ライフサイエンスコーパス: hyperlipidemic

1 , and these patients are generally obese and hyperlipidemic.

2 essing high levels of apoE2 (>50 mg/dl) were hyperlipidemic.

3 ed MI were more frequently men (86% vs 68%), hyperlipidemic (62% vs 40%), and smokers (59% vs 37%), w

4 lipoprotein receptor (Ldlr(-/-)), which are hyperlipidemic; 9 weeks later, mice were fed either regu

5 Hyperlipidemic Acta2R149C/+Apoe-/- mice have a 2.5-fold

6 nth study with 60 patients, in more advanced hyperlipidemic, also evaluating the intima-media thickne

7 show that mice lacking calcineurin Abeta are hyperlipidemic and develop age-dependent insulin resista

8 OA1(Tg) mice were severely hyperglycemic and hyperlipidemic and had markedly elevated plasma APOB lev

9 The OC and PC diets were equally hyperlipidemic and hypercholesterolemic.

10 ighlighting the promise of nanomedicines for hyperlipidemic and metabolic syndromes.

11 symptomatic hepatomegaly who are diabetic or hyperlipidemic and present with an unrelated medical pro

12 h periodontal disease and atherosclerosis in hyperlipidemic and proatherogenic ApoE(-/-) mice.

13 healing, antiulcer, anti-inflammatory, anti-hyperlipidemic and slimming effects.

14 n low-density lipoprotein receptor-deficient hyperlipidemic and streptozotozin-induced diabetic mice,

15 le environment of large arteries in healthy, hyperlipidemic, and atherosclerotic conditions.

16 s, we found that imd mutants weigh more, are hyperlipidemic, and have impaired glucose tolerance.

17 ZF rats were obese, hyperlipidemic, and normoglycemic.

18 clerotic lesions were clearly visible in all hyperlipidemic animal gamma-imaging.

19 We demonstrate that hyperlipidemic animals succumbed to a non-lethal dose of

20 Strikingly, survival of hyperlipidemic animals was restored when the nuclear imp

21 lerate atherosclerotic lesion development in hyperlipidemic animals.

22 errying SRTFs and ChREBPs, protected 70-100% hyperlipidemic animals.

23 We observed that while female hyperlipidemic apoE KO mice fed a 0.2% adenine diet for

24 sclerosis by inducing a Th17 response in the hyperlipidemic apoE KO mouse model.

25 rophage progenitor cells were upregulated in hyperlipidemic ApoE(-/-) and LDL-R(-/-) mice, with adven

26 uman-like lipoprotein metabolism that unlike hyperlipidemic Apoe(-/-) and Ldlr(-/-) mice expresses fu

27 AP, a marker of the acute-phase response, in hyperlipidemic apoE(-/-) mice and suggest a probability

28 inhibits atherosclerosis and inflammation in hyperlipidemic Apoe(-/-) mice in vivo.

29 Hyperlipidemic Apoe(-/-) mice were fed a western diet to

30 In hyperlipidemic Apoe(-/-) mice, Mif-2-deficiency and phar

31 cts of atherosclerotic lesions isolated from hyperlipidemic apoE(-/-) mice.

32 tives (CAP-PEs) are present in the plasma of hyperlipidemic ApoE(-/-) mice.

33 tion and vascular atherosclerosis in vivo in hyperlipidemic ApoE(-/-) mice.

34 . denticola infection and atherosclerosis in hyperlipidemic ApoE(-/-) mice.

35 ion of apoB(+) T(regs) in lineage tracing of hyperlipidemic Apoe(-/-) mice.

36 stimulation protects from atherosclerosis in hyperlipidemic APOE*3-Leiden.CETP mice, a well-establish

37 LXRbeta-deficient mice crossed to the hyperlipidemic ApoE-deficient background or challenged w

38 or continuous infusion of angiotensin II in hyperlipidemic ApoE-knockout mice (Ang II model).

39 lipid, and [(3)H]PAF clearance was slowed in hyperlipidemic apolipoprotein (apo)E(-/-) mice with exce

40 n from platelet-specific ERK5 null mice into hyperlipidemic apolipoprotein E null mice showed decreas

41 betaarr2(+/+) and betaarr2(-/-) mice on the hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) ba

42 infection of the aorta occurred in 11 of 31 hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) mi

43 First, atherosclerotic lesion development in hyperlipidemic apolipoprotein E-deficient (ApoE(-/-)) mi

44 AAAs were induced in hyperlipidemic apolipoprotein E-deficient mice by chroni

45 nt was effective at reducing lipid levels in hyperlipidemic apolipoprotein E-deficient mice, it impai

46 etween the strains C3H/HeJ and C57BL/6J on a hyperlipidemic apolipoprotein E-null background.

47 of age, normolipidemic, wild-type (WT), and hyperlipidemic, apolipoprotein E-deficient (apoE-/-) mic

48 Here we demonstrate that MafB promotes hyperlipidemic atherosclerosis by suppressing foam-cell

49 ostanoid receptor together with mPges-1 on a hyperlipidemic background (low-density lipoprotein recep

50 /- mice on wild-type (PKM2fl/flLysMCre+) and hyperlipidemic background (PKM2fl/flLysMCre+Apoe-/-).

51 osis development on an apolipoprotein E null hyperlipidemic background, but it did lead to a signific

52 These effects did not increase in severe hyperlipidemic blood from aged mice and upon feeding a h

53 hages to aortas from both normolipidemic and hyperlipidemic C57BL/6J mice and apolipoprotein E (ApoE)

54 Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice sh

55 ins C and E restores endothelial function in hyperlipidemic children.

56 ers for oxidative stress and inflammation in hyperlipidemic children.

57 specific percentile were defined as combined hyperlipidemic (CHL).

58 Genetic deletion of cd36 in the hyperlipidemic condition reduced proinflammatory chemoki

59 I-1 on the arterial response to injury under hyperlipidemic conditions are unknown.

60 ncreased their MHC class II expression under hyperlipidemic conditions both in vivo and in vitro.

61 enic role of CD1b-autoreactive T cells under hyperlipidemic conditions in a mouse model of spontaneou

62 hage cholesterol accumulation on exposure to hyperlipidemic conditions in vitro, ex vivo, and in vivo

63 Platelet reactivity in hyperlipidemic conditions is enhanced when platelet scav

64 ptor serves a pro-atherogenic function under hyperlipidemic conditions, as both apolipoprotein E and

65 y which EC contribute to atherogenesis under hyperlipidemic conditions.

66 to reduce atherosclerotic plaque size under hyperlipidemic conditions.

67 cytes and fibroblasts under hyperglycemia or hyperlipidemic conditions.

68 gulation of the MCP-1/CCR2 chemokine axis in hyperlipidemic conditions.

69 nt on diabetes-induced dyslipidemia, because hyperlipidemic diabetic and nondiabetic mice with simila

70 ral artery denudation in ApoE(-/-) mice on a hyperlipidemic diet was used to induce accelerated ather

71 els of atherosclerosis receiving a normal or hyperlipidemic diet.

72 after initiation of diabetes mellitus and a hyperlipidemic diet.

73 lipid mediators involved in inflammatory and hyperlipidemic diseases.

74 To assess the power of hyperlipidemic Diversity Outbred (DO) mice in facilitati

75 ere all increased by hyperlipidemia, whereas hyperlipidemic double mutant BMGFP(+)LDLr(-/-)TLR2(-/-)

76 percholesterolemic mice to determine how the hyperlipidemic environment affected transplanted hearts.

77 lood from chimeric mice, suggesting that the hyperlipidemic environment altered the wild-type platele

78 loped in a normolipidemic as compared with a hyperlipidemic environment and of the coronary atheroscl

79 arts compared with native hearts in the same hyperlipidemic environment.

80 n BP homeostasis in response to high salt in hyperlipidemic female mice.

81 als in unmedicated middle-aged men, one in a hyperlipidemic group (HYL group; n = 40) and one in a no

82 In the hyperlipidemic group, BOP was significantly correlated w

83 In this study with hyperlipidemic hamsters fed lovastatin only, lovastatin

84 y modulating lipid levels in hApoA1 mice and hyperlipidemic hamsters, while normalizing glucose level

85 The retinas of hyperglycemic, hyperlipidemic (HGHL, apolipoprotein E(-/-) db/db) mice

86 In the hyperlipidemic (HL) chow group, there was a 2.3-fold inc

87 aP2/DTA mice fed a control diet were hyperlipidemic, hyperglycemic, and had hyperinsulinemia

88 activation were analyzed on renal damage in hyperlipidemic-hyperglycemic mice.

89 pha in macrophages significantly ameliorated hyperlipidemic-hyperglycemic nephropathy.

90 Thus, the mechanism of hyperlipidemic hypersensitivity to lethal microbial infl

91 present a new evidence for the mechanism of hyperlipidemic hypersensitivity to microbial inflammatio

92 cing IL-2 or IFN-gamma remained increased in hyperlipidemic IL-6-deficient mice.

93 roducing IL-2 or IFN-y remained increased in hyperlipidemic IL-6-deficient mice.

94 duals heterozygous for the mutation are also hyperlipidemic, indicating that this is a codominant dis

95 DHA is warranted in both normolipidemic and hyperlipidemic individuals.

96 In hyperglycemic-hyperlipidemic kidneys, the accumulation of Tip47-positi

97 pes in an independent normolipidemic and the hyperlipidemic LCAS populations were significantly diffe

98 ls treated with native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice th

99 Hyperlipidemic LDL-R--deficient mice transgenic for an O

100 ts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR(-/-) mice, including cross-link addu

101 reduced atherosclerotic plaque formation in hyperlipidemic LDLR(-/-) mice.

102 arrow (BM) cells with 98.5% WT BM cells into hyperlipidemic Ldlr-/- mice.

103 was sufficient to cause dermal xanthomas in hyperlipidemic LDLR-deficient mice.

104 was attenuated when MacKOs were crossed into hyperlipidemic low-density lipoprotein receptor knockout

105 In the AngII-infused hyperlipidemic low-density lipoprotein receptor-deficien

106 ial cells (EC-mPGES-1-KOs) were crossed into hyperlipidemic low-density lipoprotein receptor-deficien

107 esic medications (OR = 0.21, P = .002), anti-hyperlipidemic medications (OR = 0.39, P = .004), macrol

108 In contrast to prior data among hyperlipidemic men, the current data suggest that Lp-PLA

109 ic blood pressure in both normolipidemic and hyperlipidemic men, with significant diastolic blood pre

110 tion and lesional macrophage accumulation in hyperlipidemic mice after vascular injury.

111 Administration of BBR to hyperlipidemic mice and hamsters lowered circulating PCS

112 t markedly increased levels in the plasma of hyperlipidemic mice and in the plasma of humans with low

113 tivation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice and that oxidatively modified LDL (o

114 When hyperlipidemic mice are given a high fat diet, CC appear

115 Ang II induced AAA in 9 (90%) of 10 hyperlipidemic mice deficient in apoE (apoE-/-/uPA+/+ mi

116 Furthermore, hyperlipidemic mice deficient in haematopoietic ANGPTL4

117 tro and to the aorta from normolipidemic and hyperlipidemic mice ex vivo.

118 Furthermore, the hyperlipidemic mice exhibited numerous foam cells, a pro

119 SMC-specific deletion (SM22-Delta) protects hyperlipidemic mice from AngII-mediated aneurysm formati

120 AT2) (A2), especially in the liver, protects hyperlipidemic mice from diet-induced hypercholesterolem

121 phages protects mice from atherosclerosis in hyperlipidemic mice in a gender-dependent manner.

122 Accelerated rejection in hyperlipidemic mice is also associated with increased se

123 chronic lipid accumulation and inflammation, hyperlipidemic mice lacking ABCG1 develop smaller athero

124 osclerotic lesion development in uninfected, hyperlipidemic mice lacking expression of either lipopol

125 ese results show that CD8alpha(+) DC loss in hyperlipidemic mice profoundly reduces cross-priming abi

126 PKM2 in myeloid cells in either wild-type or hyperlipidemic mice reduced infarcts and enhanced long-t

127 We suggest that accelerated rejection in hyperlipidemic mice results from IL-6 driven anti-donor

128 er cells in recipient LDL receptor-deficient hyperlipidemic mice revealed accelerated foam-cell apopt

129 hat absence of caveolin-1 (Cav1)/caveolae in hyperlipidemic mice strongly inhibits atherosclerosis, w

130 n low density lipoprotein receptor-deficient hyperlipidemic mice substantially decreased expression o

131 these uncertainties by subjecting normal and hyperlipidemic mice to transient middle cerebral artery

132 Apolipoprotein E-deficient hyperlipidemic mice treated for 6 weeks with constant ad

133 Apolipoprotein E-deficient spontaneously hyperlipidemic mice underwent uninephrectomy (UNx) or sh

134 Importantly, enhancing mitophagy in aged, hyperlipidemic mice via oral administration of spermidin

135 Platelets from hyperlipidemic mice were also found to have a diminished

136 Treatment of wild-type as well as hyperlipidemic mice with mAb 5.50.3 resulted in reduced

137 letion of COX-2 accelerates atherogenesis in hyperlipidemic mice, a process delayed by selective enzy

138 6(+) valvular endothelial cells increased in hyperlipidemic mice, and the conservation of PPARgamma a

139 urysm formation induced by angiotensin II in hyperlipidemic mice, coincident with a reduction in oxid

140 eloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, coincident with iNOS-mediated oxida

141 When crossed into ApoE-deficient hyperlipidemic mice, COX-2 deletion accelerated atheroge

142 In hyperlipidemic mice, expression of TF and active caspase

143 apoE results in increased atherosclerosis in hyperlipidemic mice, possibly as a consequence of altere

144 ophages in vitro as well as in the aortas of hyperlipidemic mice, suggesting that direct actions of L

145 kin-6 act as metabolic regulators in SMCs of hyperlipidemic mice.

146 not influence atherosclerosis development in hyperlipidemic mice.

147 differential association of Hb with HDL from hyperlipidemic mice.

148 ncreased atherosclerotic lesion formation in hyperlipidemic mice.

149 ioglitazone reduces valvular inflammation in hyperlipidemic mice.

150 ease pro-atherogenic remnant lipoproteins in hyperlipidemic mice.

151 hypercholesterolemia and atherosclerosis in hyperlipidemic mice.

152 targeting with a small molecule inhibitor in hyperlipidemic mice.

153 limited atherosclerotic lesion formation in hyperlipidemic mice.

154 revealed an altered lipid profile in mildly hyperlipidemic mice.

155 proatherogeneic impact of COX-2 deletion in hyperlipidemic mice.

156 tively reduces progression of the disease in hyperlipidemic mice.

157 ession, dyslipidemia, and atherosclerosis in hyperlipidemic Mir155 knockout mice.

158 t rodent pancreas, even in hyperglycemic and hyperlipidemic models or 1.5-year-old mice.

159 tty liver disease (SJL/J) and in a humanized hyperlipidemic mouse model (LDLr(-/-), apoB(100/100)).

160 The hyperlipidemic mouse model HypoE/SRBI(-/-) has been show

161 -A) does not ameliorate atherosclerosis in a hyperlipidemic mouse model, suggesting receptors other t

162 Studies in hyperlipidemic mouse models suggest that prominent activ

163 t mouse onto both the Ldlr and Apoe knockout hyperlipidemic mouse models.

164 g PLTP (PLTP-deficient mice) using different hyperlipidemic mouse strains.

165 response to P. gingivalis in the presence of hyperlipidemic PA levels as opposed to OA cultures, whic

166 ol (LDL-C), total cholesterol (TC) and TG in hyperlipidemic patients and in mice by mechanisms involv

167 significantly lower in the immunosuppressed hyperlipidemic patients than in normolipidemic controls.

168 d, double-blind study, 1,220 type IIa or IIb hyperlipidemic patients were randomized to treatment wit

169 ay provide additional therapeutic benefit to hyperlipidemic patients with concomitant NAFLD.

170 ary 1, 1998 and June 31, 2002: Cohort 1: 342 hyperlipidemic patients with elevated baseline enzymes (

171 who were prescribed a statin; cohort 2: 1437 hyperlipidemic patients with normal transaminases who we

172 sensitive CRP (hs-CRP) levels, especially in hyperlipidemic patients.

173 been shown to decrease cholesterol levels in hyperlipidemic patients.

174 an mid-intensity monotherapy among high-risk hyperlipidemic patients.

175 enic mice leads to either a hypolipidemic or hyperlipidemic phenotype.

176 vivo such as within atherosclerotic lesions, hyperlipidemic plasma, and plasma with low high-density

177 rough its ability to enhance HDL function in hyperlipidemic plasma, apoE is now known to suppress ath

178 In hyperlipidemic post-menopausal women, statin therapy ind

179 gression of coronary artery calcium (CAC) in hyperlipidemic post-menopausal women.

180 -blind, multicenter trial, we randomized 615 hyperlipidemic, postmenopausal women to intensive (atorv

181 Expression of tk in balloon-injured hyperlipidemic rabbit arteries followed by ganciclovir t

182 Smooth muscle cells from hyperlipidemic rabbit arteries infected with adenoviral

183 18 hours, P<0.001) in the Watanabe heritable hyperlipidemic rabbit model but also significantly impro

184 acceleration of atherosclerosis in a mildly hyperlipidemic rabbit model but is prevented by treatmen

185 cerivastatin to immature Watanabe heritable hyperlipidemic rabbits (cerivastatin group, n=10, ceriva

186 ed 1 carotid artery in 43 Watanabe heritable hyperlipidemic rabbits and performed local gene transduc

187 e in lesion-prone aortic sites was longer in hyperlipidemic rabbits before lesion formation than in t

188 al LDL residence times in normolipidemic and hyperlipidemic rabbits before lesion formation were simi

189 placebo (n=10) to mature Watanabe heritable hyperlipidemic rabbits for 52 weeks.

190 Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro ag

191 Watanabe heritable hyperlipidemic rabbits underwent serial MRI at baseline

192 Watanabe heritable hyperlipidemic rabbits were less susceptible to C. pneum

193 ocardial infarction-prone Watanabe heritable hyperlipidemic rabbits with age ranging between new-born

194 in LDL receptor deficient Watanabe Heritable Hyperlipidemic rabbits.

195 e responses to balloon injury were tested in hyperlipidemic rabbits.

196 therosclerotic lesions in Watanabe heritable hyperlipidemic rabbits.

197 ranase expression in the neointima of obese, hyperlipidemic rats in comparison to lean rats.

198 ght loss in the visceral fat mass of HFD-fed hyperlipidemic rats without affecting the normal feeding

199 fold in the urine of PM-treated diabetic and hyperlipidemic rats, compared with control animals.

200 mulation was tested in poloxamer 407-induced hyperlipidemic rats.

201 iton WR-1339 and high fat diet (HFD)-induced hyperlipidemic rats.

202 The hyperlipidemic response to a high-sucrose diet was great

203 Furthermore, hyperlipidemic serum enhanced IL-6 secretion by CD1b+ DC

204 intimal formation in both normolipidemic and hyperlipidemic settings and raise the possibility that s

205 itionally inducing VSMC apoptosis in situ in hyperlipidemic SM22alpha-hDTR/ApoE(-/-) mice to levels s

206 ensity lipoproteins (oxLDL) generated in the hyperlipidemic state may contribute to unregulated plate

207 28 days) decreased the insulin-resistant and hyperlipidemic states and increased food consumption and

208 eration at predilection sites in response to hyperlipidemic stress through upregulation of Dlk1 expre

209 d binding, and apoE2/E2 VLDL from a Type III hyperlipidemic subject did not bind.

210 llitus (n=36), smokers (n=10), and untreated hyperlipidemic subjects (n=10) were studied.

211 A longer study, with more advanced hyperlipidemic subjects is suggested.

212 Hyperlipidemic subjects showed higher TF (237+/-63 versu

213 e the risk of hepatotoxicity from statins in hyperlipidemic subjects with elevated baseline serum tra

214 bsorption shifting (IFAS) can be obtained in hyperlipidemic subjects with polyglucosamine biopolymer

215 ltered the lipoprotein profile in moderately hyperlipidemic subjects without significantly affecting

216 trategy for reducing the impact of stroke in hyperlipidemic subjects.

217 We have extended our study to smokers and hyperlipidemic subjects.

218 reater female vulnerability in hypertensive, hyperlipidemic Tg25 rats.

219 Here we report that, in heritable hyperlipidemic Watanabe rabbits, adenoviral gene transfe

220 of atherosclerosis in the Watanabe Heritable Hyperlipidemic (WHHL) rabbit, a model that spontaneously

221 metabolic defect in the Watanable heritable hyperlipidemic (WHHL) rabbit, an animal model for homozy

222 r in isolated aortas from Watanabe heritable hyperlipidemic (WHHL) rabbits (2 to 4 years old) compare

223 O transgenic rabbits with Watanabe heritable hyperlipidemic (WHHL) rabbits and found that the lesion

224 muscle cells (ASMC) from Watanabe heritable hyperlipidemic (WHHL) rabbits and skin fibroblasts from

225 e used as cell donors and Watanabe heritable hyperlipidemic (WHHL) rabbits were used as cell recipien

226 sma lipoprotein levels in Watanabe-heritable hyperlipidemic (WHHL) rabbits, which are a model for hum

227 ealand white (NZW) and 15 Watanabe heritable hyperlipidemic (WHHL) rabbits.

228 , Japanese White (JW) and Watanabe heritable hyperlipidemic (WHHL) rabbits.

229 T2D rats were obese and severely hyperlipidemic, with impaired glucose and insulin tolera

230 tensive vs. hypertensive, normolipidemic vs. hyperlipidemic, with vs. without diabetes mellitus), ang