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1 n Americans from MESA (Multi-Ethnic Study of Atherosclerosis).
2 r disease in the MESA (Multi-Ethnic Study of Atherosclerosis).
3 s, with higher values indicating more severe atherosclerosis).
4 cipants from the MESA (Multi-Ethnic Study of Atherosclerosis).
5 c events in stable patients with symptomatic atherosclerosis.
6 ses against lipoprotein particles that drive atherosclerosis.
7 had a greater burden of subclinical coronary atherosclerosis.
8 A TLR7 antagonist may mitigate atherosclerosis.
9 that IRF5 maintains CD11c(+) macrophages in atherosclerosis.
10 mpaired resolution during the progression of atherosclerosis.
11 besity, including the metabolic syndrome and atherosclerosis.
12 ifestyle are risk factors for HIV-associated atherosclerosis.
13 HIV alone accelerates atherosclerosis.
14 ase (eNOS) uncoupling, is an initial step in atherosclerosis.
15 R results in severe hypercholesterolemia and atherosclerosis.
16 in the development of obesity, diabetes, and atherosclerosis.
17 ke, which consequently results in attenuated atherosclerosis.
18 19 participants in the Multi-Ethnic Study of Atherosclerosis.
19 ular Health Study, and Multi-Ethnic Study of Atherosclerosis.
20 odulators of inflammatory processes, such as atherosclerosis.
21 sidered as a medicine to treat patients with atherosclerosis.
22 cting the presence and extent of subclinical atherosclerosis.
23 gate the functional role of P2X7 knockout in atherosclerosis.
24 rction, various types of cardiomyopathy, and atherosclerosis.
25 ammatory IL-1beta levels, leading to reduced atherosclerosis.
26 Endothelial cells (EC) play a key role in atherosclerosis.
27 n the lesions, and limits the development of atherosclerosis.
28 ity, but also ameliorated significant aortic atherosclerosis.
29 RA and might be linked to the development of atherosclerosis.
30 es associated with complex diseases, such as atherosclerosis.
31 promotes lesion formation and progression of atherosclerosis.
32 n interesting potential new target to combat atherosclerosis.
33 nflammation is central in the development of atherosclerosis.
34 er indication for the roles of ROS and NO in atherosclerosis.
35 several prevalent human diseases, including atherosclerosis.
36 as a potential therapeutic strategy against atherosclerosis.
37 a new era of anti-inflammatory therapies for atherosclerosis.
38 terms intracranial stenosis and intracranial atherosclerosis.
39 involved in a number of diseases, including atherosclerosis.
40 volumes of exercise may accelerate coronary atherosclerosis.
41 ed a potential link between hypertension and atherosclerosis.
42 n increases monocyte recruitment and worsens atherosclerosis.
43 x1 may be a potential therapeutic target for atherosclerosis.
44 with a proinflammatory status and increased atherosclerosis.
45 roles of vascular oxidative stress and NO in atherosclerosis.
46 s of antiplatelet therapies in patients with atherosclerosis.
47 r plaque stabilization in mice with advanced atherosclerosis.
48 ammasome activation and reduced experimental atherosclerosis.
49 s foam cell formation and the progression of atherosclerosis.
50 l roles in the progression and regression of atherosclerosis.
51 nk augmented sGC expression to lower risk of atherosclerosis.
52 latory properties of MSCs from patients with atherosclerosis.
53 s for analyses of cargo proteins relevant to atherosclerosis.
54 ults in vascular inflammation and ultimately atherosclerosis.
55 e is known regarding the epigenetic basis of atherosclerosis.
56 disease, autoimmunity, allergy, cancer, and atherosclerosis.
57 n by As3MT was required for arsenic-enhanced atherosclerosis.
58 mokine and cytokine genes that contribute to atherosclerosis.
59 feeding them an atherogenic diet to produce atherosclerosis.
60 e layer of initiation for the progression of atherosclerosis.
61 w shear stress sites that are predisposed to atherosclerosis.
62 ling during restenosis after angioplasty and atherosclerosis.
63 n assess both anatomy and biology of carotid atherosclerosis.
64 ght into the protective role of C1q in early atherosclerosis.
65 cardial dysfunction and accelerated coronary atherosclerosis.
66 was inflammatory response in the process of atherosclerosis.
67 r than 300 Agatston units, reflecting severe atherosclerosis.
68 d epigenome signatures associated with human atherosclerosis.
69 Many CVRF-free middle-aged individuals have atherosclerosis.
70 echanism by which sIgM deficiency aggravates atherosclerosis.
71 sterol concentrations, obesity, and coronary atherosclerosis.
72 ress is an early event in the development of atherosclerosis.
73 l responses and functions may be involved in atherosclerosis.
74 o [(18)F]FDG PET imaging in 42 patients with atherosclerosis.
75 the potential for using BCD in treatment of atherosclerosis.
76 treatment of the clinical manifestations of atherosclerosis.
77 y improves endothelial function and prevents atherosclerosis.
78 t vasodilation, blood vessel remodeling, and atherosclerosis.
79 otein E-deficient (Apoe(-/-)) mouse model of atherosclerosis.
80 ession of ARID5B to be associated with human atherosclerosis.
81 opose potential mechanisms of HIV-associated atherosclerosis.
82 e potential for proresolving therapeutics in atherosclerosis.
83 f1 were protected from high-fat diet-induced atherosclerosis.
84 associated with growth-factor signaling and atherosclerosis.
85 Radiation therapy often accelerates atherosclerosis.
86 l wall play critical roles in the process of atherosclerosis.
87 iR-155 deficiency in apoE(-/-) mice inhibits atherosclerosis; 2) apoE(-/-)/miR-155(-/-) (double knock
89 From a population-based study on subclinical atherosclerosis, 40 participants with IPH at baseline ma
90 participants of MESA ([Multi-Ethnic Study of Atherosclerosis] 68.7 years, 53.0% women, white 42.2%, C
91 participants in MESA (Multi-Ethnic Study of Atherosclerosis), a cohort initially free of overt cardi
92 ants enrolled in MESA (Multi-Ethnic Study of Atherosclerosis), a population-based cohort aged 45-84 y
93 diabetes cases in the Multi-Ethnic Study of Atherosclerosis, a multicenter US study of Caucasian, Af
95 of endothelial ADK in mice leads to reduced atherosclerosis and affords protection against ischemia/
96 ic potential for limiting the progression of atherosclerosis and aneurysms and protecting them from r
101 o target inflamed endothelium, shows reduced atherosclerosis and CC formation in ApoE (-/-) mice.
102 rally associated with higher risk of carotid atherosclerosis and clinical cardiovascular disease but
103 ic risk have a greater burden of subclinical atherosclerosis and derive greater relative and absolute
105 mplications for novel vaccine strategies for atherosclerosis and in understanding the impacts of immu
106 were associated with progression to advanced atherosclerosis and incidence of cardiovascular disease
107 cigarette smoke is known to promote coronary atherosclerosis and increase the likelihood of myocardia
108 ance is highly prevalent among patients with atherosclerosis and is associated with an increased risk
109 icantly associated with surrogate markers of atherosclerosis and is linked to the presence of cardiov
111 Inflammation is a critical factor in early atherosclerosis and its progression to myocardial infarc
112 ypercholesterolemia is a key risk factor for atherosclerosis and leads to the uptake of native and ox
114 k is associated with more severe symptomatic atherosclerosis and more intensive antiplatelet therapy
116 as decreased IgM, associated with increased atherosclerosis and necrotic cores, and a decrease in pl
117 ction during the pathological development of atherosclerosis and offer novel prevention and therapeut
118 , which can be advanced for the treatment of atherosclerosis and other inflammatory disorders in the
119 We examined the role of vascular CXCR4 in atherosclerosis and plaque composition by inducing an en
120 the specific role of MC1-R in the context of atherosclerosis and possible regulatory pathways of MC1-
121 are a foundation for defining mechanisms of atherosclerosis and potential targets of drugs to preven
122 ng mouse Angptl3 retarded the progression of atherosclerosis and reduced levels of atherogenic lipopr
123 lammation resolution may become defective in atherosclerosis and the potential for proresolving thera
124 lammation in many common diseases, including atherosclerosis and type 2 diabetes, driving the product
125 h Study, MESA (Multiethnic European Study of Atherosclerosis), and the AGE-RS (Age, Gene/Environment
126 sal role in the development of hypertension, atherosclerosis, and associated cardiovascular events su
127 disease (PVOD) is a common manifestation of atherosclerosis, and it has a high rate of morbidity.
128 ledge about lycopene's preventive effects in atherosclerosis, and other cardiovascular diseases, must
130 n two well-established preclinical models of atherosclerosis, and the molecular and cellular mechanis
131 lasma lipoproteins and spontaneously develop atherosclerosis, ApoE(-/-)/AMPKalpha1(-/-) mice showed r
135 (added to titrated insulin therapy) reduced atherosclerosis, as measured by progression of common ca
136 ly men and postmenopausal women with carotid atherosclerosis, as well as with risk of stroke in this
137 ted by measuring (1) presence of subclinical atherosclerosis, assessed by coronary artery calcificati
139 ntibody deficiency significantly accelerated atherosclerosis at both the aortic root and aortic arch.
141 These data suggest a relationship between atherosclerosis burden and VTE risk, and they support in
143 development of hypercholesterolemia-induced atherosclerosis, but may play a role when an additional
144 t in chronic inflammatory processes, such as atherosclerosis, but the control of the vascular inflamm
145 epigenetically controlled enhancer, promotes atherosclerosis by dysregulating immunometabolism toward
146 died whether myeloid Bmal1 deletion promotes atherosclerosis by enhancing monocyte recruitment to ath
147 hat Bmal1 deficiency in macrophages promotes atherosclerosis by enhancing recruitment of Ly6c(hi) mon
149 se alpha1 (AMPKalpha1) in monocytes promotes atherosclerosis by increasing monocyte differentiation a
150 clearly establish that vascular CXCR4 limits atherosclerosis by maintaining arterial integrity, prese
152 ion may regulate the progression to advanced atherosclerosis by regulating smooth muscle proliferatio
155 r 7 or 18 weeks developed significantly more atherosclerosis compared to Apoe (-/-) Il27ra (+/-) cont
156 y associated with both ARID5B expression and atherosclerosis, consistent with this CpG residing in an
158 ull) mice deficient in miR-146a develop less atherosclerosis, despite having highly elevated levels o
159 s intrahepatic T-cell differentiation during atherosclerosis development and indicates that intrahepa
160 ll content within arterial plaques and limit atherosclerosis development in a context of moderate hyp
165 ammatory bowel disease), metabolic diseases (atherosclerosis, diabetes and obesity) and major infecti
166 r detection of high-risk plaques in patients.Atherosclerosis diagnosis relies primarily on imaging an
167 ed PEMT showed that they were protected from atherosclerosis, diet-induced obesity, and insulin resis
168 Cholesterol is an important risk factor of atherosclerosis, due to its active uptake by monocytes/m
172 omen and 1124 men (>/=45 years) with carotid atherosclerosis, from prospective population-based RS (R
173 t of dysregulated inflammation resolution in atherosclerosis has been known for several decades.
175 tter understand the TF-related mechanisms in atherosclerosis, here we investigated the role of 12/15-
176 was shown to suppress T cells activation in atherosclerosis, however it's possible role in myeloid c
177 effects and reduces periodontal diseases and atherosclerosis; however, its role in regulating periodo
178 o confirm a direct role of TSP-1 in diabetic atherosclerosis, hyperglycemic TSP-1(-/-)/ApoE(-/-) doub
179 sis, have been linked to pathologies such as atherosclerosis, hypertension, heart failure, chronic ki
180 cur in the absence of comorbidities, such as atherosclerosis, hypertension, renal dysfunction, and di
186 terial thrombosis was related to accelerated atherosclerosis in animal models; however, contrasting f
187 chlamydia pneumonia) in stabilizing advanced atherosclerosis in Apob(tm2Sgy)/Ldlr(tm1Her/J) mice.
188 ion (Baffr deficiency) significantly reduces atherosclerosis in Apoe (-/-) mice infused with AngII.
189 ntify biological components that may promote atherosclerosis in chronic inflammatory conditions.
191 ression protected against the development of atherosclerosis in LDL-receptor/ApoB48-deficient mice.
195 This study confirms increased prevalence of atherosclerosis in RA and provides data to support the h
202 hroughout its spectrum; that is, subclinical atherosclerosis, incident atherosclerotic cardiovascular
203 ber of human diseases, such as arthritis and atherosclerosis, include characteristic pathology in spe
204 function are critical in the pathogenesis of atherosclerosis, including in the setting of diabetes.
205 dds of prevalent noncoronary and generalized atherosclerosis independently of the presence of convent
206 , aortic arch and aorta in acute and chronic atherosclerosis induced in apolipoprotein E-deficient mi
216 d activation of immune cells to the aorta in atherosclerosis is regulated by adhesion molecules, chem
220 (NK) cells in experimental animal models of atherosclerosis, it is not yet clear whether NK cells be
223 servational studies suggest that symptomatic atherosclerosis may be associated with risk of venous th
224 elines that include detection of subclinical atherosclerosis may help to identify HIV-infected adults
225 ere consistently associated with subclinical atherosclerosis measures (coronary calcium score and car
227 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with SBP between 120 and 179 mm H
228 pared with that in the Multi-Ethnic Study of Atherosclerosis (MESA), a Human Immunodeficiency Virus (
229 Using data from the Multi-Ethnic Study of Atherosclerosis (MESA), we evaluated associations of nei
235 articipants from MESA (Multi-Ethnic Study of Atherosclerosis) (n=6621) and the Dallas Heart Study (n=
236 diagnosis, and treatment of stroke caused by atherosclerosis of the major intracranial arteries.
237 TS: In a rat model of ageing that is free of atherosclerosis or hypertension, E/A, a diagnostic measu
238 69 participants in the Multi-Ethnic Study of Atherosclerosis, or MESA, who were free of prior myocard
239 To assess whether P2X7 may have a role in atherosclerosis, P2X7 expression was analyzed in aortic
240 hylated regions (DMR) could be identified in atherosclerosis patients, related to epigenetic control
241 n cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inf
244 -I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, an
245 ample nested within the prospective Salzburg Atherosclerosis Prevention Program in Subjects at High I
249 erosclerotic plaques and in western diet-fed atherosclerosis-prone Ldlr(-/-) and ApoE(-/-) mice.
250 reg cells relocated to the inflamed aorta in atherosclerosis-prone low-density lipoprotein receptor d
252 associated with increased susceptibility to atherosclerosis, provides a clinical human model that ca
253 work portraits rheumatoid arthritis, asthma, atherosclerosis, pulmonary diseases and Crohn's disease
254 arteries of Macaca fascicularis subjected to atherosclerosis regression diet, and in endothelial cell
255 tial association of the M2 polarization with atherosclerosis regression remain poorly understood.
257 down reduced expression of genes involved in atherosclerosis-related inflammatory and lipid metabolis
261 n age-related and chronic conditions such as atherosclerosis, rheumatoid arthritis, psoriasis, and Cr
262 y number using exome sequencing reads in the Atherosclerosis Risk in Communities (ARIC) Study, a comm
265 were classified in 6118 participants in the Atherosclerosis Risk in Communities study (67-91 years o
266 studies: Cardiovascular Health Study (CHS), Atherosclerosis Risk in Communities Study (ARIC), and Mu
267 case-fatality among blacks and whites in the Atherosclerosis Risk in Communities study (ARIC), the Ca
268 ters) from 6,793 individuals from the Dental Atherosclerosis Risk in Communities Study (DARIC) were u
270 omen's Health Initiative clinical trials and Atherosclerosis Risk in Communities Study subpopulations
271 luded 11,715 middle-aged adults in the ARIC (Atherosclerosis Risk In Communities) cohort with heart r
273 5801 elderly participants in the ARIC study (Atherosclerosis Risk in Communities; age range, 67-90 ye
274 e used ECG measurements from the ARIC study (Atherosclerosis Risk in Communities; n=6731 subjects) an
275 olecular phenotypes associated with coronary atherosclerosis severity in patients at least 65 years o
276 Strokes were classified as large artery atherosclerosis, small vessel occlusion, or cardioemboli
277 2.2%) PESA (Progression of Early Subclinical Atherosclerosis) study participants (age 45.8 +/- 4.3 ye
279 sity with obesity and complexity of coronary atherosclerosis (SYNTAX score) in a cohort of 351 adults
281 itudinal data from the Multi-Ethnic Study of Atherosclerosis that were linked to foreclosure data fro
282 ic exposure is known to increase the risk of atherosclerosis, the contribution of arsenic methylation
284 tes and monocyte-derived macrophages promote atherosclerosis through increased inflammation and vascu
285 wall ameliorates the disturbed flow-induced atherosclerosis through, at least in part, targeting cel
286 ate the association of thyroid function with atherosclerosis throughout its spectrum; that is, subcli
287 rly subjects were positively associated with atherosclerosis throughout the whole disease spectrum, i
288 ciation guidelines, and subclinical coronary atherosclerosis was assessed by computed tomography.
293 To test a direct participation of TLR7 in atherosclerosis, we crossbred TLR7-deficient (Tlr7 (-/-)
295 be associated with a high risk of developing atherosclerosis.We estimated the no-observed-adverse-eff
296 ects of constitutively active CD40 in DCs on atherosclerosis were examined using low-density lipoprot
297 dlr(-/-) mice accelerates the development of atherosclerosis, which is prevented by reconstitution wi
298 ayers in the development and exacerbation of atherosclerosis, which prompts the question as to whethe
299 considered to be a manifestation of systemic atherosclerosis with associated adverse cardiovascular a
300 the role of interleukin-1beta inhibition in atherosclerosis, with the aim of establishing whether in
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