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1 HDL cholesterol levels, apolipoprotein A-I, cholesterol
2 HDL from AgNO3-injected mice lacking Saa1.1 and Saa2.1 e
3 HDL from HD patients were enriched in SAA, LBP, ApoC-III
4 HDL functionality and particle size were determined.
5 HDL particles are captured from the blood stream by the
6 HDL size gradually decreased, i.e. nibbling, with the co
7 HDL that contains apoC-III was associated with a higher
8 HDL that increased IL-6 secretion were enriched in ApoC-
9 HDL triglyceride concentrations predict post-MI LVEF and
10 HDL were purified from healthy controls (n = 13), subjec
11 HDL-C level is unlikely to represent a CV-specific risk
12 HDL-c rate of change throughout pregnancy was negatively
13 HDLs were isolated, and lipidomics and differential prot
15 ty (OR/SD, 0.89; 95% CI, 0.72-1.10; P=0.28), HDL cholesterol (OR/SD, 0.82; 95% CI, 0.66-1.02; P=0.08)
16 , HDL particle number was the strongest of 4 HDL-related biomarkers as an inverse predictor of incide
17 -5.73, -2.84), DBP -2.56 mmHg (-3.40, 1.71), HDL +0.85 mg/dL (-0.10, 1.60), and TC -5.34 mg/dL (-9.72
19 holesteryl ester transfer protein activity), HDL antioxidant properties (paraoxonase-1 arylesterase a
22 s: "gobbling," i.e. one-step transfer of all HDL-CE to the cell and "nibbling," multiple successive c
23 , 0.62; 95% CI, 0.42-0.92; P=0.02), although HDL particle number again emerged as the strongest predi
26 For both baseline and on-statin analyses, HDL particle number was the strongest of 4 HDL-related b
28 ta-carotene and BMI (-0.27), WC (-0.30), and HDL cholesterol (0.31) after accounting for multiple com
29 ol, paraoxonase-1 arylesterase activity, and HDL vasodilatory capacity (relative to control, P=0.039,
30 apoB and apoA-I as well as between LDL-C and HDL-C may be an etiological mechanism for ALS and needs
31 rotein A-I, cholesterol efflux capacity, and HDL particle number were assessed at baseline and 12 mon
33 039) and a decrease in total cholesterol and HDL cholesterol (beta = 3.766; 95% CI: 1.092, 6.440; P =
35 ith HDL cholesterol, apolipoprotein A-I, and HDL particle number (Spearman r= 0.39, 0.48, and 0.39 re
37 ociated with plasma adiponectin, insulin and HDL cholesterol concentrations, obesity, and coronary at
39 med by immobilizing the MREs of both LDL and HDL on the same GDE, which was then used to detect LDL a
42 d low and high density lipoproteins (LDL and HDL, respectively) were first individually characterized
43 ith LDL cholesterol (rs17242388 in LDLR) and HDL cholesterol (rs189679427 between GOT2 and APOOP5), a
44 t capacity on low-density lipoproteins), and HDL vasodilatory capacity (HDL ability to induce the rel
49 erol, and L-HDL-free cholesterol, as well as HDL cholesterol seem to be protective against increasing
50 bbling," multiple successive cycles of SR-B1-HDL association during which a few CEs transfer to the c
55 scores and polygenic profile scores for BMI, HDL cholesterol, low-density lipoprotein cholesterol, co
57 ALS patients had increasing levels of LDL-C, HDL-C, apoB, and apoA-I, whereas gradually decreasing le
58 .62; 95% CI = 0.42-0.93), whereas high LDL-C/HDL-C (>/=3.50; HR = 1.50; 95% CI = 1.15-1.96) and high
61 ipoproteins), and HDL vasodilatory capacity (HDL ability to induce the release of nitric oxide in end
62 erol transport (cholesterol efflux capacity, HDL ability to esterify cholesterol, and cholesteryl est
63 several HDL quality-related characteristics (HDL particle oxidation, resistance against oxidative mod
64 terol concentration of HDL (HDL cholesterol (HDL-C)) without apoC-III was inversely associated with r
66 nce of high-density lipoprotein cholesterol (HDL-C) as a specific risk factor for cardiovascular (CV)
67 vel of high-density lipoprotein cholesterol (HDL-C) is also considered to be a predictor for stroke.
68 C) and high-density lipoprotein cholesterol (HDL-C) were either directly measured or calculated from
69 n mean high-density lipoprotein cholesterol (HDL-C), LDL-C, and apolipoprotein B (apoB) levels in par
70 (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and
71 (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and
73 es and high-density lipoprotein cholesterol (HDL-C; cg27243685; P=8.1E-26 and 9.3E-19) was associated
74 [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], tot
76 tintervention values of TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, triglycerides, SBP,
77 d diastolic blood pressure, LDL cholesterol, HDL cholesterol, total cholesterol, triglycerides, and f
78 ood total cholesterol (TC), LDL cholesterol, HDL cholesterol, triglycerides, ratio of TC to HDL chole
79 g (-1.2, 1.5 mm Hg) for TC, LDL cholesterol, HDL cholesterol, triglycerides, TC:HDL cholesterol, SBP,
81 %), respectively], and the total-cholesterol:HDL-cholesterol ratio [-0.0% (95% CI: -4.3%, 4.8%) compa
82 e LIPC gene region that increase circulating HDL-cholesterol have the opposite direction of associati
83 region associated with increased circulating HDL-cholesterol also associate with increased AMD risk,
84 ncy led to reduced production of circulating HDL and increased liver damage upon high-dose LPS challe
88 lesterol, triglycerides (TGs), high-density (HDL-C), and low-density lipoprotein cholesterol (LDL-C)
92 31.1 mg/dl; non-HDL-C: 124.0 +/- 33.5 mg/dl; HDL-C: 53 +/- 12.8 mg/dl; and apoB: 90.7 +/- 24 mg/dl; m
94 rmacological thermogenic activation enhances HDL remodelling, which is associated with specific lipid
95 er adjustment for conventional risk factors, HDL-C levels still showed no significant association wit
96 05, 95% CI: 0.50, 2.21; P-trend = 0.44) (for HDL-C with apoC-III vs. HDL-C without apoC-III, P-hetero
97 no significant differences between diets for HDL cholesterol and triglyceride.In comparison with a co
98 that signals observed at ABCA1 and LIPC for HDL cholesterol and NCAN/MAU2 for triglycerides are inde
102 iations with high-density lipoprotein (HDL), HDL-diameter, HDL-C, HDL2-C, and HDL3-C (all P < 0.003).
103 ld correspond to the glassy states of high- (HDL) and low-density liquid (LDL) in the metastable part
104 cardiometabolic risk-factor profile (higher HDL cholesterol, lower BMI, lower C-reactive protein, lo
110 we studied at the single molecule level how HDL particles interact with synthetic lipid membranes.
115 olesterolemia induced an important change in HDL-transported proteins (576 spots in HL-HDL vs. 621 sp
117 reduction was associated with an increase in HDL cholesterol (beta = -0.452; 95% CI: -0.880, -0.023;
121 relative to baseline, P=0.028) and increased HDL ability to esterify cholesterol, paraoxonase-1 aryle
122 % CI, -13.3 to +10.2; P=0.80), but increased HDL cholesterol (+7.7%), apolipoprotein A-I (+4.3%), and
124 risk factor for AMD risk and that increasing HDL-cholesterol (particularly via CETP inhibition) will
125 emonstrate that hypercholesterolemia induces HDL lipidomic changes, losing phosphatidylcholine-lipid
126 -HDL phospholipids, L-HDL cholesterol, and L-HDL-free cholesterol, as well as HDL cholesterol seem to
127 DL-free cholesterol, XL-HDL phospholipids, L-HDL cholesterol, and L-HDL-free cholesterol, as well as
128 ic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting i
129 e effect of the genetic risk score for large HDL particle numbers, such that each risk allele of the
131 ssociated with lower concentrations of large HDL particles at follow-up in the lifestyle arm (beta=-0
133 ment, the phospholipid content of very large HDL was lower in metformin than in placebo-treated patie
135 d transferred from high density lipoprotein (HDL) - a main carrier of cholesterol in the blood stream
137 ere independent of high-density lipoprotein (HDL) and non-HDL cholesterol, and extended to stroke and
139 he ratio of TGs to high-density lipoprotein (HDL) cholesterol (beta = 2.689; 95% CI: 0.373, 5.003; P
140 The causal role of high-density lipoprotein (HDL) cholesterol in cardioprotection has been questioned
141 new experience and high-density lipoprotein (HDL) cholesterol levels are most positively genetically
142 drugs that raised high-density lipoprotein (HDL) cholesterol levels to reduce cardiovascular events
144 y lipoprotein, and high-density lipoprotein (HDL) cholesterol, but not in the total-to-HDL cholestero
145 -reactive protein, high-density lipoprotein (HDL) cholesterol, forced expiratory volume, grip strengt
146 tor profile [lower high-density lipoprotein (HDL) cholesterol, higher total homocysteine, and higher
147 (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, or triglycerides at a genome-wide leve
148 (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triacylglycerols, apolipoproteins A-I
149 ircumference (WC), high-density lipoprotein (HDL) cholesterol, triglycerides, fat mass (FM), systolic
152 logically relevant high-density lipoprotein (HDL) receptor whose primary role is to mediate selective
153 MI measurements of high-density lipoprotein (HDL) triglycerides (HDL-TG) predicted LVEF (beta=1.90 [9
154 cant interference: high-density lipoprotein (HDL) yields 4-6% of the LDL signal, very-low-density-lip
156 associations with high-density lipoprotein (HDL), HDL-diameter, HDL-C, HDL2-C, and HDL3-C (all P < 0
157 lood lipid traits (high-density lipoprotein (HDL), low-density lipoprotein (LDL), plasma concentratio
158 nated by selective high density lipoprotein (HDL)-cholesteryl ester (CE) uptake, mediated by scavenge
160 ) and circulating (high-density lipoprotein, HDL) synergize to facilitate Abeta transport across bioe
161 tions in high- and low-density lipoproteins (HDL and LDL) particles measured by standardized clinical
162 main receptor for high density lipoproteins (HDL) and mediates the bidirectional transport of lipids,
165 ficial effects of high-density lipoproteins (HDL) seem altered in patients with symptomatic cardiovas
166 ical functions of high-density lipoproteins (HDLs) contribute to explaining the cardioprotective role
168 en with abdominal obesity and relatively low HDL-cholesterol concentrations were assigned to sequence
169 s in normal-weight participants and with low HDL concentrations and elevated glycated hemoglobin in o
170 pregnancy baseline concentration and a lower HDL-c rate of change during pregnancy were associated wi
171 sting insulin levels adjusted for BMI, lower HDL cholesterol levels and higher triglyceride levels) a
172 eline total cholesterol and LDL-C, but lower HDL-C and higher triglycerides than controls (P < .001).
175 deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol
181 mmol/L; 95% CI: -0.46, -0.25 mmol/L) and non-HDL cholesterol (MD: -0.32 mmol/L; 95% CI: -0.46, -0.19
183 nt of high-density lipoprotein (HDL) and non-HDL cholesterol, and extended to stroke and myocardial i
185 ss the effect of KJM on LDL cholesterol, non-HDL cholesterol, and apolipoprotein B.Medline, Embase, C
188 33.1 mg/dl; LDL-C: 109.9 +/- 31.1 mg/dl; non-HDL-C: 124.0 +/- 33.5 mg/dl; HDL-C: 53 +/- 12.8 mg/dl; a
190 trates that the most accurate method for non-HDL-P quantification in native serum samples implies dai
191 deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol
192 r study population) had a lower level of non-HDL cholesterol than noncarriers, a difference of 15.3 m
193 fference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 m
194 s to be largely explained by lowering of non-HDL-C (high-density lipoprotein cholesterol), rather tha
195 erolemic (HL) diet for 10 days, reaching non-HDL cholesterol concentrations of 38.2 +/- 3.5 mg/dl and
196 2% (95% CI: -2.3%, 7.8%), respectively], non-HDL cholesterol [-5.3% (95% CI: -8.6%, 2.1%) compared wi
199 aphy to measure the apoA-I concentrations of HDL that contains and lacks apoC-III in 2 prospective st
203 al model, whether the reported impairment of HDL cardioprotective function was associated with altera
205 bbling mechanisms, media from incubations of HDL with CHO-SR-B1 cells were analyzed by non-denaturing
206 increased interest in alternative indices of HDL quality, such as cholesterol efflux capacity, and HD
207 is to mediate selective uptake or influx of HDL-derived cholesteryl esters into cells and tissues.
208 At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12
211 P score was associated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corre
213 We used the average between the negative of HDL-C z-score and TGs z-score to give similar weight to
216 ntiadhesive and antithrombotic properties of HDL/ApoA-I may connect the pathology of microvasculature
218 ssed the effects of both TMDs on the role of HDL particles on reverse cholesterol transport (choleste
221 concentrations of apoC-III and subspecies of HDL defined by the presence or absence of apoC-III with
222 yte lipoprotein lipase and hepatic uptake of HDL by scavenger receptor B-I are the driving forces of
223 rom cheese and butter has similar effects on HDL cholesterol but differentially modifies LDL-choleste
225 isk marker for diabetes, and its presence on HDL may impair the antidiabetogenic properties of HDL.
228 reactivities to lipid-free apoA-I and plasma HDL, suggesting the possibility of these mAbs to detect
229 ot a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (ii
230 ictor of graft failure independent of plasma HDL cholesterol levels in renal transplant recipients.
232 urthermore, thermogenic stimulation promotes HDL-cholesterol clearance and increases macrophage-to-fa
235 within residues 44-65 against reconstituted HDL particles, indicating that these mAbs specifically r
236 minate discoidal and spherical reconstituted HDL particles despite their great reactivities to lipid-
237 and risks including acne, alopecia, reduced HDL cholesterol, increased triglycerides, and a possible
238 elevated blood pressure, 40.98% for reduced HDL-cholesterol, 23.33% for elevated triglycerides, 18.9
240 dicines, i.e., high-density lipoprotein ([S]-HDL), polymeric micelles ([S]-PM), and liposomes ([S]-LI
243 rbohydrate diet (fat: 25%, SFAs: 5.8%).Serum HDL-cholesterol concentrations were similar after the ch
244 also studied the effects of a TMD on several HDL quality-related characteristics (HDL particle oxidat
246 onally, elevated HDL components, i.e., small HDL triglycerides, might have a causal role of elevating
247 RRMS patients show increased levels of small HDL (sHDL), accompanied by larger, triglyceride (TG)-ric
249 ycerides, ratio of TC to HDL cholesterol (TC:HDL), and systolic and diastolic blood pressures (SBP an
250 ts, TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, triglycerides, and DBP, but not SBP, de
251 of TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, triglycerides, SBP, and DBP; calculated
253 sma glucose (p = 0.008), TG (p = 0.003), TG: HDL-C ratio (p = 0.010), and vWF levels (p = 0.004).
256 ose with no event (HD-) (n = 12) showed that HDL from HD+ patients were enriched in SAA but had lower
260 and 124 mg/dL) along with an increase in the HDL/LDL ratio, and improved glucose levels were document
261 implemented to assess the connection of the HDL-C levels and the prevalence of asymptomatic ICAS.
263 tudy (4D Study), we investigated whether the HDL cholesterol efflux capacity is predictive for cardio
266 L cholesterol, triglycerides, ratio of TC to HDL cholesterol (TC:HDL), and systolic and diastolic blo
267 re, heart rate, HbA1c, blood glucose, LDL-to-HDL cholesterol ratio, C-reactive protein, angiotensin I
269 araoxonase-1 arylesterase activity and total HDL antioxidant capacity on low-density lipoproteins), a
270 re negative than the relative risk for total HDL (relative risk, 0.80; 95% confidence interval, 0.74-
271 , 0.85; P-trend = 0.002), more so than total HDL-C (HR = 0.60, 95% CI: 0.35, 1.03; P-trend = 0.04), w
272 igh-density lipoprotein (HDL) triglycerides (HDL-TG) predicted LVEF (beta=1.90 [95% confidence interv
273 ponents: waist circumference, triglycerides, HDL-c, glucose, and systolic and diastolic blood pressur
274 We assessed changes in HbA1c, triglycerides, HDL cholesterol and BMI in a mixed effects longitudinal
276 detect structural transition of apoA-I upon HDL formation, we developed novel monoclonal antibodies
277 , which is more lipophilic than apoAI, using HDL-[(3)H]CE labeled with [(125)I]apoAI or [(125)I]apoAI
281 95% CI: 0.35, 1.03; P-trend = 0.04), whereas HDL-C with apoC-III was not associated (HR = 1.05, 95% C
282 95% confidence interval, 1.01-1.18), whereas HDL that lacks apoC-III was associated with lower risk (
283 of this pilot study was to determine whether HDL glycoprotein composition affects HDL's immunomodulat
286 < 5 x 10-8) three novel loci associated with HDL-C near CD163-APOBEC1 (P = 7.4 x 10-9), NCOA2 (P = 1.
288 erides and only 1-3% of the association with HDL-cholesterol, blood pressure, and insulin concentrati
289 iate between clinical groups, correlate with HDL's immunomodulatory capacity, and may be predictive o
290 flux capacity was moderately correlated with HDL cholesterol, apolipoprotein A-I, and HDL particle nu
291 .24 to -0.13) and positive correlations with HDL cholesterol (alpha-carotene = 0.17; beta-carotene =
293 ; P-trend = 0.006) and lung cancer risk with HDL cholesterol (HR: 0.59; 95% CI: 0.38, 0.93; P-trend =
294 iations included colorectal cancer risk with HDL cholesterol (HR: 0.63; 95% CI; 0.41, 0.98; P-trend =
297 In contrast, large (L) and extra large (XL) HDL lipid components, i.e., XL-HDL cholesterol, XL-HDL-f
298 HDL cholesterol, XL-HDL-free cholesterol, XL-HDL phospholipids, L-HDL cholesterol, and L-HDL-free cho
299 pid components, i.e., XL-HDL cholesterol, XL-HDL-free cholesterol, XL-HDL phospholipids, L-HDL choles
300 ra large (XL) HDL lipid components, i.e., XL-HDL cholesterol, XL-HDL-free cholesterol, XL-HDL phospho
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