ライフサイエンスコーパス: free cholesterol

1 ated at the SML equivalent of about 30 mol % free cholesterol.

2 s by increasing the availability of cellular free cholesterol.

3 crophages was considered the major source of free cholesterol.

4 glands from Lxralphabeta-/- mice accumulated free cholesterol.

5 lesterol is secreted into bile, primarily as free cholesterol.

6 o exhibited absence or dramatic reduction in free cholesterol.

7 due in part to the secondary accumulation of free cholesterol.

8 he pathways are involved in the secretion of free cholesterol.

9 ing the formation of cholesterol esters from free cholesterol.

10 sphingomyelin, which has a high affinity for free cholesterol.

11 n (HDL) cholesteryl esters and the efflux of free cholesterol.

12 polipoprotein B-100, phospholipids, and some free cholesterol.

13 incorporation of dipalmitoyl-PC, but not by free cholesterol.

14 d cholesteryl esters to free fatty acids and free cholesterol.

15 ould be inhibited by replenishing cells with free cholesterol.

16 rhage with deposition of erythrocyte-derived free cholesterol.

17 sferases (ALT/AST) and hepatic triglycerides/free cholesterol.

18 e cholesterol but poorly with hepatic tissue free cholesterol.

19 absence of changes in the concentrations of free cholesterol.

20 Adipose harbors a large depot of free cholesterol.

21 olesterol oxidase-sensitive pool of membrane free cholesterol, 2) mediate cholesterol efflux to HDL,

22 differ significantly from those labeled with free cholesterol ((3)H-FC).

23 phospholipid (26%), cholesteryl ester (24%), free cholesterol (37%), and apoAI (22%).

24 crease in VLDL and LDL phospholipids (210%), free cholesterol (60%), and cholesteryl ester (40%) with

25 cholesterol (63%), cholesteryl ester (63%), free cholesterol (67%), non-high density lipoprotein (HD

26 l esters but does not play a primary role in free cholesterol absorption.

27 Although free cholesterol accumulated in late endocytic organelle

28 Investigating further, we found that free cholesterol accumulated in PMN lipid raft fractions

29 Free cholesterol accumulated in the endoplasmic reticulu

30 Unexpectedly, free cholesterol accumulates within swollen lysosomes, s

31 cholesterol homeostasis causes intracellular free cholesterol accumulation and hepatocyte injury.

32 This was accompanied by free cholesterol accumulation and increased endoplasmic

33 ccumulation in lysosomal storage disease and free cholesterol accumulation in cell membranes in ather

34 the capacity of glucolipotoxicity to induce free cholesterol accumulation in human pancreatic islets

35 f this phospholipid response to keep up with free cholesterol accumulation in lesional macrophages in

36 e domains but lacks the START domain, caused free cholesterol accumulation in lysosomes and inhibited

37 PC2 (progressive neurodegenerative symptoms, free cholesterol accumulation in lysosomes).

38 and MBL also significantly reduced levels of free cholesterol accumulation in monocytes and human mon

39 m macrophages to protect against toxicity of free cholesterol accumulation in the cell.

40 nhibition of cholesteryl ester synthesis and free cholesterol accumulation in the endoplasmic reticul

41 ged Sort1 knock-out mice showed less hepatic free cholesterol accumulation, increased bile acid synth

42 size for 1 SD higher DeltavitE (+4 umol/mmol free-cholesterol-adjusted alpha-TOH) was roughly one-qua

43 itive endocytic recycling compartment, where free cholesterol also accumulated as revealed by filipin

44 macrophages with 7-ketocholesterol, but not free cholesterol, also inhibited expression of SR-BI.

45 th Abeta and submicromolar concentrations of free cholesterol alter the trafficking of a population o

46 terol ester concentrations and reductions in free cholesterol amounts.

47 Compared with baseline values, serum free cholesterol, an index of tissue cholesterol mobiliz

48 an enzyme that converts cholesteryl ester to free cholesterol, an indispensable process in cholestero

49 a [(3)H]benzophenone-modified photoactivable free cholesterol analogue ((3)H-FCBP) did not differ sig

50 ncreased proportion of total plasma, and HDL free cholesterol and a marked (>10-fold) reduction in mo

51 ed blood cell membranes are a rich source of free cholesterol and accumulated red blood cells within

52 ree fatty acids, esterified cholesterol, and free cholesterol and also a much higher content of satur

53 etion is tightly coupled to the secretion of free cholesterol and bile salts.

54 oading-induced intracellular accumulation of free cholesterol and cholesterol esters in macrophages.

55 ycin decreased intracellular accumulation of free cholesterol and cholesterol esters induced by the e

56 d intracellular accumulation of cholesterol (free cholesterol and cholesterol esters), whereas activa

57 ylated lipid and Pry1 and Pry2 proteins bind free cholesterol and cholesteryl acetate in vitro.

58 /-)-->LDLr(-/-) mice had significantly lower free cholesterol and cholesteryl ester levels in the bra

59 ty of the polar lipids, but left significant free cholesterol and fatty acids, and small but critical

60 in NPC disease exhibit extensive storage of free cholesterol and glycosphingolipids (GSLs), includin

61 Blocking GRAMD1B function decreases free cholesterol and lipid droplets.

62 ptor signaling by reducing cellular membrane free cholesterol and lipid raft content, indicating a ro

63 iated through alterations in plasma membrane free cholesterol and lipid raft content.

64 rhage into the necrotic core are a source of free cholesterol and may become a driving force in the p

65 Two analogues (1, 2) of free cholesterol and one analogue (3) of the immunosuppr

66 caveolin expression is regulated by cellular free cholesterol and plasma levels of low-density lipopr

67 oncogenic APC in increasing plasma membrane free cholesterol and rigidity, thereby modulating Wnt si

68 c potential, to prevent the increase in both free cholesterol and ROS levels induced by glucolipotoxi

69 facilitation of the intestinal absorption of free cholesterol and the modification of plasma lipoprot

70 c plaque may contribute to the deposition of free cholesterol and thereby the enlargement of the necr

71 t reagentless biosensor for determination of free cholesterol and total cholesterol has been realized

72 cm(-2) and 760 microA mM(-1) cm(-2) towards free cholesterol and total cholesterol respectively with

73 mitoyl-2-oleoyl-sn-glycero-3-phosphocholine, free cholesterol, and apoA-I.

74 e loss of large HDL particles, increased HDL-free cholesterol, and decreased HDL protein in CBS(-/-)/

75 ation of intraplaque hemorrhage, accumulated free cholesterol, and necrotic core expansion is beginni

76 iglycerides, with less definite ones between free cholesterol, and phospholipids for a specific group

77 lipoprotein (HDL) composed of phospholipid, free cholesterol, and protein, primarily apoE and apoJ.

78 by negative-stain electron microscopy of the free cholesterol- and phospholipid-enriched IDL/LDL frac

79 f CE and a surface enriched in phospholipid, free cholesterol, apoA-II, and apoE.

80 As expected, increases in hepatic free cholesterol are associated with decreases in 3-hydr

81 cells in atherosclerotic lesions accumulate free cholesterol as well as cholesteryl ester.

82 phospholipids, L-HDL cholesterol, and L-HDL-free cholesterol, as well as HDL cholesterol seem to be

83 smembrane pore depend on the availability of free cholesterol at the membrane surface, while changes

84 Free cholesterol at very low concentrations regulated Ca

85 R stress correlates strongly with hepatic ER free cholesterol but poorly with hepatic tissue free cho

86 of function was shown to lower intracellular free cholesterol, causing upregulation of HMG Co-A reduc

87 in selective cholesteryl ester uptake and in free cholesterol cellular efflux.

88 Triglyceride, free cholesterol, cholesterol ester, and phospholipid co

89 combination of effects directed by elevated free cholesterol, cholesterol esters and cholic acid, an

90 ucose or 1-[(14)C]acetate incorporation into free cholesterol, cholesterol esters, triglycerides, fre

91 a mechanism whereby the elevation of hepatic free cholesterol concentrations by dietary cholesterol,

92 lgus monkeys but not in green monkeys, liver free cholesterol concentrations were elevated when chole

93 lungs, accompanied with decreased pulmonary free cholesterol content and suppressed tumor cell proli

94 m ABCA1(-A/-A) mice had a 2-fold increase in free cholesterol content compared with wild-type mice an

95 C transfer by PLTP decreases with increasing free cholesterol content in rHDL and with decreasing HDL

96 Total and free cholesterol content was significantly higher in 25

97 n direct correlation with increased cellular free cholesterol content.

98 ncluding free fatty acid toxicity, increased free cholesterol, cytokine-mediated injury and activatio

99 LAL overexpression increased levels of BAT free cholesterol, decreased SREBP targets, and induced t

100 d inflammation may therefore in part reflect free cholesterol- dependent changes in lipid raft struct

101 F expression was equally sufficient to cause free cholesterol-dependent apoptosis in podocytes by act

102 TNF-stimulated free cholesterol-dependent apoptosis in podocytes was me

103 sm in which local TNF is sufficient to cause free cholesterol-dependent podocyte injury irrespective

104 l pool in J774-SRBI cells, suggests that the free cholesterol derived from the hydrolysis of choleste

105 -) astrocytes secrete little phospholipid or free cholesterol despite comparable apoJ expression, sug

106 of free cholesterol transport, and modulates free cholesterol distribution between the plasma membran

107 ified cholesterol but did not reduce hepatic free cholesterol due to a compensatory increase in the r

108 sterification, in combination with increased free cholesterol efflux acceptors, has positive effects

109 holesteryl esters (CEs) and thereby enhances free cholesterol efflux and reduces cellular CE content.

110 ABCA1 facilitates free cholesterol efflux from peripheral tissues.

111 Free cholesterol efflux to HDL was increased ( approxima

112 Indeed, beyond its role in mediating free cholesterol efflux to HDL, the ABCG1 transporter eq

113 These studies suggest that free cholesterol enrichment of either plasma or endosoma

114 r baseline gamma-tocopherol, higher baseline free cholesterol, European ancestry (as opposed to Afric

115 Renal cortical-free cholesterol (FC) and cholesterol ester (CE) levels

116 es indicate that acute tubular injury causes free cholesterol (FC) and cholesteryl ester (CE) accumul

117 The quantification of free cholesterol (FC) and cholesteryl ester (CE) in mamm

118 Using gas chromatographic analysis, free cholesterol (FC) and esterified cholesterol (CE) we

119 to apoA-I, and had a significant increase in free cholesterol (FC) and membrane lipid rafts without i

120 in atherosclerotic lesions accumulate excess free cholesterol (FC) and phospholipid.

121 phages in atherosclerotic lesions accumulate free cholesterol (FC) as well as cholesteryl ester and a

122 ing stimulation of the bidirectional flux of free cholesterol (FC) between cells and HDL and changes

123 SR-BI stimulates the bi-directional flux of free cholesterol (FC) between cells and lipoproteins, an

124 (SR-BI) stimulates the bidirectional flux of free cholesterol (FC) between HDL and SR-BI-expressing c

125 tein (HDL) cholesteryl ester, stimulation of free cholesterol (FC) efflux from cells to HDL and phosp

126 unregulated, extracellular acceptor-mediated free cholesterol (FC) efflux is rate limited by the intr

127 Phospholipid (PL) and free cholesterol (FC) efflux maintain homeostasis.

128 By promoting cellular free cholesterol (FC) efflux, HDL and its apolipoprotein

129 dividing cells during S-phase, together with free cholesterol (FC) efflux.

130 ow-density lipoprotein (LDL) reduced CER (1% free cholesterol (FC) esterified/h) compared to B6 (6% F

131 There is increasing interest in cellular free cholesterol (FC) excess as an inducer of lesional m

132 that scavenger receptor BI (SR-BI) promotes free cholesterol (FC) exchange between high density lipo

133 g, selective uptake of HDL-CE and release of free cholesterol (FC) from cells to HDL.

134 yers, an increase in the selective uptake of free cholesterol (FC) from plasma low density lipoprotei

135 After removal of inhibitor, free cholesterol (FC) homeostasis was determined at inte

136 showed toxic effects because of an excess of free cholesterol (FC) in macrophages, which can cause en

137 cause of macrophage death is accumulation of free cholesterol (FC) in the ER, leading to activation o

138 give rHDL increases as the level of membrane free cholesterol (FC) increases up to 20 mol % when the

139 Free cholesterol (FC) is selectively internalized from l

140 l metabolism, causing a 4.8-fold increase in free cholesterol (FC) levels and a 4-fold increase in th

141 atively direct effects of ceramide (Cer) and free cholesterol (FC) on meibomian lipid films (MLF) usi

142 erminus for a major pathway of intracellular free cholesterol (FC) transport.

143 lphosphatidylcholine (POPC) with and without free cholesterol (FC) was studied by isothermal titratio

144 diacylglycerol (DAG), triacylglycerol (TAG), free cholesterol (FC), cholesterol ester, and phospholip

145 Isolation of free cholesterol (FC), cholesteryl ester (CE), and trigl

146 eath is intracellular accumulation of excess free cholesterol (FC), which is known to occur in vivo.

147 Lipoprotein Z (LP-Z) is an abnormal free cholesterol (FC)-enriched LDL-like particle discove

148 LCAT bound to (3)H-free cholesterol (FC)-labeled pre-beta(1)-HDL generated

149 as inactive in binding phospholipids (PL) or free cholesterol (FC).

150 raphy (FPLC) after radiolabeling with [(3)H]-free cholesterol (FC).

151 d SU by FFA was secondary to changes in cell-free cholesterol (FC).

152 hydrolyzed by liposomal lipases to generate free cholesterol (FC).

153 accumulate large amounts of unesterified or "free" cholesterol (FC), a process that is thought to con

154 A1-mediated efflux of cellular unesterified (free) cholesterol (FC) and phospholipid (PL) is not well

155 poA-I modification on cellular unesterified (free) cholesterol (FC) efflux, three recombinant human a

156 (PC), sphingomyelin (SM), and unesterified (free) cholesterol (FC) from J774 macrophages, in which A

157 Unesterified, or "free," cholesterol (FC) is a potent inducer of macrophag

158 nd macrophages with excess unesterified, or "free," cholesterol (FC).

159 ccumulate large amounts of unesterified, or "free," cholesterol (FC).

160 ds, peptide cross-linked by photoactivatable free cholesterol (FCBP)], (iv) selectivity for interacti

161 forms of HDL, followed by the conversion of free cholesterol (FCh) contained in HDL into cholesteryl

162 We conclude that SR-BI-mediated free cholesterol flux is highly sensitive to HDL phospho

163 id in scavenger receptor BI (SR-BI)-mediated free cholesterol flux was examined by manipulating HDL(3

164 L phospholipid composition on SR-BI-mediated free cholesterol flux were not correlated with changes i

165 roles for serum albumin and erythrocytes in free cholesterol flux.

166 glycerides, wax esters, squalene, ceramides, free cholesterol, free fatty acids, and cholesterol and

167 y in organs predisposed to the extraction of free cholesterol from bilayers, such as the skin, lung,

168 o disruption may involve the accumulation of free cholesterol from erythrocyte membranes.

169 We also found rapid in vivo transfer of free cholesterol from HDL to apoB-lipoproteins in ABCA1-

170 otects against vascular disease by accepting free cholesterol from macrophage foam cells in the arter

171 The clearance of free cholesterol from plasma lipoproteins by tissues is

172 n identified and free fatty acids as well as free cholesterol have been identified as toxic species.

173 s storage is accompanied by sequestration of free cholesterol in a manner similar to that observed in

174 nhancing ACAT activity, reduce the amount of free cholesterol in a putative regulatory pool that feed

175 Glucolipotoxicity treatment increased free cholesterol in beta-cells, which was accompanied by

176 We furthermore identified decreased HDL-3 free cholesterol in genetic PD cases compared to sporadi

177 lytical performance for the determination of free cholesterol in human serum samples.

178 ol esterification, cause the accumulation of free cholesterol in intracellular membranes, deplete end

179 mbosis, whereas their macrophages accumulate free cholesterol in late endosomes and show increased ca

180 s provide detailed insights into the role of free cholesterol in LD and adipocyte function and sugges

181 known coregulation and association of SM and free cholesterol in lipid rafts.

182 ed the accumulation of cholesteryl ester and free cholesterol in liver that was induced under the var

183 in enhanced oxidative damage, and increased free cholesterol in liver under stress accompanied by lo

184 umulation of low density lipoprotein-derived free cholesterol in lysosomes, is caused by mutations in

185 levels and the intracellular accumulation of free cholesterol in lysosomes.

186 activated in response to the accumulation of free cholesterol in macrophages.

187 able to discriminate between esterified and free cholesterol in milk.

188 a and LXRbeta) in preventing accumulation of free cholesterol in mouse adrenal glands by controlling

189 terification and changes the distribution of free cholesterol in neurons.

190 ld-type and M 19 CHO cells, with most of the free cholesterol in normal and mutant CHO cells located

191 f intraplaque hemorrhage as a contributor of free cholesterol in plaques and point to its provocative

192 Free cholesterol in plaques is an emerging contributing

193 Quantitative analysis of free cholesterol in serum using reactive DESI was demons

194 ysregulated lipoprotein parameters (e.g. low free cholesterol in small high-density lipoproteins) and

195 perlipidemia can lead to the accumulation of free cholesterol in the artery wall, and that this promo

196 These results suggest that reducing excess free cholesterol in the CNS could be a viable ALS treatm

197 se element reporter assay, we confirmed that free cholesterol in the ER was also reciprocally modulat

198 We find that accumulation of free cholesterol in the late endosomes/lysosomes of Arf6

199 MTP reduces cholesteryl esters and enhances free cholesterol in the liver and intestine without dimi

200 ed to be much less toxic than the buildup of free cholesterol in the lysosomes of patients with mutat

201 than 100 fold less than the exchange rate of free cholesterol in the same conditions.

202 apoA-I-/- mice, promoted the accumulation of free cholesterol in the very low-density lipoprotein (VL

203 ed hypertriglyceridemia, the accumulation of free cholesterol in VLDL and HDL, and the formation of d

204 Paradoxically, the amount of free cholesterol increased on the surface of LDs in ACAT

205 Several lines of evidence demonstrated that free-cholesterol-induced autophagy, which led to increas

206 esterol that could increase the partition of free cholesterol into membranes.

207 o equilibrate, indicating that bulk cellular free cholesterol is isolated from that participating in

208 An increase in free cholesterol is observed in aggregates contained in

209 The released, free cholesterol is then exported from lysosomes for cel

210 tals to which recycling or newly synthesized free cholesterol is transported prior to efflux or redis

211 Free cholesterol is very efficiently removed from cells

212 sition of natural HDL and, importantly, bind free cholesterol (K(d) = 4 nM).

213 cyl groups from phospholipids to the 3-OH of free cholesterol, leading to the removal of excess chole

214 y, ACAT-1 inhibition increased intracellular free cholesterol level, which was associated with elevat

215 Treatments that change cellular free cholesterol levels also modulate the trafficking of

216 gidity was associated with a reduction in PM free cholesterol levels and the intracellular accumulati

217 ory chain dysfunction elevates intracellular free cholesterol levels and therefore attenuates the exp

218 Increased extracellular free cholesterol levels are toxic to neurons; this toxic

219 ly LXRalpha provides a safety valve to limit free cholesterol levels as a basal protective mechanism

220 tudies have shown that increases in cellular free cholesterol levels stimulate apoE transcription in

221 lls showed significant reduction in cellular free cholesterol levels, with no cytotoxicity up to 5 mi

222 s associated with a small decrease in plasma-free cholesterol levels, without a change in cholesteryl

223 anism to avoid toxicity associated with high free cholesterol levels.

224 verexpression of GRAMD1B increases levels of free cholesterol, lipid droplets, and impairs autophagy

225 hese observations, we fed TNFalpha-secreting free cholesterol-loaded apoptotic macrophages to a healt

226 TNFalpha is released by free cholesterol-loaded apoptotic macrophages, and the c

227 StarD5 expression increased 3-fold in free cholesterol-loaded macrophages, which activate the

228 HDL reversed impaired chemotaxis in free cholesterol-loaded WT macrophages but was without e

229 age death, macrophages rendered apoptotic by free cholesterol loading (FC-AMs) were incubated briefly

230 ophages undergo ER stress and apoptosis upon free cholesterol loading (FCL).

231 In contrast free cholesterol loading of macrophages leads to imbalan

232 arious stimuli such as nutrient deprivation, free cholesterol loading, and oxidized LDL.

233 ring endoplasmic reticulum stress induced by free cholesterol loading.

234 ORMDL1 degradation was specific to free-cholesterol loading as autophagy induced by serum s

235 By contributing to the deposition of free cholesterol, macrophage infiltration, and enlargeme

236 rane of target cells is dictated by how much free cholesterol molecules are present.

237 that alpha-toxin may increase the number of free cholesterol molecules in the membrane.

238 reverse cholesterol transport by esterifying free cholesterol on HDL particles.

239 CAT1/2 overexpression increases the level of free cholesterol on the LD surface, thereby impeding adi

240 olesterol oxidase-sensitive pool of membrane free cholesterol on the other.

241 r, and ultimately into the bile and feces as free cholesterol or bile acids.

242 After P. falciparum initially acquired free cholesterol or inner erythrocytic membrane-derived

243 wed increased apoptosis when challenged with free cholesterol or oxidized LDL loading.

244 hages from apoptosis induced by loading with free cholesterol or oxidized LDL.

245 ree major branches of the UPR in response to free cholesterol or oxysterol loading in insulin-resista

246 reased apoptosis in response to loading with free cholesterol or oxysterol, but underlying mechanisms

247 ations in apoA-I(-/-) HDL particle diameter, free cholesterol or phospholipid content, or the apoE or

248 zyme 1beta, a combined reduction of cellular free cholesterol or triglyceride or both and MTP activit

249 Only traces of free cholesterol oxides were found (25-OH, 7-k, 7alpha-O

250 ble increase in cholesterol esters, although free cholesterol persisted at wild type levels, which mi

251 onstrating a direct relationship between the free cholesterol: phospholipid ratio and cellular necros

252 an adaptive response to prevent the cellular free cholesterol: phospholipid ratio from reaching cytot

253 lasma cholesterol, cholesteryl esters (CEs), free cholesterol, phospholipids, HDL cholesterol, and ap

254 bined with the measurement of the smaller ER free cholesterol pool in J774-SRBI cells, suggests that

255 though J774-SRBI cells manifested a smaller free cholesterol pool in the endoplasmic reticulum.

256 etains the membrane condensing properties of free cholesterol regardless of the chemistry or position

257 High-density lipoproteins, responsible for free cholesterol removal, are reduced in patients with i

258 Adipose tissue (AT) is the body's largest free cholesterol reservoir and abundantly expresses ATP

259 o chylomicrons, absorption of phospholipids, free cholesterol, retinol, and vitamin E also involves H

260 mained significantly higher than that of the free cholesterol, suggesting that cholesterol derived fr

261 e reduced macrophage immunostaining and more free cholesterol than control lesions.

262 ey molecules involved in the accumulation of free cholesterol that are selectively induced in high-ri

263 e membranes is their high relative levels of free cholesterol; the mole ratio of cholesterol to phosp

264 converted approximately 0.1-2% of total cell-free cholesterol to [14C]cholesteryl esters.

265 pression alters the distribution of membrane-free cholesterol to a caveolar fraction or alters the ac

266 The efflux of cellular phospholipid and free cholesterol to apolipoprotein A-I promoted by ABCA1

267 Although esterification of free cholesterol to cholesteryl ester in the liver is kn

268 CAT1 and ACAT2) are two enzymes that convert free cholesterol to cholesteryl esters.

269 demonstrate the unique ability of exogenous free cholesterol to disrupt plasma membrane homeostasis

270 The efflux of free cholesterol to HDL was the same in sense and antise

271 golipid, C8-lactosylceramide (C8-LacCer), or free cholesterol to human fibroblasts at 10 degrees C ca

272 The addition of free cholesterol to ldlA7-SRBI cells also stimulated cho

273 inositol, sphingomyelin, and partial loss of free cholesterol transfer activities.

274 The MLN64 START domain stimulated free cholesterol transfer from donor to acceptor mitocho

275 Almost all the free cholesterol transferred from lipoproteins to cells

276 Only 5% of the free cholesterol transferred to cells was esterified, in

277 f SR-BI in macrophages increases the rate of free cholesterol transport, and modulates free cholester

278 tive selective uptake rate constants for CE, free cholesterol, triglycerides (triolein), and phosphat

279 icking of these vesicles may be regulated by free cholesterol under physiological conditions.

280 s system for quick and reliable detection of free cholesterol using unaided eye.

281 The clearance of lysosomal free cholesterol was also associated with a decrease in

282 The absorption of free cholesterol was also not significantly different be

283 The reduction in cellular free cholesterol was associated with correction of abnor

284 ndent accumulation of cholesteryl esters and free cholesterol was detected in the plaques of the chol

285 as quantified.Measurements and Main Results: Free cholesterol was largely increased by 60-fold and ch

286 essing GX sPLA(2) was reversed when cellular free cholesterol was normalized using cyclodextrin.

287 ive blue shade product depending on level of free cholesterol, when tested on complex system of human

288 creased the ratio of cholesterol esters over free cholesterol, whereas inhibition of p38 MAPK with SB

289 E levels, fewer lipid bodies, and accumulate free cholesterol, which causes injurious membrane effect

290 In contrast, the less-polar free cholesterol, which serves as an important biomarker

291 ABCA1)-mediated assembly of phospholipid and free cholesterol with apoA-I plays an important role in

292 We reported herewith that the presence of free cholesterol within liposomes reduces the inflammato

293 oteins (XL.HDL) on the causal pathway to AD: free cholesterol (XL.HDL.FC: 95% CI = 0.78 to 0.94), tot

294 components, i.e., XL-HDL cholesterol, XL-HDL-free cholesterol, XL-HDL phospholipids, L-HDL cholestero