First 11 pages of thesis. - OPUS - Universität Würzburg

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1.2.2 Environmental factors 1. High-fat diet High fat and high cholesterol diets have been shown to increase atherosclerosis. In experimental models, high fat diets are used to induce plaque formation. In humans, regular consumption of high fat diet results in obesity and subsequent reduction of average life expectancy. Hence, reduction of body weight through diets is one of the main treatment strategies to reduce the individual cardiovascular risk. Mediterranean diets rich in olive oil or nuts have proved to reduce the cardiovascular risk more effectively than a conventional low-fat diet 12 . Additionally, omega-3 fatty acid rich diets reduce the risk of cardiovascular diseases 13 . 2. Smoking It has been calculated that about 30% of cardiovascular deaths are due to smoking 14 . Cigarette smoking increases total cholesterol, triglycerides and LDL- cholesterin and decreases the cardio-protective HDL-cholesterin. Smoking is an established independent risk factor for atherosclerosis development even among young individuals 15 . 3. Infectious disease/chronic inflammatory disease Recent studies have shown that inflammation plays a fundamental role in development of atherosclerosis 16, 17 . The signalling cascades that are triggered in response to inflammation have a proatherogenic role. Epidemiological and basic scientific studies have shown that pathogens like Chlamydia pneumonia 18 - 8 -
and Porphyromonas gingivalis 19 are associated with atherosclerosis development. Chronic inflammatory disease secondary to infection, like acquired immunodeficiency syndrome (AIDS) due to infection of human immunodeficiency virus (HIV) 20 and auto immune diseases like systemic lupus erythematosus and rheumatoid arthritis also accelerate atherosclerosis development 21 . 4. Lack of exercise Lack of physical exercise and a sedentary life style is an independent risk factor for various cardiovascular diseases. Regular exercise results in reduction of body fat, LDL cholesterol, triglyceride levels and blood pressure and increases atheroprotective HDL cholesterol levels 22 . Physical exercise is of paramount importance as it positively influences many independent cardiovascular disease risk factors. 5. Oxidative stress Increased levels of oxidants or decreased levels of anti-oxidants secondary to dyslipidemia, hypertension, diabetes and smoking are implicated in the pathogenesis of atherosclerosis. Oxidation of LDL is considered to be the critical step involved in ‘foam cell’ formation 23 . Oxidation of LDL results in many structural modifications and generation of numerous ‘oxidation specific epitopes’ such as malondialdehyde (MDA)-lysines and 4-hydroxynonenal (4-HNE)–lysine’ which are highly immunogenic. Immunization of mice with MDA and native LDL resulted in a significant reduction of atherosclerosis indicating the proatherosclerotic role of oxidized LDL (ox-LDL) 24 . - 9 -
Page 1 and 2: Insight into oxidative stress media
Page 3 and 4: Eidesstattliche Erklärungen Hiermi
Page 6 and 7: Acknowledgements First and foremost
Page 8 and 9: “Research is to see what everybod
Page 10 and 11: Chapter 2 37 2.0 Materials and Meth
Page 12 and 13: Summary and Hypothesis 76 Zusammenf
Page 14 and 15: 1.0 Introduction Atherosclerosis, t
Page 16 and 17: which contribute to the lipid rich
Page 18 and 19: 1.2 Risk Factors Atherosclerosis ha
Page 22 and 23: 1.3 Oxidative Stress Oxidative stre
Page 24 and 25: peroxynitrite 38 which by itself ca
Page 26 and 27: Pharmacological inhibition of nitri
Page 28 and 29: 1.4 The nitric oxide pathway in ath
Page 30 and 31: of NADPH, FAD and FMN, whereas the
Page 32 and 33: isoforms to the regulatory and targ
Page 34 and 35: perinuclear/golgi region within the
Page 36 and 37: nNOS interacts with several protein
Page 38 and 39: iNOS expression is regulated transc
Page 40 and 41: transport pathway and is an essenti
Page 42 and 43: Interestingly, BH4 supplementation
Page 44 and 45: the survival rate, as apoE/nNOS dko
Page 46 and 47: The seemingly opposing effects of i
Page 48 and 49: The purpose of the study presented
Page 50 and 51: 2.0 Materials and Methods 2.1 Mater
Page 52 and 53: Reagents Source For Immunohistochem
Page 54 and 55: Others Reagents Source Pegulated Su
Page 56 and 57: 2.2 Methods 2.2.1 Detection of free
Page 58 and 59: 2.2.1.2 Principle of ESR ESR spectr
Page 60 and 61: spectra 190 . Addition of exogenous
Page 62 and 63: ings were prepared as mentioned abo
Page 64 and 65: X-band EMX spectroscope (Bruker Bio
Page 66 and 67: minutes. At last sections were wash
Page 68 and 69: 3.0 Results 3.1 eNOS is a significa
Page 70 and 71:
3.2 eNOS deletion decreases vascula
Page 72 and 73:
3.3 nNOS contributes little to vasc
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3.5 iNOS contributes significantly
Page 76 and 77:
Figure 13. Determination of iNOS de
Page 78 and 79:
3.8 iNOS deletion influences NADPH
Page 80 and 81:
4.0 Discussion 4.1 eNOS is a major
Page 82 and 83:
in our apoE/eNOS dko model, these a
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under conditions of substrate or co
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vessels with the iNOS specific inhi
Page 88 and 89:
Summary and Hypothesis The principl
Page 90 and 91:
Zusammenfassung und Hypothese Stick
Page 92 and 93:
Bibliography 1. Gimbrone MA, Jr. Va
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xanthine oxidase contributes to vas
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expression of adhesion molecules an
Page 98 and 99:
transforming growth factor-beta 1.
Page 100 and 101:
generation from neuronal nitric oxi
Page 102 and 103:
148. Lee PC, Wang ZL, Qian S, Watki
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174. Mayr U, Zou Y, Zhang Z, Dietri
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implications in intracellular fluor
Page 108 and 109:
Definitions Thesaurus • Allograft
Page 110 and 111:
• Claudication refers to leg pain
Page 112 and 113:
cases per year in the US. It is a n
Page 114 and 115:
Curriculum Curriculum vitae vitae N
Page 116 and 117:
presentation at the 37 th Annual co
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First 11 pages of thesis. - OPUS - Universität Würzburg

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