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. Testosterone as a protective factor against atherosclerosis--immunomodulation and influence upon plaque development and stability. J Endocrinol. 2003; 178(3):373–80. 5. Phillips GB. Is atherosclerotic cardiovascular disease an endocrinological disorder? The estrogen-androgen paradox. J Clin Endocrin Metab. 2005; 90(5):2708-2711. 6. Burke A.P., Farb A., Malcom G., Virmani R.. Effect of menopause on plaque morphologic characteristics in coronary atherosclerosis, Am Heart J, 2001; vol. 141 2:58-62. 7. Rossouw JE, Prentice PL, Manson JE, et al. Postmenopausal hormone therapy and

Other Societies on Cardiovascular Disease Prevention in Clinical Practice. Eur Heart J 2003; 24: 1601-10. Das B, Daga MK, Gupta SK. Lipid Pentad Index: A novel bioindex for evaluation of lipid risk factors for atherosclerosis in young adolescents and children of premature coronary artery disease patients in India. Clin Bioch 2007; 40 (1-2): 18-24. Bogavac-Stanojević N, Jelić-Ivanović Z, Spasojević-Kalimanovska V, Spasić S, Kalimanovska-Oštrić D. Lipid and inflammatory markers for the prediction of coronary artery disease: A multi-marker approach. Clin Biochem

References Ives DG, Fitzpatrick AL, Bild DE, et al. Surveillance and ascertainment of cardiovascular events: the Cardiovascular Health Study. Ann Epidemiol. 1995;5:278-285. doi:10.1016/1047-2797(94)00093-9 PMID:8520709 Kuller L, Borhani N, Furberg C, et al. Prevalence of subclinical atherosclerosis and cardiovascular disease and association with risk factors in the Cardiovascular Health Study. Am J Epidemiol. 1994;139(12):1164-1179. PMID:8209875 Ballotta E, Da Giau G, Renon L, Abbruzzese E, Saladini M, Baraccini C, Menegehetti G. Symptomatic and

115Kunihiro S. et al.: Tetrahydrobiopterin Slows Atherosclerosis Pteridines/Vol. 18/No. 4 Correspondence to: Yoshiyuki Hattori, MD, Department of Endocrinology & Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan. E-mail yhattori@dokkyomed.ac.jp Pteridines Vol. 18, 2007, pp. 115 - 121 Tetrahydrobiopterin Slows the Progression of Atherosclerosis Suzuki Kunihiro1, Yoshiyuki Hattori1, Teruo Jojima1, Atsuko Tomizawa1, Toshie Okayasu1, Hiroyuki Kase1, Yoshiaki Kawagoe1, Nobuyuki Banba1, Tsuyoshi Monden1, Nobuo Nakanishi2, Kikuo Kasai1 1

Clin Chem Lab Med 2007;45(12):1667–1677 2007 by Walter de Gruyter • Berlin • New York. DOI 10.1515/CCLM.2007.349 2007/360 Article in press - uncorrected proof Review Measuring subclinical atherosclerosis: is homocysteine relevant? Ahmad B. Sarwar1, Ammar Sarwar2, Boaz D. Rosen3 and Khurram Nasir2,* 1 Hahnemann University Hospital, Drexel University College of Medicine Philadelphia, Philadelphia, PA, USA 2 Cardiac MR PET CT Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA 3 Harbor Hospital Baltimore, Baltimore, MD, USA Abstract

Introduction Despite considerable therapeutic advances over the past 50 years, cardiovascular events are the leading causes of death worldwide. This is primarily due to the increasing prevalence of atherosclerosis (AS) which is associated with a sedentary and obesogenic life style increasingly present in the so-called Western, industrialized world. Atherosclerosis is a sub-acute inflammatory condition of the vascular wall, characterized by the infiltration of macrophages and T-cells which interact with one another and with the arterial wall cells (1). The chronic

Qingbo Xu et at. : Serum hsp 65 antibodies, neopterin, autoantibodies and atherosclerosis Pte ridines Vol. 5, 1994, pp. 139-141 Relationship among Serum hsp65 Antibodies, Neopterin, Autoantibodies and Atherosclerosis Qingbo Xu, # Georg Wick/ ' Helmut Wachter" and Gilbert Reibnegger*§ II Institute for Biomedical Aging Research, Austrian Academy of Sciences, Rennweg 10, A-6020 Innsbruck, Austria t Institute for General and Experimental Pathology, University of Innsbruck , t Institute for Medical Chemistry and Biochemistry, University of Innsbruck, Fritz

senescence-associated β-galactosidase (SA-β-GAL) activity [ 2 ]; (2) increased expression level of senescence-associated proteins (e.g., P53/P21 and P16); and (3) increased expression level of pro-inflammation cytokines (e.g., IL-18 and IL1β) and adhesion molecules (e.g., ICAM-1 and VCAM-1). In recent years, senescent-associated diseases, especially cardiovascular diseases, have endangered human health worldwide. Senescence-associated atherosclerosis is a major cause of cardiovascular diseases, which is considered the leading cause of mortality and morbidity. Senescence in

Introduction Atherosclerosis is a long-term process characterized by plaque formation in middle and large arterial blood vessels [ 1 ]. Atherosclerosis is one of the leading causes of stroke, heart attack and peripheral arterial disease [ 2 , 3 ]. The prevalence and degree of atherosclerosis increases with increasing age, body mass index (BMI), increased blood pressure (BP), and serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) [ 4 ]. An elevated level of LDL is directly associated with development of atherosclerotic cardiovascular

Introduction Atherosclerosis is one of the most common cardiovascular diseases (CVDs) in human societies. According to reports of the World Health Organization (WHO), it will be the cause of the most mortality and morbidity in the future ( Fleming, 2003 ). The term ‘atherosclerosis’ is a combination of two Latin words, ‘athero’ means gruellike, soft, pasty materials and ‘sclerosis’ means hardening. It develops by the formation of atheromatous plaque within the artery wall resulting in vessel stenosis and failure of blood flow. It occurs as a result of three