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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
14                                        The 2 HDL subspecies showed opposing associations, with risk o
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
18 ion (IR) that hypercholesterolemia abolishes HDL-related cardioprotection.
19 holesteryl ester transfer protein activity), HDL antioxidant properties (paraoxonase-1 arylesterase a
20 whether HDL glycoprotein composition affects HDL's immunomodulatory function.
21 ydrophobic channel in the receptor, or after HDL endocytosis.
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
24  apoAII, cholesterol, and phospholipid among HDL species as a function of incubation time.
25  lipid-free apoAI; apoAII was retained in an HDL remnant.
26    For both baseline and on-statin analyses, HDL particle number was the strongest of 4 HDL-related b
27 rol (+7.7%), apolipoprotein A-I (+4.3%), and HDL particle number (+5.2%).
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
32 ty, such as cholesterol efflux capacity, and HDL quantity, such as HDL particle number.
33 039) and a decrease in total cholesterol and HDL cholesterol (beta = 3.766; 95% CI: 1.092, 6.440; P =
34 nd positively with free fatty acid (FFA) and HDL after control for age and sex.
35 ith HDL cholesterol, apolipoprotein A-I, and HDL particle number (Spearman r= 0.39, 0.48, and 0.39 re
36                          Body mass index and HDL cholesterol were negatively correlated with molecula
37 ociated with plasma adiponectin, insulin and HDL cholesterol concentrations, obesity, and coronary at
38                                 Mean LDL and HDL cholesterol concentrations were 2.35 mmol/L (91 mg/d
39 med by immobilizing the MREs of both LDL and HDL on the same GDE, which was then used to detect LDL a
40 e GDE, which was then used to detect LDL and HDL simultaneously in mixed solution.
41           The optimal frequencies of LDL and HDL were found to be 81.38Hz and 5.49Hz, respectively, w
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
45                                       TG and HDL-C concentrations were not associated with risk of in
46 n APOC3 (rs138326449) with triglycerides and HDL-C.
47 her mimetic peptides that form a belt around HDL.
48 l efflux capacity, and HDL quantity, such as HDL particle number.
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
51                                     Baseline HDL particle number was inversely associated with incide
52               An inverse association between HDL cholesterol levels and the incidence of RHOA was obs
53  risk factors evaluated associations between HDL-related biomarkers and incident CVD.
54  The study showed little correlation between HDL-C levels and asymptomatic ICAS.
55 scores and polygenic profile scores for BMI, HDL cholesterol, low-density lipoprotein cholesterol, co
56 x-, and region-specific z-scores for WC, BP, HDL-C, and TGs.
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
59 whereas gradually decreasing levels of LDL-C/HDL-C and apoB/apoA-I ratios.
60 ptor, class B, type I (SR-BI), the so-called HDL receptor.
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
65  resistance, triglycerides, HDL cholesterol (HDL-C), and C-reactive protein].
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
72 nd low high-density lipoprotein cholesterol (HDL-C).
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
75     Among all subjects, TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, triglycerides, and
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,
80  assess the causal roles of LDL-cholesterol, HDL-cholesterol, and triglycerides on AMD risk.
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
85 t Study [n=5835]) were screened for combined HDL cholesterol and Lp(a) elevations.
86                               In conclusion, HDL cholesterol efflux capacity is not a prognostic card
87                               In conclusion, HDL-cholesterol efflux normalised to apoA-I was inversel
88 lesterol, triglycerides (TGs), high-density (HDL-C), and low-density lipoprotein cholesterol (LDL-C)
89 proteomics tests were performed to determine HDL molecular changes.
90  humans caused elevation of 2 small diameter HDL fractions and 1 large diameter fraction.
91 igh-density lipoprotein (HDL), HDL-diameter, HDL-C, HDL2-C, and HDL3-C (all P < 0.003).
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
93                       Additionally, elevated HDL components, i.e., small HDL triglycerides, might hav
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
99                        The relative risk for HDL lacking apoC-III was even more negative than the rel
100 cently labelled amphiphilic lipid probe from HDL particles to the lipid bilayer upon contact.
101        The cholesterol concentration of HDL (HDL cholesterol (HDL-C)) without apoC-III was inversely
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
105 es differentially clustered in NC-HDL and HL-HDL.
106                             Functionally, HL-HDL showed lower antioxidant activity (-35%) and a reduc
107 in HDL-transported proteins (576 spots in HL-HDL vs. 621 spots in NC-HDL).
108                                           HL-HDLs presented a core enriched in cholesteryl esters and
109                                           HL-HDLs showed a reduced content of lipocalin retinol bindi
110  we studied at the single molecule level how HDL particles interact with synthetic lipid membranes.
111 pecific lipidomic changes in mouse and human HDL.
112 hen enriched with virgin olive oil, improved HDL atheroprotective functions in humans.
113 nduced these beneficial changes by improving HDL oxidative status and composition.
114  function was associated with alterations in HDL remodeling and functionality.
115 olesterolemia induced an important change in HDL-transported proteins (576 spots in HL-HDL vs. 621 sp
116 rplasia (BPH) and liver-mediated decrease in HDL-C.
117 reduction was associated with an increase in HDL cholesterol (beta = -0.452; 95% CI: -0.880, -0.023;
118 3-1.44) per 1 standard deviation increase in HDL-cholesterol.
119          There were significant increases in HDL cholesterol, LDL cholesterol, and triacylglycerols,
120 otein cholesterol), rather than increases in HDL-C.
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
123 ulation of thermogenesis linked to increased HDL levels in APOE*3-Leiden.CETP mice.
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
130 he 3 diets increased the percentage of large HDL particles (relative to baseline, P<0.001).
131 ssociated with lower concentrations of large HDL particles at follow-up in the lifestyle arm (beta=-0
132 duces the phospholipid content in very large HDL particles.
133 ment, the phospholipid content of very large HDL was lower in metformin than in placebo-treated patie
134          Hypercholesterolemia induced larger HDL particles.
135 d transferred from high density lipoprotein (HDL) - a main carrier of cholesterol in the blood stream
136 or that binds both high-density lipoprotein (HDL) and low-density lipoprotein.
137 ere independent of high-density lipoprotein (HDL) and non-HDL cholesterol, and extended to stroke and
138 apoA1) and nascent high-density lipoprotein (HDL) assembly is not well understood.
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
143 vels and increases high-density lipoprotein (HDL) cholesterol levels.
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
150  (RCT) and reduces high-density lipoprotein (HDL) function in vivo.
151 ring remodeling of high-density lipoprotein (HDL) particles.
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
155 s, 35% in GWASs of high-density lipoprotein (HDL), and 23% in GWASs of schizophrenia.
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
159  on the surface of high-density lipoprotein (HDL).
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,
163 the maturation of high-density lipoproteins (HDL) from discoidal to spherical particles.
164 nic properties of high-density lipoproteins (HDL) is unknown.
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
167 tal muscle IR, hypertriglyceridemia, and low HDL-C become fully established.
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).
173 lso associated with higher rather than lower HDL cholesterol.
174 tty acids, indicating the presence of mature HDL particles with low surface fluidity.
175  deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol
176 nd out that, upon contact with the membrane, HDL becomes integrated into the lipid bilayer.
177 lipid species differentially clustered in NC-HDL and HL-HDL.
178 ins (576 spots in HL-HDL vs. 621 spots in NC-HDL).
179  to efflux cholesterol (-60%) compared to NC-HDL (p < 0.05).
180 noic acid binding protein 1 (p < 0.05 vs. NC-HDL).
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
182 /d for reductions in LDL cholesterol and non-HDL cholesterol of 10% and 7%, respectively.
183 nt of high-density lipoprotein (HDL) and non-HDL cholesterol, and extended to stroke and myocardial i
184 ion in LDL (low-density lipoprotein) and non-HDL-C.
185 ss the effect of KJM on LDL cholesterol, non-HDL cholesterol, and apolipoprotein B.Medline, Embase, C
186 ed the effect of KJM on LDL cholesterol, non-HDL cholesterol, or apolipoprotein B.
187 ity-lipoprotein particle concentrations (non-HDL-P).
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
189               The genetic risk score for non-HDL cholesterol confers CAD risk beyond that of LDL chol
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
197 onocytes was used as a prototypical assay of HDL's immunomodulatory capacity.
198             The cholesterol concentration of HDL (HDL cholesterol (HDL-C)) without apoC-III was inver
199 aphy to measure the apoA-I concentrations of HDL that contains and lacks apoC-III in 2 prospective st
200                            Concentrations of HDL-bound serum amyloid A (SAA), lipopolysaccharide bind
201               The cardioprotective effect of HDL is thought to be largely determined by its cholester
202 enger receptor B-I are the driving forces of HDL-cholesterol disposal in liver.
203 al model, whether the reported impairment of HDL cardioprotective function was associated with altera
204 wed no gradual decrease with the increase of HDL-C levels.
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
209                             Higher levels of HDL cholesterol appear to protect against RHOA after 11
210                             Normal levels of HDL-C are not an independent risk factor for asymptomati
211 P score was associated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corre
212 gonist GW501516 to increase plasma levels of HDL-cholesterol.
213  We used the average between the negative of HDL-C z-score and TGs z-score to give similar weight to
214 odulatory capacity, and may be predictive of HDL's ability to protect from infection.
215 ay impair the antidiabetogenic properties of HDL.
216 ntiadhesive and antithrombotic properties of HDL/ApoA-I may connect the pathology of microvasculature
217 s for monitoring formation and remodeling of HDL particles.
218 ssed the effects of both TMDs on the role of HDL particles on reverse cholesterol transport (choleste
219 esis that apoC-III may mark a subfraction of HDL that is associated with higher risk of CHD.
220        We investigated whether subspecies of HDL defined by apoC-III are associated with coronary hea
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
224 to detect structural transition of apoA-I on HDL.
225 isk marker for diabetes, and its presence on HDL may impair the antidiabetogenic properties of HDL.
226 s a traditional Mediterranean diet [TMD]) on HDL function in humans.
227 ps or between groups for changes in total or HDL cholesterol or triglycerides.
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.
231 r risk that extend beyond traditional plasma HDL cholesterol concentrations.
232 urthermore, thermogenic stimulation promotes HDL-cholesterol clearance and increases macrophage-to-fa
233  role of the lipoprotein beyond quantitative HDL cholesterol levels.
234 ower LDL-cholesterol concentrations or raise HDL-cholesterol concentrations.
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
239                      New measures reflecting HDL structure and function may provide novel insights fo
240 dicines, i.e., high-density lipoprotein ([S]-HDL), polymeric micelles ([S]-PM), and liposomes ([S]-LI
241                                Moreover, [S]-HDL and [S]-PM showed higher uptake by plaque macrophage
242          Finally, the SR-B1-linked selective HDL-cholesteryl ester uptake pathway is now being evalua
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
245             These remodeling changes shifted HDL particles toward a dysfunctional state.
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
248 with a single antioxidant have improved some HDL functions.
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
252 lesterol, HDL cholesterol, triglycerides, TC:HDL cholesterol, SBP, and DBP, respectively].
253 sma glucose (p = 0.008), TG (p = 0.003), TG: HDL-C ratio (p = 0.010), and vWF levels (p = 0.004).
254                 Our results demonstrate that HDL glycoprotein composition, including the site-specifi
255                        We find evidence that HDL-cholesterol is a causal risk factor for AMD, with an
256 ose with no event (HD-) (n = 12) showed that HDL from HD+ patients were enriched in SAA but had lower
257          Some genetic evidence suggests that HDL-cholesterol is a causal risk factor for AMD risk and
258         However, the association between the HDL-C level and asymptomatic ICAS is uncertain.
259 r, specific residues on PON1 involved in the HDL-PON1 interaction remain unclear.
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.
262 reased systemic cholesterol flux through the HDL compartment.
263 tudy (4D Study), we investigated whether the HDL cholesterol efflux capacity is predictive for cardio
264 change from baseline in total cholesterol to HDL-cholesterol ratio.
265                Novel measures that relate to HDL function may contribute new information to the predi
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
268 n (HDL) cholesterol, but not in the total-to-HDL cholesterol ratio.
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
275  (HbA1c), insulin resistance, triglycerides, HDL cholesterol (HDL-C), and C-reactive protein].
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
278  roughly uniform-sized factions with varying HDL-C levels.
279 ns ApoA-IV and ApoC-II, contributing to VLDL/HDL distribution and lipolysis.
280 P-trend = 0.44) (for HDL-C with apoC-III vs. HDL-C without apoC-III, P-heterogeneity = 0.002).
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
284                      We investigated whether HDL cholesterol efflux capacity is associated with cardi
285  levels were also positively associated with HDL cholesterol.
286 < 5 x 10-8) three novel loci associated with HDL-C near CD163-APOBEC1 (P = 7.4 x 10-9), NCOA2 (P = 1.
287 e, only rs1729407 showed an association with HDL-cholesterol (P = 7.1 x 10 (-) (07)).
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 =
292 tes by a dynamic lid until it interacts with HDL to allow transesterification to proceed.
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 =
295 enal metabolism and/or an interaction within HDL particles.
296 R-885-5p levels associated inversely with XL HDL cholesterol levels.
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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