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1 and PC diets were equally hyperlipidemic and hypercholesterolemic.
2 urveys, 60.7% to 64.3% of hypertensives were hypercholesterolemic.
3 vascular and platelet function in untreated hypercholesterolemics.
4 nted in hypertensive (215+/-44%; p=0.02) and hypercholesterolemic (172+/-71%; p=0.02) patients compar
5 n hypertensive (37+/-11%; p=0.01) but not in hypercholesterolemic (85+/-21%; p=0.78) patients compare
6 ega6/omega3 (0.08-0.21), hypocholesterolemic/hypercholesterolemic acid ratios (HH) (0.87-2.43), ather
7 ed system showed superior performance in all hypercholesterolemic adults (AUC=0.94-0.97) as well as i
13 ween relative weight and CVD risk factors in hypercholesterolemic and nonhypercholesterolemic childre
14 , it is clear that saturated fatty acids are hypercholesterolemic and that unsaturated fatty acids el
15 in/kexin type 9 (PCSK9) show promise as anti-hypercholesterolemic and, therefore, anti-atheroscleroti
21 ts show that in vivo biopanning selection in hypercholesterolemic animals makes it possible to identi
23 induced atherosclerotic plaque formation in hypercholesterolemic ApoE mice by placing semiconstricti
27 rophage ACAT1 accelerates atherosclerosis in hypercholesterolemic apoE-/- mice but has no effect when
28 d rHDL, infusion of PEG-rHDL (40 mg/kg) into hypercholesterolemic Apoe-/- mice led to more pronounced
29 PEG-rHDL was estimated after injection into hypercholesterolemic Apoe-/- mice; the half-life of pegy
30 i) monocyte subset increased dramatically in hypercholesterolemic apoE-deficient mice consuming a hig
33 ApoE(-/-), and ApoE(-/-)Glut1(+/-) mice into hypercholesterolemic ApoE-deficient mice, we found that
34 could restore normal endothelial function in hypercholesterolemic apolipoprotein (apo) E-null mice.
35 -poor lesions in the flow cessation model in hypercholesterolemic apolipoprotein E knockout (ApoE KO)
36 ces a significant reduction of restenosis in hypercholesterolemic apolipoprotein E knockout mice subj
38 olysis, and osteogenesis in aortic valves of hypercholesterolemic apolipoprotein E-deficient mice (30
40 embrane injection into neointimal lesions of hypercholesterolemic apolipoprotein E-deficient mice.
41 senescence and atherosclerosis in aortas of hypercholesterolemic apolipoprotein E-deficient mice.
43 y, we performed a series of assessments with hypercholesterolemic (apolipoprotein E-null [ApoE(-/-)])
44 , plasminogen-deficient mice were crossed to hypercholesterolemic, apolipoprotein E-deficient mice pr
49 ly oxidized LDL subfraction present in human hypercholesterolemic but not normolipidemic plasma can i
54 n carbohydrate intake and HDL cholesterol in hypercholesterolemic children consuming fat-restricted d
55 with lower HDL-cholesterol concentrations in hypercholesterolemic children consuming reduced-fat diet
56 n blood lipids and other CVD risk factors in hypercholesterolemic children, although the strength of
58 adaptive immune response prevails under the hypercholesterolemic conditions present in atheroscleros
63 ation of vasa vasorum occurs in experimental hypercholesterolemic coronary arteries and may be a part
67 e fed either a normal diet (control, n=7), a hypercholesterolemic diet (HCC, n=7), or a hypercholeste
69 8.5 to 16.0] for wild-type mice on chow and hypercholesterolemic diet and for apolipoprotein E-defic
70 ring of all groups (n=136) were fed a mildly hypercholesterolemic diet for up to a year and had simil
71 of TGF-beta signaling in Apoe(-/-) mice on a hypercholesterolemic diet led to development of aortic a
73 a hypercholesterolemic diet (HCC, n=7), or a hypercholesterolemic diet with supplemental resveratrol
74 ere placed on a normal chow diet (N) or on a hypercholesterolemic diet without (HC) or with vitamin C
75 e placed on a normal diet (N; n = 7) or on a hypercholesterolemic diet without (HC; n = 6) or with ET
79 s was fed control chow and 8 groups were fed hypercholesterolemic diets Chol 1 (yielding plasma chole
81 ike 1 transporter with ezetimibe reduced the hypercholesterolemic effect of [Thr28, Nle31]-CCK in LDL
86 embrane and improvement in relaxation in the hypercholesterolemic group given fish oils was seen (r=.
87 high-performance liquid chromatography in 49 hypercholesterolemic (HC) and 31 normocholesterolemic (N
89 d tomography after a 12-week normal (n=7) or hypercholesterolemic (HC, n=7) diet, RAS (n=6), or concu
90 DS AND In normocholesterolemic (NC, n=7) and hypercholesterolemic (HC, n=7) Yucatan male pigs, the le
91 s elevated (P<0.0005) in homozygous familial hypercholesterolemic (HFH) patients (85+/-5.5; n=38) com
92 Pigs were fed a normocholesterolemic (NC) or hypercholesterolemic (HL) diet for 10 days, reaching non
93 lectronegative LDL subfraction isolated from hypercholesterolemic human plasma with a recombinant pla
95 t diet, male apoB/BATless mice became obese, hypercholesterolemic, hypertriglyceridemic, and hyperins
99 in 2 dissimilar models of vascular disease: hypercholesterolemic LDL receptor-null (Ldlr(-/-)) mice
101 Study for nonobese 5-6-y-old black and white hypercholesterolemic (LDL cholesterol > 75th percentile;
102 total resistance to atherogenesis, even on a hypercholesterolemic (LDL receptor-null) background.
105 vasodilation and arterial wall thickness in hypercholesterolemic Ldlr(-/-) mice and Ldlr(-/-)/apoA-I
106 ctor 2 (KLF2) accelerates atherosclerosis in hypercholesterolemic Ldlr(-/-) mice due to the enhanced
107 , whereas the disrupted liver homeostasis in hypercholesterolemic Ldlr(-/-) mice led to intrahepatic
111 t endothelial Kir channels are suppressed by hypercholesterolemic levels of lipoproteins in vitro and
112 ress and high atherosclerosis-prone areas of hypercholesterolemic low-density lipoprotein receptor kn
113 ogenesis, we investigated arterial growth in hypercholesterolemic low-density lipoprotein receptor(-/
115 Step I diet, 13 normocholesterolemic and 13 hypercholesterolemic men aged 20-50 y were enrolled in a
119 d, crossover, metabolic-ward study, 7 mildly hypercholesterolemic men were fed 3 natural-food diets s
120 vention Study, a primary prevention trial in hypercholesterolemic men) exhibited a similar, although
125 IGFBPs was replicated in wild-type SMCs from hypercholesterolemic mice and confirmed by silencing apo
126 xamined CD11c on blood leukocytes in apoE-/- hypercholesterolemic mice and found that compared with w
129 e that is assumed by the microvasculature of hypercholesterolemic mice and suggest that T lymphocytes
130 nt autoimmunity and suppress inflammation in hypercholesterolemic mice by attenuating lymphocyte chol
131 n or collapse of adventitial vasa vasorum in hypercholesterolemic mice by stimulating an increase in
133 eractions and ameliorates ischemic injury in hypercholesterolemic mice independently of lipid-lowerin
137 ormal erythrocyte morphology was observed in hypercholesterolemic mice lacking the high-density lipop
139 iae infection accelerates atherosclerosis in hypercholesterolemic mice predominantly through a TLR/My
142 l hypertrophy, inflammation, and fibrosis in hypercholesterolemic mice with diabetes, suggesting that
143 by genetic inactivation of the mttp gene in hypercholesterolemic mice with early aortic valve diseas
145 poprotein (oxLDL) and active immunization of hypercholesterolemic mice with oxLDL ameliorates atherog
146 in bone marrow cells reduced coagulation in hypercholesterolemic mice, consistent with a major role
149 macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a tra
150 progenitors in the bone marrow and spleen of hypercholesterolemic mice, effects that were partially r
151 O in macrophages promotes atherosclerosis in hypercholesterolemic mice, raising the possibility that
165 n coronary restenosis, PTCA was performed in hypercholesterolemic minipigs whose left anterior descen
167 to 53%, compared with offspring of untreated hypercholesterolemic mothers (P<0.01), with the greatest
169 e expression between offspring of normo- and hypercholesterolemic mothers persist long after birth, s
173 and MyD88 signaling in atherosclerosis in a hypercholesterolemic mouse model, providing a pathophysi
175 but was not significantly different between hypercholesterolemic (n = 27) and nonhypercholesterolemi
180 ession was increased in aortae obtained from hypercholesterolemic, oophorectomized animals supplement
181 ss of whether they were primed in vivo under hypercholesterolemic or control conditions, demonstratin
182 apoptosis and L4 had a mild effect, whereas hypercholesterolemic or normolipidemic L1-L3 had negligi
186 (NC), 11 hypertensive patients (HT), and 12 hypercholesterolemic patients (HChol), arteries (interna
188 Using a double-blind design, newly diagnosed hypercholesterolemic patients (n = 51) with asymptomatic
189 in healthy subjects (p=0.004 vs. saline) and hypercholesterolemic patients (p=0.03 vs. saline), but n
190 eous gluteal fat biopsies were taken from 16 hypercholesterolemic patients (serum total cholesterol,
192 parate occasion, to ET-1 were measured in 12 hypercholesterolemic patients and 12 normal control subj
194 broader lipid-altering effects when treating hypercholesterolemic patients at high risk for atheroscl
195 al subjects, 12 hypertensive patients and 10 hypercholesterolemic patients before and during NO synth
196 n-delivered nutrition intervention trial for hypercholesterolemic patients conducted in Worcester, Ma
197 apparently healthy individuals and genotyped hypercholesterolemic patients from clinical trial cohort
198 ous studies have shown that hypertensive and hypercholesterolemic patients have impaired endothelium-
201 to examine the effects of fish oils given to hypercholesterolemic patients on small artery function i
202 inuing arginine treatment), the platelets of hypercholesterolemic patients once again became hyperagg
206 and cytokine levels were compared between 11 hypercholesterolemic patients treated with simvastatin a
207 ctivity of endogenous endothelin-1 (ET-1) in hypercholesterolemic patients using antagonists of ET-1
208 gen showed increased aggregability (68.6% in hypercholesterolemic patients vs. 54.5% in normocholeste
209 ow-density lipoprotein apheresis in severely hypercholesterolemic patients who are refractory to lipi
210 s evolocumab compared with oral ezetimibe in hypercholesterolemic patients who are unable to tolerate
212 tography of LDL samples from 7 asymptomatic, hypercholesterolemic patients yielded subfractions L1-L5
213 a small molecule intended to lower LDL-C in hypercholesterolemic patients, and has been previously s
214 fy FBF from baseline (p = 0.78); however, in hypercholesterolemic patients, BQ-123 administration res
216 isoprostanes was significantly increased in hypercholesterolemic patients, whereas substrate AA in u
217 r activity of endogenous ET-1 is enhanced in hypercholesterolemic patients, whereas their sensitivity
218 oves nitric oxide-mediated vasodilatation in hypercholesterolemic patients, which is consistent with
223 herosclerotic lesion burden and phenotype in hypercholesterolemic PD-L1/2(-/-)LDLR(-/-) mice and LDLR
232 n of vasa vasorum in normal and experimental hypercholesterolemic porcine coronary arteries, using a
234 operties that may benefit the vasculature of hypercholesterolemic postmenopausal women, even if they
238 content were investigated in 66 free-living, hypercholesterolemic, postmenopausal women during a 6-mo
242 labeled with (64)Cu for noninvasive PET in a hypercholesterolemic rabbit with atherosclerotic-like le
244 s vasodilatory responses to acetylcholine in hypercholesterolemic rabbits and atherosclerotic humans.
245 yte adhesion and subendothelial migration in hypercholesterolemic rabbits and whether any gender diff
246 y found that administration of L-arginine to hypercholesterolemic rabbits induces regression of preex
248 shown that gene therapy with NO synthase in hypercholesterolemic rabbits substantially reverses the
251 a significant vascular protective effect in hypercholesterolemic rabbits, most likely by attenuation
258 th muscle cells was significantly greater in hypercholesterolemic recipients than in normocholesterol
259 ndices (higher atherogenic, thrombogenic and hypercholesterolemic saturated fatty acids and lower des
260 ificantly reduced serum LDL-C in healthy and hypercholesterolemic statin-treated subjects, including
262 was performed and included fifty moderately hypercholesterolemic subjects (mean LDL cholesterol = 16
265 20; P<0.05) was also increased in moderately hypercholesterolemic subjects (n=24) compared with their
269 mg) to a placebo administered once daily to hypercholesterolemic subjects greater than 18 years of a
270 ease (CAD) progression and cardiac events in hypercholesterolemic subjects is now widely accepted.
272 esterolemic control subjects, platelets from hypercholesterolemic subjects stimulated with 5 microgra
274 dose pravastatin (80 mg/day) administered to hypercholesterolemic subjects with chronic liver disease
277 sma total cholesterol and LDL cholesterol in hypercholesterolemic subjects, but the responsible soy c
284 eration and healing response in the familial hypercholesterolemic swine model of femoral restenosis.
287 applicable methods was markedly inhibited in hypercholesterolemic swine with coronary endothelial dys
291 cardial perfusion was significantly lower in hypercholesterolemic than in normocholesterolemic swine,
292 nificantly lower in the lateral territory of hypercholesterolemic versus normocholesterolemic animals
297 apeutic effects on vascular fatty lesions of hypercholesterolemic zebrafish by atorvastatin is notabl
298 henotypes are present in large quantities in hypercholesterolemic zebrafish larvae and support the us