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Atherosclerosis
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1. Effects of arsenic exposure and genetic polymorphisms of p53, glutathione S-transferase M1, T1, and P1 on the risk of carotid atherosclerosis in Taiwan.
Match Strength: 6.544

To evaluate the joint effects between genetic polymorphisms of glutathione S-transferase M1, T1, P1, and p53, and arsenic exposure through drinking well water on the risk of carotid atherosclerosis, 605 residents including 289 men and 316 women were recruited from a northeastern area of Taiwan. Carotid atherosclerosis was diagnosed by either a carotid artery intima-media thickness (IMT) of >1.0mm, a plaque score of >/=1, or stenosis of >50%. A significant age- and gender-adjusted odds ratio of 3.3 for the development of carotid atherosclerosis was observed among the high-arsenic ... Read More »
» Published in Atherosclerosis. 2006 Sep 12;

2. The RXR agonist bexarotene improves cholesterol homeostasis and inhibits atherosclerosis progression in a mouse model of mixed dyslipidemia.
Match Strength: 5.692

OBJECTIVE: The activity of the antitumoral agent bexarotene (Targretin, Bexarotene) depends on its binding to the nuclear retinoid-X receptor (RXR) and subsequent transcriptional regulation of target genes. Through RXR activation, bexarotene may modulate numerous metabolic pathways involved in atherosclerosis. Here, we investigated the effect of bexarotene on atherosclerosis progression in a dyslipidemic murine model, the human apolipoprotein E2 knockin mouse, that develops essentially macrophage-laden lesions. METHODS AND RESULTS: Atherosclerotic lesions together with different metabolic ... Read More »
» Published in Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2731-7. Epub 2006 Sep 28.

3. Interaction between Chlamydia pneumoniae seropositivity, inflammation and risk factors for atherosclerosis in patients with severe coronary stenosis.
Match Strength: 5.635

OBJECTIVE: To investigate whether Chlamydia pneumoniae (Cpn) seropositivity in patients with suspected coronary artery disease (CAD) (n = 81) is associated with increases in markers of inflammation, the severity of coronary atherosclerosis, and traditional risk factors for cardiovascular events. MATERIAL AND METHODS: The severity of coronary atherosclerosis was ranked by Gensini score. Inflammation and endothelial dysfunction were evaluated using white blood cell counts and levels of high-sensitivity C-reactive protein (hs-CRP), ferritin, tumour necrosis factor-alpha (TNF-alpha), interleukins ... Read More »
» Published in Scand J Clin Lab Invest. 2006;66(6):523-34.

4. HO-1 and VGEF gene expression in human arteries with advanced atherosclerosis.
Match Strength: 5.497

OBJECTIVES: Both heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) have been shown to be involved in the progression of atherosclerosis. The relationship between HO-1 and VEGF gene expression and their proteins in endothelial cells from human atherosclerotic arterial specimens was investigated. DESIGN AND METHODS: The study included seventeen human arterial specimens with early and six specimens with advanced atherosclerotic lesions. Ten specimens were obtained from healthy young adults undergoing arterial reconstruction for trauma and were considered as non-atherosclerotic ... Read More »
» Published in Clin Biochem. 2006 Nov;39(11):1057-62. Epub 2006 Aug 25.

5. Apolipoprotein A-I mimetic peptides and their role in atherosclerosis prevention.
Match Strength: 5.205

The importance of apolipoprotein A-I (apoA-I) in atherosclerosis was established by testing in animal models, and its potential usefulness in humans has been confirmed in preliminary studies. ApoA-I is a large protein comprising 243 amino acids, which means that venous administration is necessary. In addition, manufacture of apoA-I is difficult and expensive. Research has, therefore, been directed towards finding smaller peptide mimetics that produce similar results to apoA-I, but that are easier to manufacture and administer. The earliest peptides mimicked some of the lipid-binding properties ... Read More »
» Published in Nat Clin Pract Cardiovasc Med. 2006 Oct;3(10):540-7.

6. A 1,3-diacylglycerol-rich oil induces less atherosclerosis and lowers plasma cholesterol in diabetic apoE-deficient mice.
Match Strength: 5.201

OBJECTIVE: Recent studies have demonstrated that 1,3-diacylglycerol (1,3-DAG) has several metabolic advantages over triacylglycerol (TAG) in humans and in animal models despite both oils having a similar fatty acid composition. In our current study, we have examined the effects of long-term feeding of a 1,3-DAG-rich oil on the dyslipidemia and atherosclerosis in the experimental model of the diabetic apolipoprotein E (apoE)-deficient mouse that develops accelerated atherosclerosis. METHODS AND RESULTS: Diets containing 1,3-DAG-rich oil or TAG oil were administered to control non-diabetic apoE ... Read More »
» Published in Atherosclerosis. 2006 Sep 20;

7. T cells in atherogenesis: for better or for worse?
Match Strength: 4.966

The idea that atherosclerosis is an inflammatory disease is no longer controversial. Instead, much of the current research is now focused on understanding what drives this inflammation and how it is regulated. Adaptive immunity, in particular T cells, is highly involved in atherogenesis. It is well known that different subsets of T cells can drive or dampen inflammatory processes, but we still have much to learn about the regulation of this balance in the context of atherosclerosis. This review summarizes our knowledge of T cells in atherogenesis, their potential antigens, their contact ... Read More »
» Published in Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2421-32. Epub 2006 Sep 14.

8. Smooth muscle cells in atherosclerosis originate from the local vessel wall and not circulating progenitor cells in ApoE knockout mice.
Match Strength: 4.887

OBJECTIVE: Recent studies of bone marrow (BM)-transplanted apoE knockout (apoE-/-) mice have concluded that a substantial fraction of smooth muscle cells (SMCs) in atherosclerosis arise from circulating progenitor cells of hematopoietic origin. This pathway, however, remains controversial. In the present study, we reexamined the origin of plaque SMCs in apoE-/- mice by a series of BM transplantations and in a novel model of atherosclerosis induced in surgically transferred arterial segments. METHODS AND RESULTS: We analyzed plaques in lethally irradiated apoE-/- mice reconstituted with sex ... Read More »
» Published in Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2696-702. Epub 2006 Sep 28. Comment in: Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2579-81.

9. Loss of the lysophosphatidylcholine effector, G2A, ameliorates aortic atherosclerosis in low-density lipoprotein receptor knockout mice.
Match Strength: 4.712

OBJECTIVE: Lysophosphatidylcholine is a major product of low-density lipoprotein (LDL) oxidation and secretory phospholipase A2-mediated lipid hydrolysis within atherosclerotic lesions. The G2A receptor mediates chemotaxis of cultured macrophages and T cells to lysophosphatidylcholine, supporting a pro-atherogenic role for this receptor in vivo. We investigated the ability of G2A to modulate atherosclerosis in mice. METHODS AND RESULTS: We measured atherosclerosis in G2A+/+ and G2A-/- LDL receptor knockout (LDLR-/-) mice. Consistent with a previous study, early lesion size at the aortic sinus ... Read More »
» Published in Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2703-9. Epub 2006 Sep 21.

10. Dietary measures and exercise training contribute to improvement of endothelial function and atherosclerosis even in patients given intensive pharmacologic therapy.
Match Strength: 4.519

PURPOSE: Atherosclerosis contributes to cardiovascular mortality and morbidity even with aggressive lipid management. Our objective is to determine whether a combined pharmacological and lifestyle intervention can improve atherosclerosis. METHODS: We conducted a 2-year observational study at a specialized clinic in a tertiary care hospital. One hundred fifty-six subjects with coronary disease were enrolled in an intensive pharmacological management and lifestyle measures (including counseling and exercise training) program designed to reach specific targets. The main outcome measures were ... Read More »
» Published in J Cardiopulm Rehabil. 2006 Sep-Oct;26(5):288-93.

11. Biomechanical modulation of endothelial phenotype: implications for health and disease.
Match Strength: 4.461

The functional phenotypic plasticity of the vascular endothelium relies on the ability of individual endothelial cells to integrate and transduce both humoral and biomechanical stimuli from their surrounding environments. Increasing evidence strongly suggests that biomechanical stimulation is a critical determinant of endothelial gene expression and the functional phenotypes displayed by these cells in several pathophysiological conditions. Herein we discuss the types of biomechanical forces that endothelial cells are constantly exposed to within the vasculature, explain how these ... Read More »
» Published in Handb Exp Pharmacol. 2006;(176 Pt 2):79-95.

12. The conundrum of claudication.
Match Strength: 4.067

Stable claudication has traditionally been treated conservatively by many clinicians as operative therapies involve considerable risk for a condition that is often slowly progressive and non-fatal. The relative safety of less invasive endovascular techniques brings potential survival benefits from the increased exercise tolerance that result. We aimed to revisit and clarify the aetiologies of intermittent claudication in a review of the rarer causes that can mimic atherosclerotic occlusive disease. An extensive search of Medline, Embase and the Cochrane databases was carried out to compile ... Read More »
» Published in ANZ J Surg. 2006 Oct;76(10):916-27.

13. Effects of treatment for diabetes mellitus on circulating vascular progenitor cells.
Match Strength: 3.893

The circulating endothelial progenitor cells (EPCs) have an important role in angiogenesis, and the smooth muscle progenitor cells (SMPCs) participate in atherosclerosis. However, little is known about the effects of treatment of diabetes mellitus (DM) on EPCs and SMPCs. Therefore, we investigated the relations between the number of circulating vasucular progenitor cells before and after the treatment for DM. Ten previously untreated DM patients were enrolled in this study. Blood samples were collected before and after treatment. The peripheral mononuclear cells were purified and cultured to ... Read More »
» Published in J Pharmacol Sci. 2006 Sep;102(1):96-102.

14. The relationship between oxidized LDL and other cardiovascular risk factors and subclinical CVD in different ethnic groups: The Multi-Ethnic Study of Atherosclerosis (MESA).
Match Strength: 3.812

Several groups have demonstrated an association between established CHD and elevated oxidized LDL (oxLDL). The relation with cardiovascular risk factors and subclinical CVD is less clear. Therefore, we examined this association in the Multi-Ethnic Study of Atherosclerosis cohort: 879 persons without CHD, all non-statin users, examined cross-sectionally. oxLDL was measured with a monoclonal antibody 4E6-based ELISA. The presence of subclinical CVD was defined as plaque occurrence in carotid arteries with >/=25 stenosis, ankle-brachial blood pressure index (ABI) <0.9 and coronary ... Read More »
» Published in Atherosclerosis. 2006 Sep 16;

15. Optical coherence tomography accurately identifies intermediate atherosclerotic lesions-An in vivo evaluation in the rabbit carotid artery.
Match Strength: 3.761

OBJECTIVE: We tested the ability of optical coherence tomography (OCT) to identify very early stages of atherosclerosis in vivo. METHODS: Twelve New Zealand white male rabbits (weight 3.5-4.0kg) underwent perivascular electrical injury of the common carotid arteries, and were then fed a cholesterol-rich diet. At 43+/-16 (range 27-63) days after injury, arteries were imaged by OCT, then rabbits were euthanized and vessels processed for histology. RESULTS: A total of 14 carotid arteries were imaged by OCT and histology; 22 atherosclerotic lesions were identified, 16 (73%) occurring at the site ... Read More »
» Published in Atherosclerosis. 2006 Sep 26;

16. Toll-like receptor 4 signalling is neither sufficient nor required for oxidised phospholipid mediated induction of interleukin-8 expression.
Match Strength: 3.690

OBJECTIVE: Toll-like receptor (TLR)-4 signalling has been shown to accelerate atherosclerosis. As oxidised phospholipids are present in atherosclerotic plaque and have been shown to modulate TLR4 signalling, we investigated the role of oxidised 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine (OxPAPC) in the regulation of TLR 1, 2, 4 and 6 signalling. METHODS AND RESULTS: Unlike established TLR agonists, OxPAPC did not induce NF-kappaB-dependent gene expression in monocytic THP-1 cells, human aortic endothelial cells or TLR-deficient HEK-293 cells transfected with TLRs 1, 2, 4 or 6. ... Read More »
» Published in Atherosclerosis. 2006 Sep 16;

17. Effects of Quyu Xiaoban Capsule on vascular endothelial function in patients with atherosclerosis.
Match Strength: 3.596

OBJECTIVE: To evaluate the therapeutic effects of Quyu Xiaoban Capsule (QYXBC) on endothelial dependent vascular relaxation (EDVR) function in patients with atherosclerosis (AS) with ultrasonic technique. METHODS: Tested were the endothelial function and blood lipids of 42 patients with AS in the treated group and 30 healthy volunteers in the control group. And re-examination of these parameters was carried out on the AS patients after they had been treated with QYXBC for 10 months. RESULTS: Before treatment, the reactive hyperemia induced changes in artery diameter in the treated group was ... Read More »
» Published in Chin J Integr Med. 2006 Sep;12(3):171-4.

18. Predictors of carotid atherosclerotic plaque progression as measured by noninvasive magnetic resonance imaging.
Match Strength: 3.555

The purpose of this in vivo MRI study was to quantify changes in atherosclerotic plaque morphology prospectively and to identify factors that may alter the rate of progression in plaque burden. Sixty-eight asymptomatic subjects with >/=50% stenosis, underwent serial carotid MRI examinations over an 18-month period. Clinical risk factors for atherosclerosis, and medications were documented prospectively. The wall and total vessel areas, matched across time-points, were measured from cross-sectional images. The normalized wall index (NWI=wall area/total vessel area), as a marker of disease ... Read More »
» Published in Atherosclerosis. 2006 Sep 13;

19. Coffee and sweetened beverage consumption and the risk of type 2 diabetes mellitus: the atherosclerosis risk in communities study.
Match Strength: 3.518

The authors analyzed data from a prospective, community-based cohort to assess the risk of incident type 2 diabetes mellitus associated with coffee and sweetened beverage consumption. They included 12,204 nondiabetic, middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) Study (1987-1999). Consumption of each beverage was assessed by food frequency questionnaire and classified into categories of cups per day. They found an inverse association, after adjusting for potential confounders, between increased coffee consumption and risk of type 2 diabetes mellitus in men (for ... Read More »
» Published in Am J Epidemiol. 2006 Dec 1;164(11):1075-84. Epub 2006 Sep 18.

20. The role of estrogens in cardiovascular disease in the aftermath of clinical trials.
Match Strength: 3.379

The effects of estrogens on reproductive tissues and climacteric symptoms are unambiguous. However, their effects on other tissues and, in particular, the cardiovascular system remain controversial. In general, premenopausal women are protected from coronary heart disease (CHD) compared with aged-matched men but this ;female protection' appears to be lost after menopause, suggesting beneficial effects of female sex hormones on the cardiovascular system. This view has been supported by observational studies showing that estrogen replacement therapy (ERT) is associated with a 30% to 50% decrease ... Read More »
» Published in Hormones (Athens). 2004 Jul-Sep;3(3):171-83.

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