ライフサイエンスコーパス: plaque

1 2% of zOTUs in saliva; 2.5% to 38% in dental plaque).

2 atite deposition in atherosclerotic coronary plaque.

3 d carotid intima-media thickness and carotid plaque.

4 d with a reduced progression of noncalcified plaque.

5 on saliva and supragingival and subgingival plaque.

6 aque rupture, intraplaque cavity, or layered plaque.

7 gue dorsum, buccal mucosa, and supragingival plaque.

8 litus mainly led to an increase in calcified plaque.

9 region continued to significantly accumulate plaques.

10 ue Tregs is a common signature of regressing plaques.

11 ith AD significantly dissociated hippocampal plaques.

12 inium (Gd) imaging agent, for MRI of amyloid plaques.

13 on for the acute stabilization of late-stage plaques.

14 process of T cell homing to atherosclerotic plaques.

15 c-3-positive macrophage-rich atherosclerotic plaques.

16 e levels for in vivo imaging of beta amyloid plaques.

17 ics than the parental virus and forms larger plaques.

18 erogeneity of macrophages in atherosclerotic plaques.

19 present in tissues including atherosclerotic plaques.

20 matory macrophages and human atherosclerotic plaques.

21 coexist as neurotoxic heteromers within the plaques.

22 g ligand with high affinity for amyloid-beta plaques.

23 enterovirus infect cells in atherosclerotic plaques.

24 e to an atherogenic diet to develop advanced plaques.

25 xposure, presence of asbestosis, and pleural plaques.

26 tify substrates that are cleaved in ruptured plaques.

27 europathy tended to be higher with the 15-mm plaque (2% vs. 9%; P = 0.054).

28 er's disease pathological hallmarks: amyloid plaques (A), phosphorylated tau (T), and accompanying ne

29 the close relationship between vascular and plaque Abeta deposition, several factors favour one or t

30 Plaque abundance was elevated in PS2APP;Trem2(ko) female

31 On day 21, at the time of maximum plaque accumulation, the GI of the APE test group was a

32 ure (17 patients with irregular or ulcerated plaque and 27 with smooth plaque; P = .54).

33 increased progression of calcified coronary plaque and a reduced progression of noncalcified coronar

34 t rPEDV-D350A formed a significantly smaller plaque and had significant defects in viral protein synt

35 al dissection, non-calcified atherosclerotic plaque and intraluminal thrombus.

36 Removal of dental plaque and local application of local chemical adjuncts,

37 o exhibited more dendritic spine loss around plaque and more neurofilament light chain in CSF.

38 h increased prevalence of high-risk coronary plaque and risk of cardiovascular events.

39 mmatory response may precede insoluble Abeta plaque and tau tangle formation.

40 For AD-related pathologies of amyloid plaques and Braak stage, e2 had large and highly signifi

41 er and provides excellent contrast for Abeta plaques and cerebral amyloid angiopathy.

42 ear pores in mammalian cells to amyloid-beta plaques and dendrites in brain tissues and elastic fiber

43 The deposition of amyloid beta (Abeta) plaques and fibrils in the brain parenchyma is a hallmar

44 us in cell culture, but it displayed smaller plaques and impaired fitness in direct competition assay

45 marked by amyloid beta (Abeta) extracellular plaques and intracellular neurofibrillary tangles, const

46 with both extracellular amyloid-beta (Abeta) plaques and intracellular tau-containing neurofibrillary

47 mentia associated with deposition of amyloid plaques and neurofibrillary tangles, formed by amyloid b

48 The emergence of PET probes for amyloid plaques and neurofibrillary tangles, hallmarks of Alzhei

49 r's disease (AD) is characterized by amyloid plaques and progressive cerebral atrophy.

50 Non-invasively detecting atherosclerotic plaques and stenosis using NETs may lay a groundwork for

51 hanistic insight into the formation of PrPSc plaques and suggest that PrP posttranslational modificat

52 ntia long ago, but subsequently, Alzheimer's plaques and tangles have received more attention.

53 by the accumulation of amyloid-beta (Abeta) plaques and tau neurofibrillary tangles in the brain.

54 ligation to mimic vulnerable atherosclerotic plaques and their rupture leading to MI.

55 mplete 3D reconstructions of atherosclerotic plaques and uncovers their volume, geometry, acellular c

56 ples (saliva, supragingival, and subgingival plaque) and was correlated with AAA diameters and volume

57 liva, gingival crevicular fluid, subgingival plaque, and blood samples were obtained at the same time

58 ased carotid intima-media thickness, carotid plaque, and carotid stenosis increased consistently with

59 ased carotid intima-media thickness, carotid plaque, and carotid stenosis.

60 actin networks at the gap junction formation plaque, and the formation of F-actin patches plays a cri

61 (82.0%) were male, 1,315 (31.0%) had pleural plaques, and 1,353 (32.0%) had radiographic asbestosis.

62 copic features include linear furrows, white plaques, and concentric rings.

63 in VSMCs in human and mouse atherosclerotic plaques, and in human VSMCs derived from plaques or unde

64 These plaques are formed by aggregation of polypeptides that a

65 D) brain deposits of amyloid peptides called plaques are neither single pixels nor ROIs.

66 However, rupture-prone plaques are often distinguished by their internal compos

67 ts that contribute to the formation of Abeta plaques are well addressed at the intra- and intercellul

68 POKO mice had significantly decreased aortic plaque area as compared with CKD-bMPOWT mice.

69 l-to-noise ratio in a fluorescent Dulbecco's plaque assay, leading to the construction of a multirepo

70 Proteinaceous plaques associated with neurodegenerative diseases conta

71 PCSK6 upregulation in human atherosclerotic plaques associated with smooth muscle cells (SMCs), infl

72 rm large rafts of clustered channels, called plaques, at cell appositions.

73 lEVs accumulated in plaque atherosclerotic lesions depending on the progress

74 ore, which describes the density of neuritic plaques based on certain key locations in the neocortex.

75 On a per-plaque basis, increasing age (beta=0.070; P=0.058) and h

76 Dental plaque biofilm is considered to be the underlying cause

77 iscs were inoculated with human peri-implant plaque biofilms and mechanical antimicrobial interventio

78 le interval, 4.0-5.7) years, low-attenuation plaque burden correlated weakly with cardiovascular risk

79 Patients with low-attenuation plaque burden greater than 4% were nearly 5 times more l

80 stenosis not intended for PCI but with IVUS plaque burden of >=65% were randomized to treatment of t

81 near-infrared spectroscopy-IVUS, the median plaque burden was 73.7%, the median MLA was 2.9 mm(2), a

82 of angiographically mild lesions with large plaque burden was safe, substantially enlarged the follo

83 Low-attenuation plaque burden was the strongest predictor of myocardial

84 Plaque burden, not stenosis per se, is the main predicto

85 nformation about the bifurcation anatomy and plaque burden, thereby enabling planning, education, and

86 dence-based preventive therapies informed by plaque burden.

87 did not reduce the incidence of new carotid plaques but produced significantly greater regression of

88 1 plaque [interquartile range (IQR): -1 to 3 plaques] by 2DVUS; 7.6 mm(3) [IQR: -32.2 to 57.6 mm(3)]

89 Quartiles were calculated for noncalcified plaque, CAC, and average carotid wall volume and were co

90 steogenic phenotypes likely to contribute to plaque calcification and plaque destabilization.

91 -lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS).

92 nd endothelial lineage tracing to survey all plaque cell types and rigorously determine their origin.

93 This plaque characterization approach is fully automated, rob

94 ons of CCTA based on hemodynamic indices and plaque characterization may provide personalized risk as

95 s, we developed an automated atherosclerotic plaque characterization method that used a hybrid learni

96 to be up-regulated in human atherosclerotic plaques compared with normal vessel.

97 reflecting calcification of the noncalcified plaque component.

98 sease (AD) is cerebral deposition of amyloid plaques composed of amyloid beta (Abeta) peptides and th

99 gically by presence of extracellular amyloid plaques composed of fibrillar amyloid beta (Abeta) pepti

100 investigations have focused on structure and plaque composition as signs of plaque vulnerability, but

101 was 2.9 mm(2), and the median maximum lipid plaque content was 33.4%.

102 Inadequate plaque control, peri-implant inflammation, history of pr

103 However, studying plaque deposition and mineral composition in this spatia

104 mitochondrial Ca(2+) levels associated with plaque deposition and neuronal death in a transgenic mou

105 We characterized fibrillar plaque deposition in 6, 12, and 18-22 months old APP/PS1

106 ies in patients with AD, indicate that Abeta plaque deposition precedes cortical tau pathology.

107 Amyloid plaque deposits in the brain are indicative of Alzheimer

108 ly to contribute to plaque calcification and plaque destabilization.

109 nation of the role of ROS in pathogenesis of plaque destabilization.

110 eterious effects of TWEAK on atherosclerotic plaque development and progression.

111 loid beta (Abeta) peptide-containing amyloid plaque development.

112 -associated proteins showed that mobility in plaque domains is affected by mobility of the Cx protein

113 stography (SWE) to detect vulnerable carotid plaques, evaluating group velocity and frequency-depende

114 and proteolytic fragments in mouse and human plaque extracts.

115 prognostic implications of adverse coronary plaque features, and sex differences.

116 These plaques form 10-20 years before AD symptom onset, wherea

117 ve been recognized as key factors in amyloid plaque formation and aggravation of AD.

118 mechanisms underlying early atherosclerotic plaque formation are not completely understood.

119 mutants showed no significant differences in plaque formation compared to wild-type bacteria.

120 pose-tissue inflammation and atherosclerotic plaque formation in a mouse model of obesity.

121 pathways may therapeutically reduce amyloid plaque formation in cerebral vessels and the brain paren

122 cellular survival in macrophages and reduced plaque formation in HeLa cells.

123 on and cell death, enabling studies of viral plaque formation with single-cell resolution.

124 mutant, XG4J, was not viable on the level of plaque formation without X174 J gene complementation.

125 that CXADR is induced in macrophages during plaque formation, suggesting a mechanism by which entero

126 tilation at one of two concentrations (~1010 plaque forming units/mL or ~1011 plaque forming units/mL

127 ions (~1010 plaque forming units/mL or ~1011 plaque forming units/mL).

128 96Q mice challenged with 2 subfibrillar, non-plaque-forming prion strains instead developed plaques h

129 ed trial (vaccine-placebo ratio, 2:1) at 106 plaque-forming units (PFU) in 15 RSV-seropositive childr

130 -24 months received 1 intranasal dose of 105 plaque-forming units (PFU) of LID/DeltaM2-2/1030s (n = 2

131 solvents to yield on average 23 mL of 10(11) plaque-forming units (PFUs) per milliliter for Pseudomon

132 6-24 months received 1 intranasal dose (105 plaque-forming units [PFUs] of D46/NS2/N/DeltaM2-2-HindI

133 hronous movement of the carotid atheromatous plaque from B-mode ultrasound has been previously report

134 In total, 27 carotid plaques from 20 patients were scanned by ultrasound SWE

135 Atherosclerotic plaques from HFD-treated KO mice showed increased infilt

136 Supragingival plaque harbors hundreds of bacterial species, playing a

137 aque-forming prion strains instead developed plaques highly enriched in ADAM10-cleaved PrP and hepara

138 tauopathy) or moderate to frequent neuritic plaques (i.e. Alzheimer neuropathological change) at sub

139 mpairment at baseline and either no neuritic plaques (i.e. primary age-related tauopathy) or moderate

140 ective studies who underwent ASL and carotid plaque imaging with use of 3-T MRI in the same setting f

141 st material-enhanced MR angiography, carotid plaque imaging, and arterial spin labeling (ASL) to iden

142 Single-cell RNA-sequencing of plaque immune cells revealed that unlike Tregs from prog

143 d carotid intima-media thickness and carotid plaque in 2015 using a risk factors-based model by WHO r

144 robing (primary outcome) and lower levels of plaque in comparison with the control group after 24 mon

145 d suppression of clonal SMC expansion in the plaque in vivo.

146 structed a high-accuracy 3D-model of amyloid plaques in a fully automated fashion, employing rigid an

147 retase activity and the formation of amyloid plaques in a transgenic mouse model (5xFAD) of early amy

148 Viruses forming large plaques in A56/K2 cells increased in successive rounds o

149 (Spearman rho = 0.15; P = .33), beta-amyloid plaques in cohort 1.

150 HSV-1 DNA has been detected in AD amyloid plaques in human brains, and treatment with the antivira

151 atial navigation and had significantly fewer plaques in M1 and SS2, but not in the PFC.

152 microglia enveloping NA-containing neuritic plaques in postmortem brains of patients with AD.

153 ing to the successful PET imaging of amyloid plaques in the brains of 5xFAD mice versus those of wild

154 eta(2)-microglobulin (beta(2)m) into amyloid plaques in the joints of long-term hemodialysis patients

155 ting in an impaired response to beta-amyloid plaques in vivo.

156 uptured versus stable areas of human carotid plaques, including many of the same functional categorie

157 We propose that this plaque-independent inflammatory reaction originates from

158 bleeding on probing (BOP), and interproximal plaque index (API) were significantly improved in both g

159 Probing depth (PD), CAL, plaque index (PI), and interproximal bone height were ev

160 eriodontal parameters were recorded: visible plaque index (VPI), gingival bleeding index (GBI), probi

161 achment loss [AL], marginal bone loss [MBL], plaque index [PI], and bleeding on probing [BOP] in sham

162 Children with high plaque index and high DMFT values were more similar to e

163 of probing depth, soft tissue dehiscence and plaque index compared to non-augmented sites compared to

164 Several bacterial taxa associated with high plaque index or high DMFT were ethnic group-specific.

165 overall microbial community, compared to low plaque index or low DMFT groups in which inter-subject v

166 (Probing Pocket Depths, Bleeding On Probing, Plaque Index) and marginal bone loss were also recorded.

167 Bleeding on probing (BOP), plaque index, and probing depth (PD) were confirmed reli

168 rticipants, clinical periodontal parameters (plaque index, gingival index, sulcus bleeding index, pro

169 Disturbed flow at atheroprone regions primes plaque inflammation by enhancing endothelial NF-kappaB s

170 /ApoE(-/-) mice showed increased features of plaque instability.

171 icant atherosclerosis progression (median: 1 plaque [interquartile range (IQR): -1 to 3 plaques] by 2

172 r nonperfusion, cotton-wool spots, Kyrieleis plaques, irregular venous caliber with dilated and scler

173 t the microglial packing of Abeta into dense plaque is an important neuroprotective activity.SIGNIFIC

174 Secondary caries caused by dental plaque is one of the major reasons for the high failure

175 Amyloid-beta deposition into plaques is a pathologic hallmark of Alzheimer disease ap

176 tein fragment whose aggregation into amyloid plaques is linked with Alzheimer's disease.

177 EPRIEVE, and its substudy assessing coronary plaque, is to assess cardiovascular outcomes, the trial

178 derived from the thymus, Tregs in regressing plaques lacked Nrp1 expression, suggesting that they are

179 the test group (P <= 0.001) despite similar plaque levels (P = 0.436).

180 ;Trem2(ko) mice, notwithstanding the reduced plaque load at later ages.

181 We found a significant increase in plaque load between 6 and 12 months in all regions.

182 ent outcome of Trem2 deficiency than amyloid plaque load, suggesting that the microglial packing of A

183 suggest that implanting stents in lipid-rich plaque (LRP) may be associated with adverse outcomes.

184 w conditions on collagen and atherosclerotic plaque material, were attenuated by rivaroxaban.

185 sed removal of cerebral amyloid beta (Abeta) plaques may possibly clear tau tangles and modestly slow

186 characterize the healthy salivary and dental plaque microbiome in young children.

187 unities over time, we profiled supragingival plaque microbiomes of dizygotic and monozygotic twins du

188 tion, supporting the current knowledge about plaque morphology in the cerebellum and the fundamental

189 ve lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions.

190 SARS-CoV-2 (icSARS-CoV-2) exhibited similar plaque morphology, viral RNA profile, and replication ki

191 key proinflammatory cytokines and changes in plaque morphology.

192 d software was used to quantify noncalcified plaque (NCP), as well as its components.

193 liac, and femoral territories to determine a plaque number score; 3DVUS to quantify carotid and femor

194 alterations are observed around the amyloid plaques of Alzheimer's disease (AD), little is known abo

195 Plaques of APOA1 (tg/tg)/Apoe (-/-) mice fed F1394 showe

196 ion compared with littermate controls, while plaques of SM22alpha-hSIRT6(H133Y)/ApoE(-/-) mice showed

197 nd authors determined that parenchymal PrPSc plaques of the mouse brain preferentially incorporated u

198 an AD, and none of the cases showed neuritic plaques on any of the stains used.

199 Conclusions: The presence of pleural plaques on radiologic imaging does not confer additional

200 clades that distinctly associate with either plaque or tongue.

201 tic plaques, and in human VSMCs derived from plaques or undergoing replicative or palmitate-induced s

202 relation to the presence of generalized (>2 plaques) or incipient (0 to 2 plaques) subclinical ather

203 s. 2.8 mm) than those treated with the 15-mm plaque (P < 0.001).

204 a 2.6-fold increase in the odds of coronary plaque (P = .01), after controlling for traditional and

205 gular or ulcerated plaque and 27 with smooth plaque; P = .54).

206 e detrimental for late-stage atherosclerosis plaque pathogenesis.

207 d p-tau-181 were highly specific for amyloid plaque pathology in the discovery cohort (n = 36, AUROC

208 in metabolic wastes and amyloid-beta (Abeta) plaques, perivascular reactive astrogliosis, and misloca

209 ble-deficient mice displayed a more unstable plaque phenotype characterized by an increased lipid and

210 Polymicrobial interactions in dental plaque play a significant role in dysbiosis and homeosta

211 y cilia, caveolae, clathrin-coated pits, and plaques play additional key roles.

212 % at 10 years; P = 0.31) and associated with plaque positioning (hazard ratio [HR], 2.81 for no safet

213 reduced progression of noncalcified coronary plaque, potentially reflecting calcification of the nonc

214 ciated protein tau (p-tau) and extracellular plaques primarily comprising amyloid- beta (Abeta) pepti

215 substudy (n=40), the rate of atherosclerotic plaque progression was compared from before to after the

216 iable risk factor predictive of noncalcified plaque progression, diabetes mellitus mainly led to an i

217 s an independent determinant of noncalcified plaque progression, statin use (beta=-2.178; P=0.050) wa

218 to sustain generations of macrophages during plaque progression.

219 onsignificantly associated with annual total plaque progression.

220 The 2 plaques provided a safety margin in 43% versus 40% eyes,

221 cohort study including patients with chronic plaque psoriasis (n = 6501) being treated with biologic

222 hibitor, in patients with moderate-to-severe plaque psoriasis (NCT02969018).

223 s first line treatment of moderate-to-severe plaque psoriasis and psoriatic arthritis, and further ag

224 700841 improves clinical symptoms of chronic plaque psoriasis by inhibition of proinflammatory cytoki

225 The most rapid advancements addressing plaque psoriasis have been in its pathogenesis, genetics

226 lind trial, we randomly assigned adults with plaque psoriasis in a 1:1:1 ratio to use roflumilast 0.3

227 lacebo and Ustekinumab in Moderate to Severe Plaque Psoriasis in Subjects]) participated in a mechani

228 rapeutic advancements for moderate to severe plaque psoriasis include biologics that inhibit TNF-alph

229 Plaque psoriasis is the most common variant of psoriasis

230 atment With Brodalumab in Moderate to Severe Plaque Psoriasis Subjects], -2 [P3 Study Brodalumab in T

231 Trial of roflumilast cream for chronic plaque psoriasis.

232 rodalumab in Treatment of Moderate to Severe Plaque Psoriasis], and -3 [Efficacy and Safety of Brodal

233 transpupillary thermotherapy (0% vs. 0.4%), plaque radiotherapy (7.0% vs. 5.2%), external beam radio

234 live SARS-CoV-2 neutralisation assays (a 50% plaque reduction neutralisation assay [PRNT(50)]; a micr

235 ology test requires confirmation by either a plaque reduction neutralization test or detection of ser

236 ng antibodies were also measured by in vitro plaque reduction neutralization, the gold standard metho

237 t specimens and yields comparable results to plaque reduction neutralizing assay, the gold standard o

238 ficant correlation with titres determined by plaque reduction with infectious LASV.

239 ), and immunogenic (geometric mean serum RSV plaque-reduction neutralizing antibody titer, 1:64).

240 The PREMIER trial (Plaque Regression and Progenitor Cell Mobilization With

241 solution of atherosclerotic inflammation and plaque regression, Tregs were depleted using CD25 monocl

242 nalyses revealed that Treg depletion blocked plaque remodeling and contraction, and impaired hallmark

243 followed by repeated bi-weekly supragingival plaque removal and chlorhexidine chips application (ChxC

244 reatment protocol of bi-weekly supragingival plaque removal and local application of chlorhexidine ch

245 mm as compared with bi-weekly supra-gingival plaque removal.

246 lso inversely associated with total coronary plaque (rho = -0.19; P = .02) and noncalcified coronary

247 = -0.19; P = .02) and noncalcified coronary plaque (rho = -0.24; P = .004).

248 enicity, symptomaticity, stenosis degree and plaque risk, respectively.

249 al pathways through which proteolysis causes plaque rupture and identify substrates that are cleaved

250 proaches in mouse models of protease-induced plaque rupture and in ruptured human plaques, we aimed t

251 r, the molecular mechanisms that precipitate plaque rupture are unknown.

252 Plaque rupture is the proximate cause of most myocardial

253 6.2% (67/145) of participants, most commonly plaque rupture, intraplaque cavity, or layered plaque.

254 thrombus formation stage on atherosclerotic plaque rupture, we hypothesized that factor V Leiden may

255 Subgingival plaque samples and gingival biopsies were collected from

256 assemble metagenomes from tongue and dental plaque samples from multiple individuals and reconstruct

257 with the presence of EBV in coronary artery plaque samples in the current study.

258 Up to four subgingival plaque samples per person, each obtained from the mesio-

259 Salivary and dental plaque samples were collected from the children at 3 tim

260 The combination of degraded TBS and plaque score >=80% increased the adjusted OR to 5.71 (95

261 ilar clinical findings except for the higher plaque scores in the non-smokers at 6 months (P <0.01).

262 alis displayed significant correlations with plaque scores, bleeding on probing, and RF-IgA.

263 y an increased lipid and macrophage content, plaque size, and pro-inflammatory cytokine expression.

264 gh MC021-HA expression did not fully restore plaque size, vMC021L-HA produced amounts of EV similar t

265 or basement-membrane proteins in maintaining plaque stability.

266 well as the mechanisms by which they control plaque stability.

267 eneralized (>2 plaques) or incipient (0 to 2 plaques) subclinical atherosclerosis in 2 independent cl

268 oss is a prominent feature of ruptured human plaques, suggesting a major role for basement-membrane p

269 H and 32 patients without IPH; P = .31), and plaque surface structure (17 patients with irregular or

270 vulnerable patient, not just the vulnerable plaque, takes into account the diversity and future risk

271 ll volume (Kendall tau = 0.29), noncalcified plaque (tau = 0.16), and CAC (tau = 0.33).

272 revealed that unlike Tregs from progressing plaques that expressed markers of natural Tregs derived

273 ar at week 6 (assessed on a 5-point scale of plaque thickening, scaling, and erythema; a score of 0 i

274 The plaque-to-healthy vessel wall ratio of (68)Ga-FOL was si

275 gression, we demonstrate that an increase in plaque Tregs is a common signature of regressing plaques

276 ld recoil varied according to the underlying plaque type (lipid: 0.63+/-1.23 mm(2); calcified: 0.81+/

277 MSI image registration using structured and plaque-unrelated reference ion images.

278 line microbiota were measured in subgingival plaque using 16S rRNA sequencing.

279 , inflamed lung regions, and atherosclerotic plaques using a clinical PET/magnetic resonance imaging

280 sma levels positively correlated with global plaque volume and coronary calcification.

281 ficacy end point, percentage change in total plaque volume at 90 days by intravascular ultrasound, on

282 udy, the rate of progression of total aortic plaque volume was >3-fold higher with ICIs (from 2.1%/y

283 score; 3DVUS to quantify carotid and femoral plaque volume; and coronary artery calcium score (CACS)

284 IP expression was reduced in human and mouse plaque VSMCs and by palmitate in a p38- and c-Jun N-term

285 ein expression is reduced in human and mouse plaque VSMCs and is positively regulated by CHIP.

286 structure and plaque composition as signs of plaque vulnerability, but few studies have analyzed hemo

287 ent phase velocities as novel biomarkers for plaque vulnerability.

288 An increased risk of noncalcified/mixed plaque was only found in patients exposed to abacavir.

289 Microglial clustering around plaques was impaired, plaques were more diffuse, and the

290 less activated (P = 0.07) and the number of plaques was reduced in the cortex (P = 0.03) following N

291 induced plaque rupture and in ruptured human plaques, we aimed to illuminate biochemical pathways thr

292 gival crevicular fluid (GCF) and subgingival plaque were collected and clinical periodontal parameter

293 Melanomas treated with the 10-mm plaque were smaller (median thickness, 1.9 mm vs. 2.6 mm

294 lial clustering around plaques was impaired, plaques were more diffuse, and the Abeta42:Abeta40 ratio

295 n 3D, a substantially larger number of small plaques were observed than that indicated by the 2D-MSI

296 glia exclusively surrounded NA+ amyloid beta plaques, which accumulated in an age-dependent manner.

297 f these species are commonly found in dental plaque, while N. meningitidis is primarily found in the

298 ted neuropathology, characterized by amyloid plaques with amyloid beta (Abeta) and neurofibrillary ta

299 microcalcification is a feature of coronary plaques with an increased propensity to rupture and to c

300 fibrils accumulate at the exterior of senile plaques, yet the protofibril-fibril interplay is not wel