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1 of quantitative and qualitative features of atherosclerotic plaque.
2 ion is a modifiable step in the evolution of atherosclerotic plaque.
3 L3 deficiency showed no evidence of coronary atherosclerotic plaque.
4 ia other mechanisms than inflammation in the atherosclerotic plaque.
5 ctor-alpha, a macrophage M1 marker, in human atherosclerotic plaque.
6 e has long been a hallmark of the vulnerable atherosclerotic plaque.
7 in removing lipids and debris present in the atherosclerotic plaque.
8 (inflammatory) from stable (noninflammatory) atherosclerotic plaque.
9 n that calcification serves to stabilize the atherosclerotic plaque.
10 u and disseminates to distant sites, such as atherosclerotic plaque.
11 number of typical hallmarks of ageing in the atherosclerotic plaque.
12 tive CD4(+) T-helper cells accumulate in the atherosclerotic plaque.
13 phy angiography can characterize subtypes of atherosclerotic plaque.
14 ncreased (18)F-fluoride activity in coronary atherosclerotic plaque.
15 major cell type present at all stages of an atherosclerotic plaque.
16 tomography identifies ruptured and high-risk atherosclerotic plaque.
17 ster-enriched foam cells are the hallmark of atherosclerotic plaques.
18 e to extracellular cholesterol deposition in atherosclerotic plaques.
19 01) was significantly lower in patients with atherosclerotic plaques.
20 ng with CXCR4 transcript expression in human atherosclerotic plaques.
21 ey autophagy markers in both mouse and human atherosclerotic plaques.
22 scular cell adhesion molecule 1 (VCAM-1), in atherosclerotic plaques.
23 as surrounding the calcium deposits in human atherosclerotic plaques.
24 and neutrophils in the perivascular area of atherosclerotic plaques.
25 /wk group had a higher prevalence of CAC and atherosclerotic plaques.
26 cy in reducing macrophage burden in advanced atherosclerotic plaques.
27 clerosis and the process of T cell homing to atherosclerotic plaques.
28 both the development and the progression of atherosclerotic plaques.
29 heir efficacy to reduce macrophage burden in atherosclerotic plaques.
30 ivation of platelets at the site of ruptured atherosclerotic plaques.
31 o identify a protein signature for high-risk atherosclerotic plaques.
32 se uptake in cultured macrophages and murine atherosclerotic plaques.
33 ocalized with Mac-3-positive macrophage-rich atherosclerotic plaques.
34 se-7 (Mmp-7) reduced VSMC apoptosis in mouse atherosclerotic plaques.
35 ersity of cells present in tissues including atherosclerotic plaques.
36 esterol fecal excretion and reduces inflamed atherosclerotic plaques.
37 a key factor in the development of necrotic atherosclerotic plaques.
38 e platforms accumulated to similar levels in atherosclerotic plaques.
39 vents, such as thrombosis, is the rupture of atherosclerotic plaques.
40 on of calcium phosphate minerals in advanced atherosclerotic plaques.
41 d epigenetic heterogeneity of macrophages in atherosclerotic plaques.
42 chanism by which enterovirus infect cells in atherosclerotic plaques.
43 ound on the surface of inflamed and ruptured atherosclerotic plaques.
44 the assessment of macrophage infiltration in atherosclerotic plaques.
45 oteolytic inactivation by other proteases in atherosclerotic plaques.
46 number of apoptotic macrophages in advanced atherosclerotic plaques.
47 in murine infarcts and both mouse and rabbit atherosclerotic plaques.
48 s and that necroptosis is active in advanced atherosclerotic plaques.
49 the progression and promote the stability of atherosclerotic plaques.
50 served VSMC accumulation after injury and in atherosclerotic plaques.
51 ifically needed for CD4 T-cell homing to the atherosclerotic plaques.
52 ) play an essential role in the formation of atherosclerotic plaques.
53 mmation and are involved in the formation of atherosclerotic plaques.
54 utor to atherogenesis and the progression of atherosclerotic plaques.
55 able and vulnerable regions of human carotid atherosclerotic plaques.
56 osis, or inflammatory parameters in advanced atherosclerotic plaques.
57 CD4(+) T cells are commonly found in atherosclerotic plaques.
58 f calcification in diseased heart valves and atherosclerotic plaques.
59 or the evaluation of metabolic activities in atherosclerotic plaques.
60 ells that amplify immune cell recruitment in atherosclerotic plaques.
61 hways they can contribute to inflammation in atherosclerotic plaques.
62 c heart, and reduced myeloid cell numbers in atherosclerotic plaques.
63 is, a common feature of high-risk/vulnerable atherosclerotic plaques.
64 s that control growth and destabilization of atherosclerotic plaques.
65 ivated in inflammatory macrophages and human atherosclerotic plaques.
66 s-affine Gadofluorine P for molecular MRI of atherosclerotic plaques.
67 esterol transport, resulting in reduction of atherosclerotic plaques.
68 f atherosclerosis but are seldom detected in atherosclerotic plaques.
69 reduced plasma total cholesterol levels and atherosclerotic plaques.
70 phages are the most abundant immune cells in atherosclerotic plaques.
71 scular events are often caused by rupture of atherosclerotic plaques.
72 -cell RNA sequencing of both mouse and human atherosclerotic plaques.
73 a promising therapeutic target to stabilize atherosclerotic plaques.
74 tes, suggesting a more benign composition of atherosclerotic plaques.
75 for imaging of smooth muscle cells (SMCs) in atherosclerotic plaques.
76 are capable of Ag presentation within human atherosclerotic plaques.
77 igher in advanced than in intermediate human atherosclerotic plaques.
78 enhanced apoptosis and lipid accumulation in atherosclerotic plaques.
79 release of proinflammatory mediators inside atherosclerotic plaques.
80 was correlated in unstable symptomatic human atherosclerotic plaques.
81 strated the highest accumulation in advanced atherosclerotic-plaques after four-months of HFD, the ir
83 iseases; although their contributory role to atherosclerotic plaque and abdominal aortic aneurysm sta
87 ascular photoacoustic imaging of lipid-laden atherosclerotic plaque and perivascular fat was demonstr
88 ne, could attenuate progression of preformed atherosclerotic plaque and to identify molecular mechani
89 rvous system, bone marrow, and spleen to the atherosclerotic plaque and to the infarcting myocardium.
90 -181b was overexpressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms a
91 -181b was overexpressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms a
92 we revealed that CPB isolated from calcified atherosclerotic plaques and artificially synthesised CPB
93 ro-inflammatory myeloid cells accumulated in atherosclerotic plaques and at the myocardial infarct si
94 el mechanistic link between NE expression in atherosclerotic plaques and concomitant pro-inflammatory
95 es was located in macrophage-rich regions of atherosclerotic plaques and correlated with the intensit
96 ed increased expression of SMILR in unstable atherosclerotic plaques and detected increased levels in
97 ition of FXa promotes regression of advanced atherosclerotic plaques and enhances plaque stability.
98 nscriptome-based cellular landscape of human atherosclerotic plaques and highlights cellular plastici
99 and extracellular matrix deposition both in atherosclerotic plaques and in vascular smooth muscle ce
100 KB1 expression was examined in human carotid atherosclerotic plaques and in western diet-fed atherosc
102 lement system is a major alteration in early atherosclerotic plaques and is reflected by increased C5
104 represent a major immune cell population in atherosclerotic plaques and play central role in the pro
105 inflammatory state and macrophage burden of atherosclerotic plaques and potentially identify vulnera
106 Cholesterol crystals (CC) are abundant in atherosclerotic plaques and promote inflammatory respons
108 other ACTA2+ fibrous cap cells destabilizes atherosclerotic plaques and that there are critical gene
109 coronary artery ligation to mimic vulnerable atherosclerotic plaques and their rupture leading to MI.
110 hod generates complete 3D reconstructions of atherosclerotic plaques and uncovers their volume, geome
111 markedly reduced in VSMCs in human and mouse atherosclerotic plaques, and in human VSMCs derived from
112 ly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-14
113 ia, coronary artery calcification (CAC), and atherosclerotic plaque are risk factors for the developm
114 number and activity of T cell subsets in the atherosclerotic plaques are critical for the prognosis o
116 in injury-induced neointimal lesions and in atherosclerotic plaques are oligoclonal, derived from fe
118 phages surrounding calcium deposits in human atherosclerotic plaques are phenotypically defective bei
120 we demonstrated PCSK6 upregulation in human atherosclerotic plaques associated with smooth muscle ce
121 d physiology, and determine the formation of atherosclerotic plaques at regions of disturbed flow.
122 In vivo-administered msR4M-L1 enriches in atherosclerotic plaques, blocks arterial leukocyte adhes
124 beyond its association with total calcified atherosclerotic plaque burden as assessed by coronary ar
125 ced endothelial cell activation and elevated atherosclerotic plaque burden compared with Ldlr(-/-) mi
127 ticipated in the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Thera
132 that IL-19 can halt progression of preformed atherosclerotic plaques by regulating both macrophage in
135 that LOY is associated with the severity of atherosclerotic plaque characteristics and outcome in me
136 for accelerated, objective, and reproducible atherosclerotic plaque characterization beyond subjectiv
137 CT (IVOCT) images, we developed an automated atherosclerotic plaque characterization method that used
138 ce in haematopoietic cells results in larger atherosclerotic plaques, characterized by bigger necroti
139 cally active Ly-6C(high) monocytes, enhanced atherosclerotic plaque chemokine expression, and monocyt
141 in VSMCs in thin fibrous caps of late-stage atherosclerotic plaques compared to early fibroatheroma
142 3a/b was markedly increased in human carotid atherosclerotic plaques compared with normal arteries, a
143 viously reported to be up-regulated in human atherosclerotic plaques compared with normal vessel.
144 In vivo uptake of (18)F-FCH in human carotid atherosclerotic plaques correlated strongly with degree
147 the roles of VSMCs and VSMC-derived cells in atherosclerotic plaque development and progression.
149 ct4 serves a critical protective role during atherosclerotic plaque development by promoting smooth m
150 by plasma cells and determine the impact on atherosclerotic plaque development in mice with and with
151 eeper understanding of how B cells influence atherosclerotic plaque development is being pursued with
156 ontrast, VSMC Akt1 inhibition in established atherosclerotic plaques does not influence lesion size b
159 they may play a causative role in triggering atherosclerotic plaque formation and arterial thrombosis
165 inical goal, and treatments that can reverse atherosclerotic plaque formation are actively being soug
167 thelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endotheli
168 in enhanced adipose-tissue inflammation and atherosclerotic plaque formation in a mouse model of obe
170 with oxPAPC-driven metabolic changes reduce atherosclerotic plaque formation in mice, thereby unders
175 n high-fat diet-fed Ldlr(-/-) mice decreased atherosclerotic plaque formation, associated with decrea
176 (-/-)Apoe(-/-) knockout mice show diminished atherosclerotic plaque formation, characterized by reduc
177 olesterol diet, Tcad/ApoE-DKO mice increased atherosclerotic plaque formation, despite a 5-fold incre
178 bone marrow from Abca1(BSM) mice had reduced atherosclerotic plaque formation, similar to mice transp
185 Here Htun et al. demonstrate that vulnerable atherosclerotic plaques generate near-infrared autofluor
186 ough coronary thrombus overlying a disrupted atherosclerotic plaque has long been considered the hall
187 modelling of the stress distribution within atherosclerotic plaques has suggested that subcellular m
188 and FBS showed lower adjusted odds of having atherosclerotic plaques (ICHS odds ratio [OR]: 0.41; 95%
191 lete thrombotic occlusion developing from an atherosclerotic plaque in an epicardial coronary vessel
194 has pursued the quest to identify vulnerable atherosclerotic plaque in patients for decades, hoping t
195 coupled eNOS and reduced the size of carotid atherosclerotic plaque in rats feeding with high fat die
197 hletes despite the presence of more coronary atherosclerotic plaque in the most active participants.
199 oxaban on both newly-formed and pre-existing atherosclerotic plaques in apolipoprotein-e deficient (A
200 rophages markedly reduced the size of aortic atherosclerotic plaques in both Ldlr(-/-BMT: Flnao/fl/LC
201 lating CCR2(+) monocytes and the size of the atherosclerotic plaques in both the carotid artery and t
202 lly, calpeptin treatment reduced the size of atherosclerotic plaques in C57BL/6 mice infected with Ad
203 h cortistatin reduced the number and size of atherosclerotic plaques in carotid artery, heart, aortic
204 Snail was also expressed in EC overlying atherosclerotic plaques in coronary arteries from patien
205 B gene has been linked to the development of atherosclerotic plaques in humans and in a mouse model o
206 Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced at
208 otes macrophage emigration and regression of atherosclerotic plaques in part by liver X receptor (LXR
211 stern diet for 12 wk had significantly fewer atherosclerotic plaques in their aortas than the control
213 led accumulation of the nanoparticles in the atherosclerotic plaques increased by 3.3-fold following
214 on of CCTA vessel wall and quantification of atherosclerotic plaque, independent of the amount of ste
220 on imaging and early detection of high-risk atherosclerotic plaques is important for risk stratifica
221 n PET-positive, CT-negative regions of human atherosclerotic plaques is the result of developing micr
222 y response and deposits in foam cells at the atherosclerotic plaque, it also regulates cellular mecha
224 mulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-ca
225 cruitment into plaques, leading to increased atherosclerotic plaque macrophage content and inflammati
226 tomography (PET) is considered a measure of atherosclerotic plaque macrophages and is used for quant
228 der arterial flow conditions on collagen and atherosclerotic plaque material, were attenuated by riva
229 y GM-CSF and M-CSF in either cell culture or atherosclerotic plaques may not be distinguishable by th
230 nd in primary human coronary artery SMCs and atherosclerotic plaques obtained at carotid endarterecto
231 expression on inflammatory cells present in atherosclerotic plaques of an experimental rabbit model.
232 Male athletes had a higher prevalence of atherosclerotic plaques of any luminal irregularity (44.
233 evation in smooth muscle accumulation within atherosclerotic plaques of ApoE KO mice, suggesting plaq
235 herosclerosis, which was also found in human atherosclerotic plaques of carotid and coronary arteries
236 phils and in the inflammatory environment of atherosclerotic plaques of diabetic mice after cholester
237 were detected in vivo with PET/MR imaging in atherosclerotic plaques of the abdominal aorta and right
238 were detected in vivo with PET/MR imaging in atherosclerotic plaques of the abdominal aorta and right
239 occlusion localized at the site of high-risk atherosclerotic plaques, of which early detection and th
241 a peptide, LyP-1, which specifically targets atherosclerotic plaques, penetrates into plaque interior
242 sted LOY for association with (inflammatory) atherosclerotic plaque phenotypes and cytokines and asse
243 tokines, which are present at high levels in atherosclerotic plaques, play important roles in regulat
244 he identification of patients with high-risk atherosclerotic plaques prior to the manifestation of cl
246 is association between ICI use and increased atherosclerotic plaque progression was attenuated with c
247 , in an imaging substudy (n=40), the rate of atherosclerotic plaque progression was compared from bef
248 own an association of ADAM10 expression with atherosclerotic plaque progression, a causal role of ADA
249 However, the role of GM-CSF in advanced atherosclerotic plaque progression, the process that giv
250 alled carbon nanotubes accumulate within the atherosclerotic plaque, reactivate lesional phagocytosis
251 secondary to rupture or erosion of advanced atherosclerotic plaques represent the leading cause of d
254 dial infarction is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus f
255 onnection between myocardial infarctions and atherosclerotic plaque rupture events in the coronary ar
257 Coronary artery thrombosis is dominated by atherosclerotic plaque rupture, complex pulsatile flows
258 involved in the thrombus formation stage on atherosclerotic plaque rupture, we hypothesized that fac
261 f microcalcifications that are implicated in atherosclerotic plaque rupture; however, the mechanisms
262 ously demonstrated that both human and mouse atherosclerotic plaques show elevated expression of EphA
263 tilized the apoE(-/-) mouse model to compare atherosclerotic plaque size and composition after inorga
264 ice exhibited a significant reduction of the atherosclerotic plaque size at the aortic root and the a
265 1 (Trem-1(-/-)) showed a strong reduction of atherosclerotic plaque size in both the aortic sinus and
266 ies, and, in a hyperlipidemia model, reduced atherosclerotic plaque size while increasing markers of
267 -helper type-1 immune responses, and reduced atherosclerotic plaque size without altering the plasma
271 ur findings identify HDAC9 as a regulator of atherosclerotic plaque stability and IKK activation thus
274 essfully translated to in vivo evaluation of atherosclerotic plaque structure and biology in a precli
276 peptide expressed in the vascular system and atherosclerotic plaques that regulates vascular calcific
277 lial nitric oxide synthase, the stability of atherosclerotic plaques, the production of proinflammato
278 ivo histopathologic quantitative measures of atherosclerotic plaque tissue characteristics, as well a
279 cells and expression of CX3CL1 and LFA-3 in atherosclerotic plaque tissues from HIV-uninfected donor
281 single-cell ATAC sequencing on human carotid atherosclerotic plaques to define the cells at play and
284 rcted myocardium, inflamed lung regions, and atherosclerotic plaques using a clinical PET/magnetic re
285 ed lipids in endarterectomized human carotid atherosclerotic plaques using three-dimensional (3D) ele
288 tion on apoA-I that is abundant within human atherosclerotic plaque, was further investigated by usin
289 ports showing the presence of enterovirus in atherosclerotic plaques we hypothesized that the coxsack
294 and numbers of CD68-positive macrophages in atherosclerotic plaques were lower in Flna-deficient mic
295 MIs result spontaneously from instability of atherosclerotic plaque, whereas type 2 MIs occur in the
296 dothelium predisposes it toward formation of atherosclerotic plaque, which may be a subsequent risk f
297 valence of coronary artery calcification and atherosclerotic plaques, which are strong predictors for
298 -) mice show reduced progression to advanced atherosclerotic plaques with diminished smooth muscle an
299 vel technology that allows identification of atherosclerotic plaques with intraplaque hemorrhage and