ライフサイエンスコーパス: hyperlipidemic

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

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

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

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

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

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

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

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

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

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

11 ZF rats were obese, hyperlipidemic, and normoglycemic.

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

13 lerate atherosclerotic lesion development in hyperlipidemic animals.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 ers for oxidative stress and inflammation in hyperlipidemic children.

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

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

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

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

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

46 Platelet reactivity in hyperlipidemic conditions is enhanced when platelet scav

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

48 y which EC contribute to atherogenesis under hyperlipidemic conditions.

49 cytes and fibroblasts under hyperglycemia or hyperlipidemic conditions.

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

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

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

53 after initiation of diabetes mellitus and a hyperlipidemic diet.

54 els of atherosclerosis receiving a normal or hyperlipidemic diet.

55 lipid mediators involved in inflammatory and hyperlipidemic diseases.

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

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

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

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

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

61 In the hyperlipidemic group, BOP was significantly correlated w

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

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

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

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

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

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

68 pha in macrophages significantly ameliorated hyperlipidemic-hyperglycemic nephropathy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Furthermore, hyperlipidemic mice deficient in haematopoietic ANGPTL4

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 In hyperlipidemic mice, expression of TF and active caspase

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

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

107 differential association of Hb with HDL from hyperlipidemic mice.

108 hypercholesterolemia and atherosclerosis in hyperlipidemic mice.

109 ncreased atherosclerotic lesion formation in hyperlipidemic mice.

110 limited atherosclerotic lesion formation in hyperlipidemic mice.

111 ease pro-atherogenic remnant lipoproteins in hyperlipidemic mice.

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

113 tively reduces progression of the disease in hyperlipidemic mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 been shown to decrease cholesterol levels in hyperlipidemic patients.

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

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

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

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

133 In hyperlipidemic post-menopausal women, statin therapy ind

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

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

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

137 Smooth muscle cells from hyperlipidemic rabbit arteries infected with adenoviral

138 18 hours, P<0.001) in the Watanabe heritable hyperlipidemic rabbit model but also significantly impro

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

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

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

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

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

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

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

146 Watanabe heritable hyperlipidemic rabbits underwent serial MRI at baseline

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

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

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

150 therosclerotic lesions in Watanabe heritable hyperlipidemic rabbits.

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

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

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

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

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

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

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

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

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

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

161 28 days) decreased the insulin-resistant and hyperlipidemic states and increased food consumption and

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

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

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

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

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

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

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

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

170 reater female vulnerability in hypertensive, hyperlipidemic Tg25 rats.

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

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

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

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

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

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

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

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

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

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

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