|
Arteriosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
The aim of the study was to scrutinize the effect of Clematichinenoside (AR) on dyslipidemia-induced atherosclerosis and explore its capability on expression of Peroxisome proliferator-activated receptor-α (PPAR-alpha), apolipoprotein A-I (APOA1) and A-II (APOA2), and suppression of apolipoprotein C-III (APOC3) genes and proteins.
|
25979856 |
2015 |
|
Atherosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
The aim of the study was to scrutinize the effect of Clematichinenoside (AR) on dyslipidemia-induced atherosclerosis and explore its capability on expression of Peroxisome proliferator-activated receptor-α (PPAR-alpha), apolipoprotein A-I (APOA1) and A-II (APOA2), and suppression of apolipoprotein C-III (APOC3) genes and proteins.
|
25979856 |
2015 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
These results suggest that enrichment of apo A-II in high-density lipoprotein particles has atheroprotective effects and apo A-II may become a target for the treatment of atherosclerosis.
|
23241412 |
2013 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
These results suggest that enrichment of apo A-II in high-density lipoprotein particles has atheroprotective effects and apo A-II may become a target for the treatment of atherosclerosis.
|
23241412 |
2013 |
|
Arteriosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Our data suggest that, in the atherosclerosis-susceptible human apoB/A-II mouse model, expression of the human apoA-I(M) gene does not have protective advantage over that of the apoA-I gene.
|
16285990 |
2005 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Overexpression of human apolipoprotein (apo) A-II in transgenic mice induces high-density lipoprotein (HDL) deficiency, and increased atherosclerosis susceptibility only when fed an atherogenic diet.
|
15994442 |
2005 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Overexpression of human apolipoprotein (apo) A-II in transgenic mice induces high-density lipoprotein (HDL) deficiency, and increased atherosclerosis susceptibility only when fed an atherogenic diet.
|
15994442 |
2005 |
|
Atherosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Our data suggest that, in the atherosclerosis-susceptible human apoB/A-II mouse model, expression of the human apoA-I(M) gene does not have protective advantage over that of the apoA-I gene.
|
16285990 |
2005 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Nevertheless, some effects of apo A-II on intermediate HDL metabolism might improve reverse cholesterol transport and might reduce atherosclerosis development while some other effects might be deleterious.
|
12119188 |
2002 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Nevertheless, some effects of apo A-II on intermediate HDL metabolism might improve reverse cholesterol transport and might reduce atherosclerosis development while some other effects might be deleterious.
|
12119188 |
2002 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
New Zealand White (NZW) rabbits have low plasma total cholesterol concentrations, high cholesteryl ester transfer protein activity, low hepatic lipase (HL) activity, and lack an analogue of human apolipoprotein (apo) A-II, providing a unique system in which to assess the effects of human transgenes on plasma lipoproteins and atherosclerosis susceptibility.
|
10064724 |
1999 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
New Zealand White (NZW) rabbits have low plasma total cholesterol concentrations, high cholesteryl ester transfer protein activity, low hepatic lipase (HL) activity, and lack an analogue of human apolipoprotein (apo) A-II, providing a unique system in which to assess the effects of human transgenes on plasma lipoproteins and atherosclerosis susceptibility.
|
10064724 |
1999 |
|
Arteriosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
We report on the effect of human apolipoprotein (apo) A-II transgene expression on atherosclerosis susceptibility in two transgenic lines (25.3 and 11.1) whose plasma human apoA-II concentrations (approximately 23 and 96 mg/dl, respectively) span the normal range in humans.
|
9580110 |
1998 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
The distribution of apolipoprotein (apo) J during the development of atherosclerosis in the human aorta was evaluated by immununohistochemical observation, together with the other apolipoprotein A-I, A-II, B, C-III, and E. Although apoJ was never observed in the normal aorta (ie, without any intimal lesions or intimal thickening), it was distributed not only in the intima but also in the media of aortas with diffuse, intimal thickening or atherosclerotic lesions.
|
9555874 |
1998 |
|
Atherosclerosis
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
We report on the effect of human apolipoprotein (apo) A-II transgene expression on atherosclerosis susceptibility in two transgenic lines (25.3 and 11.1) whose plasma human apoA-II concentrations (approximately 23 and 96 mg/dl, respectively) span the normal range in humans.
|
9580110 |
1998 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
The distribution of apolipoprotein (apo) J during the development of atherosclerosis in the human aorta was evaluated by immununohistochemical observation, together with the other apolipoprotein A-I, A-II, B, C-III, and E. Although apoJ was never observed in the normal aorta (ie, without any intimal lesions or intimal thickening), it was distributed not only in the intima but also in the media of aortas with diffuse, intimal thickening or atherosclerotic lesions.
|
9555874 |
1998 |
|
Arteriosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Because LpA-I has been proposed to be more protective than LpA-I:A-II against atherosclerosis, this selective effect on the metabolism of LpA-I:A-II may provide a potential explanation why patients with classic LCAT deficiency and Fish-eye disease are not at increased risk for premature atherosclerosis despite markedly decreased levels of HDL cholesterol and apoA-I.
|
8282802 |
1994 |
|
Atherosclerosis
|
0.090 |
Biomarker
|
disease |
BEFREE |
Because LpA-I has been proposed to be more protective than LpA-I:A-II against atherosclerosis, this selective effect on the metabolism of LpA-I:A-II may provide a potential explanation why patients with classic LCAT deficiency and Fish-eye disease are not at increased risk for premature atherosclerosis despite markedly decreased levels of HDL cholesterol and apoA-I.
|
8282802 |
1994 |
|
Lecithin Acyltransferase Deficiency
|
0.040 |
Biomarker
|
disease |
BEFREE |
We characterized two species of lipoproteins containing apo A-I, one containing only apo A-I (LpA-I) and the other containing both apo A-I and apo A-II (LpA-I/A-II), in three heterozygotes for familial lecithin:cholesterol acyltransferase deficiency (LCAT).
|
7605383 |
1995 |
|
Lecithin Acyltransferase Deficiency
|
0.040 |
Biomarker
|
disease |
BEFREE |
Because LpA-I has been proposed to be more protective than LpA-I:A-II against atherosclerosis, this selective effect on the metabolism of LpA-I:A-II may provide a potential explanation why patients with classic LCAT deficiency and Fish-eye disease are not at increased risk for premature atherosclerosis despite markedly decreased levels of HDL cholesterol and apoA-I.
|
8282802 |
1994 |
|
Lecithin Acyltransferase Deficiency
|
0.040 |
Biomarker
|
disease |
BEFREE |
Lecithin-cholesterol acyltransferase mass levels and activity and apolipoproteins A-I, A-II, B and D were measured in a Japanese family who have a familial lecithin-cholesterol acyltransferase deficiency.
|
4005283 |
1985 |
|
Lecithin Acyltransferase Deficiency
|
0.040 |
Biomarker
|
disease |
BEFREE |
These presumed heterozygotes had normal levels of apolipoproteins A-I, A-II, B and D. The two subjects with LCAT deficiency had no detectable LCAT mass (below 0.1 microgram/ml) or LCAT activity (below 0.76 nmol/h/ml), apolipoprotein A-I and D levels approximately 50% of normal, and apolipoproteins B and A-II levels only 30-35% of normal.
|
7327552 |
1981 |
|
Myocardial Infarction
|
0.030 |
Biomarker
|
disease |
BEFREE |
The aim of this study was to investigate the possibility of interactions between CETP, PPARA, APOE, and APOAI polymorphisms and HDL-C, apolipoprotein (apo) A-I, lipoprotein (Lp) A-I, and Lp A-I:A-II in a sample selected from the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study population who remained free of cardiovascular events over 5 years of follow-up.
|
19217440 |
2009 |
|
Coronary heart disease
|
0.030 |
Biomarker
|
disease |
BEFREE |
A recent prospective epidemiological (PRIME) study suggests that Lp A-I (HDL containing apo A-I but not apo A-II) and Lp A-I:A-II (HDL containing apo A-I and apo A-II) were both reduced in survivors of myocardial infarction, suggesting that both particles are risk markers of CHD.
|
12119188 |
2002 |
|
Myocardial Infarction
|
0.030 |
Biomarker
|
disease |
BEFREE |
A recent prospective epidemiological (PRIME) study suggests that Lp A-I (HDL containing apo A-I but not apo A-II) and Lp A-I:A-II (HDL containing apo A-I and apo A-II) were both reduced in survivors of myocardial infarction, suggesting that both particles are risk markers of CHD.
|
12119188 |
2002 |