanied by an acute decrease in th

239 rrent evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collec

240 orphological characteristics associated with plaque rupture.

241 Inflammation drives atherosclerotic plaque rupture.

242 uman aorta tissue (n = 15) and human carotid plaque samples (n = 19).

243 Pi was detected in all dental plaque samples but not in the prostatic secretion.

244 Subgingival plaque samples were analyzed using semiquantitative poly

245 An in vitro three-species biofilm or human plaque samples were applied for bacterial adhesion to ea

246 The collection of subgingival plaque samples with paper points is time-consuming and a

247 an in vitro three-species biofilm and human plaque samples.

248 ine density was not associated with neuritic plaque score but did display negative correlation with B

249 sure versus number of teeth, bleeding score, plaque score, and periodontal severity with linear and o

250 ncluded age at death, sex, cerebral neuritic plaque scores, cerebral alpha-synuclein scores, presence

251 n or inflammation in response to accumulated plaque select for a cariogenic or periopathogenic microb

252 lcification was noted in RA, despite similar plaque size (73.3% vs 20%, p = 0.04).

253 yloid deposition led to an increase in Abeta plaque size and a reduction in plaque-associated neuriti

254 (-/-) mouse model to compare atherosclerotic plaque size and composition after inorganic arsenic, met

255 ngage from ZO-1 correlated with increased GJ plaque size and increased connexin protein half-life, wh

256 he atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which

257 mmune responses, and reduced atherosclerotic plaque size without altering the plasma lipid profiles i

258 sion (plaque number), and linear regression (plaque size), and compared between races.

259 GAPDH levels were reduced in atherosclerotic plaque SMCs, and this effect correlated with oxidative s

260 By identifying the residues that establish plaque stability, these studies lay the groundwork for e

261 a novel therapy to increase atherosclerotic plaque stability.

262 etermine the beneficial effects of statin on plaque stabilization.

263 laque instability and thereby test potential plaque-stabilizing drugs.

264 ts noted significant healing of erosions and plaques starting from the peripheral aspect within 1 to

265 reduced VZV titers (-1.5 log10), and smaller plaques than with the parental Oka (pOka) strain.

266 bbits subject to pharmacological triggering, plaques that thrombosed exhibited significantly higher C

267 The Fe (oxyhydr)oxide rind, or Fe plaque, that forms on aquatic plant roots is an importan

268 wn experimentally (in the absence of amyloid plaques) to impair hippocampal synaptic plasticity, decr

269 otrexate in patients with moderate to severe plaque-type psoriasis.

270 e is a key characteristic of atherosclerotic plaques undergoing regression.

271 The predominant strategy to characterize Fe plaque using dithionite-citrate-bicarbonate (DCB) extrac

272 arterectomized human carotid atherosclerotic plaques using three-dimensional (3D) electron microscopy

273 The spectral attributes of LCO-bound plaques varied markedly in the brain, but the mean spect

274 ological traits, including tau, amyloid beta plaques, vascular injury and Lewy bodies.

275 pt uptake was related to noncalcified aortic plaque volume (r = 0.87; P = .003) on computed tomograph

276 ncrease [95% confidence interval] in rank of plaque volume for each 10-year increase in cumulative du

277 gnificantly greater increase in noncalcified plaque volume from baseline to 12 months (from median va

278 ary outcome was noncalcified coronary artery plaque volume, as determined by coronary computed tomogr

279 progression of noncalcified coronary artery plaque volume.

280 Plaque volumes at 1 year were similar between the ramipr

281 obal plaque burden defined as the sum of all plaque volumes.

282 ization are acknowledged to be 2 features of plaque vulnerability, although their temporal expression

283 Plaque was more prevalent in the RA group (53.1% vs 37.0

284 HODS AND A high-density fixed multielectrode plaque was placed on the epicardial surface of the left

285 50 patients with periodontitis, subgingival plaque was sampled from the deepest pocket of each quadr

286 None of the excised plaques was shown to contain cells (macrophages, lymphoc

287 ILPDA is highly expressed in atherosclerotic plaques, we examined its regulation and function in muri

288 Plaques were dissected, and the culprit lesions used for

289 Braak NFT stage and the presence of neuritic plaques were not significantly associated with differenc

290 KB1 expression was markedly reduced in human plaques when compared with nonatherosclerotic vessels.

291 aneously from instability of atherosclerotic plaque, whereas type 2 MIs occur in the setting of a mis

292 o assess differences between NRS and non-NRS plaques, whereas we calculated receiver-operating charac

293 more quickly than the paxillin-rich adhesion plaques, which in turn move more quickly than the local

294 els was also significantly higher in carotid plaque with high-CE (P<0.001).

295 uced progression to advanced atherosclerotic plaques with diminished smooth muscle and collagen conte

296 tery disease burden composed of noncalcified plaques with high-risk features.

297 ction time, implant surface, and presence of plaque) with microbiologic characteristics.

298 p, however, had a more benign composition of plaques, with fewer mixed plaques and more often only ca

299 h worldwide and involves the accumulation of plaques within the artery wall that can occlude blood fl

300 rden in the presence of moderate or frequent plaques would add to the ability to predict clinical rat

301 sed for identifying fibrous cap thickness of plaques, yet cannot provide adequate depth penetration t