Problems with Sentimental Art Research Paper Example | Topics and Well Written Essays - 1000 words

Problems with Sentimental Art - Research Paper Example Same way this world is also filled with beautiful things and ugly things. Artists often portray the beautiful side of this world. However, there are instances in which artists create various art forms which may provoke sentiments knowingly or unknowingly, rather than pleasant feelings. These sentiments may cause immense damages in the remaining life of the art viewer. In other words sentimental arts cause more damages to the art viewer than goods. This paper analyses the problems with sentimental arts. (Gatalo, p.21) â€Å"Sentimentality is an ambiguous concept and it is defined as an emotional disposition that idealizes its object for the sake of emotional gratification and that is inherently corrupt because it is grounded in epistemic and moral error† (Gatalo, p.22). The above picture, Roses for Stalin, portrayed by Boris Vladimirsky extracts so many sentiments in the minds of the viewer. The above art is not generating any sense of beauty in the minds of the viewer whereas it generates lot of sentiments. In other words, this art failed to fulfil its basic and moral responsibility of satisfying the viewer through its beauty. In other words, it gave more importance to sentiments rather than beauty. A person who watches this art may develop the unpleasant memories of Stalin era and subsequently his mental agony could be intensified. Roses for Stalin is anomalous, even among sentimental artworks, because the judgments it urges us to accept are so outrageous. Stalin’s identity as a historical figure so sharply contradicts how he is represented in the painting that it renders this depiction preposterous, if not offensive. This is such an obtrusive and distracting feature of the work that it cancels out the possibility of any serious aesthetic engagement with it. Most significantly this undermines the painting’s affective power—a savvy viewer cannot partake of the warm feelings it is meant to inspire. Insofar as this feeling is central t o the design and meaning of the work, this falsity amounts to its aesthetic failure. (Gatalo, p.26). Sentimental emotions are entirely different from standard emotions. While standard emotions always generate pleasant and unpleasant feelings, sentimental emotions always generate corrupted feelings. Sentimental emotions are corrupted because of its inability in judging things with the help of sound reasoning. In other words, sentiments are always motivated emotionally rather than factually. The picture, Roses for Stalin, forces the viewer to think about the positive sides of Stalin era and it completely avoids the memories about the negative sides of Stalin era. In other words, the above picture is a deliberate attempt to portray Stalin as a saint. In short, sentimental arts often glorify a person or scene. It may keep a blind eye towards the negative aspects of the person or the scene. It is an accepted fact that during Stalin era, Soviet Union faced severe problems. However, the ab ove picture may not remind the viewer about such things. Anxious Mother: A piece of sentimental art about a young girl putting her dolls to bed (Antique Photos - Sentimental and Fine Art) In the above sentimental picture, a young girl is portrayed as putting her dolls in bed. The above painting will definitely reminds us about our childhood. The emotion in the face of the girl portrayed in this picture is very sad. It reminds us the feeling of a lonely girl who tries to keep company with dolls. In other words, feeling of loneliness is the major

Is marriage still a goal worth for pursuing Research Paper

Is marriage still a goal worth for pursuing - Research Paper Example Based on the fact that there are certain factors that have rendered the marriage institution irrelevant today like people can have children out of marriage and that compassion can be gained out of wedlock, it does not dispute the importance of marriage. Thispaper will attempt to outline the fact that marriage is worth pursuing even on the 21st century. Marriage is considered to have begun when men were being formed. Various religious groups in the world believe that marriage was ordained by the Supreme Being who rules the universe as he formed man and woman. Marriage is also based on traditional believes where people believed that men were meant to be united with a woman in a relationship that could lead to child bearing and companionship. However, different cultures believe in different types of marriages such as monogamous marriage and polygamous marriage. Marriage in some cultures is considered a mandatory engagement where all members of such societies are required to get married at a certain part of their lives. However, the society today has changed the living style and this has led to change in doctrines and principles about marriage and its worth. Careers, independence of women, and other principles have led people to realize that marriage is not as important as they used to believe (Thornton 90). Marriage is believed to be a cohabitation where children are brought up to become responsible children. Though many people may argue that children can be gained and delivered out of wedlock, it has been proved that children required both parents to raise them to become responsible adults. The children grow up knowing and depending on their father and the wife respect the husband as the head of family. Parental roles and care is expected from both the parents unless where circumstances my lead to one parent as the caretaker of the children. According to an article about arguments on non-parental care by Gheaus (1), many people disagree about the benefit if

Causes of Cardiovascular Disease | Literature Review

Causes of Cardiovascular Disease | Literature Review 2 Abstract 3 Introduction 3.1 Cardiovascular Disease Cardiovascular disease (CVD) is the broad class of diseases that involves the heart or/and blood vessels. CVD includes atherosclerosis, heart valve disease, arrhythmia, heart failure, hypertension, endocarditis, diseases of the aorta, disorders of the peripheral vascular system, and congenital heart disease [1]. However, atherosclerosis accounts for the major part of CVD (up to xx%), and sometimes CVD is misleading used as a synonym for atherosclerosis [REF]. Because atherosclerosis is the underlying disease of several CVD, part of patients, where one diagnosis of CVD became manifest, may present with further co-morbidities, especially other diagnosis of CVD are common. However, the portion of patients with co-morbidities is depending on the baseline disease [2-4]. For example 40-60% of patients with Peripheral Arterial Disease (PAD) also have coronary artery disease (CAD) and cerebral artery disease, but only 10-30% of patients with CAD have also PAD (Figure 1) [2, 4]. Further, the severity of cardiovascular co-morbidities correlates well with each other[5-7]. CVD is today responsible for ca. 30% of all deaths worldwide [8], while heart disease and stroke are the leading causes of mortality and disability in developed countries [9]. Although the mortality rates of CVD has a considerable variation across countries (xx% in xx to xx% in xx) [10], a common trend of increasing rates has been observed worldwide. Before 1900, infectious diseases and malnutrition were the most common causes of death throughout the world, and CVD was responsible for The economic burden and the public health costs are mainly driven by CVD. In terms of combined morbidity and mortality, 148 million Disability-Adjusted Life-Years (DALYs) were lost worldwide (2002), which represents about 10% of all lost DALYs [REF]. In 2008, CVD costs about 192 billion Euros a year alone in the European Union, which results in a per capita cost of 391 Euros [13]. 3.1.1 Atherosclerosis Atherosclerosis is the most frequent and important pattern of Arteriosclerosis, other forms of Arteriosclerosis are Mà ¶nckeberg medial calcific sclerosis and Arteriolosclerosis, which vary in pathophysiological and clinical presentation [14]. As described above (3.1), atherosclerosis is the leading cause of death (up to 30%) in developed countries and represents the major portion of CVD. Atherosclerosis (literal origin from Greek: athero = â€Å"gruel or paste†; sclerosis = â€Å"hardness†) is defined as â€Å"thickening and loss of elasticity of arterial walls† and describes a process, where fatty substances, cholesterol, cellular waste products, calcium and fibrin building up in the inner lining of arteries [14]. These intimal lesions are called â€Å"atheromas†, â€Å"atheromatous† or â€Å"fibrofatty plaques†, which lead into an obstruction of vascular lumens and weakness the underlying media. Even within a given arterial bed, lesions or stenoses due to atherosclerosis tend to occur focally, typically in certain predisposed regions. 3.1.1.1 Pathogenesis of Atherosclerosis Due to overwhelming importance of atherosclerosis, enormous efforts have been spent to discover its cause over the last few decades. Today, the currently accepted concept, so called â€Å"the response to injury hypothesis†, considers atherosclerosis to be a chronic inflammatory response of the arterial wall initiated by injury to the endothelium [15]. Furthermore, lesion initiation and progression are sustained by interaction between lipoproteins, macrophages, T-lymphocytes, and the normal cellular constituents of the arterial wall. This process of developing atherosclerosis, which typically lasts over a period of many years usually many decades, can be divided into several consecutive steps, as illustrated in Figure 2 [REF]. Parallel, a morphological change is observed within the artery wall, where fatty streak represents the initial morphological lesion, even so the pathogenesis has started quite earlier with a chronic endothelial injury [REF]. Figure 2: Illustration of the Pathogenesis and Morphological Development of Atherosclerosis. SMC: Smooth muscle Cell; 6 ÃŽ ¼m thick histology slices of coronary arteries stained with Movats pentachrome. A: pathological intimal thickening with a â€Å"fatty streak†; B: pathological intimal thickening with a macrophage infiltration; C: early fibroatheroma with neoangiogenesis; D: fibroatheroma with thin fibrous cap and a healed rupture; E; late fibroatheroma with a sheet calcification. * demarks necrotic scores. Histology performed by CVPath Laboratory, Maryland, MD. The below described steps of the pathogenesis of atherosclerosis shouldnt been seen as a separated processes. They are interconnected and occur parallel. Further, several mechanism of vicious circles are described [REF]. However, the stratification into the flowing six steps helps to understand the complex pathogenesis and represents the current understanding: (1) Chronic Endothelia Injury As the earliest step in the pathogenesis of atherosclerosis, endothelial activation and chronic injury, also known as endothelial dysfunction, have been described [16]. The following factors contributed in different extent to endothelial dysfunction and are partly known as traditional risk factors for atherosclerosis [17]: advancing age, dyslipidemia, hypertension, increased levels angiotensin, insulin resistance and diabetes, smoking, estrogen deficiency. Several biochemical pathways have been described for those factors increasing the endothelial dysfunction. Other factors like hyperhomocysteinemia, possible infection and especially low or oscillatory shear stress are still discussed whether they significantly contribute to endothelial dysfunction [18-22]. The phenotypic features of endothelial dysfunction are described as the reduced vasodilator and increased vasoconstrictor capacity, an enhanced leukocyte adhesion, an increase of pro-thrombotic and decrease of fibrinolytic activi ty, and an increase in growth-promoting. (2) Accommodation and Oxidation of Lipoproteins In addition and due the endothelial dysfunction lipoproteins, especially low density lipoprotein (LDL), sequestered from plasma in the extracellular space of the arterial intima. Beside the extent of endothelial dysfunction, this process is depending on the concentration of LDL in the blood circulation [23]. Even so several mechanisms have been proposed for transport of LDL into the arterial intima including vesicular ferrying through endothelial cells, passive sieving through endothelial-cell pores, passage between cells, its not finally understand. However, strong evidence exist, that the accommodation of LDL in the arterial intima is not only a passive effect by a â€Å"leaking† vascular endothelium [REF]. Part of the lipoproteins that have entered the arterial wall stay there and are modified subsequently. Especially the modification of the lipoproteins has a trapping function for die selbigen [24]. The most common modification is the oxidation of lipoproteins, giving rise to hydroperoxides, lysophospholipids, oxysterols, and aldehydic breakdown products of fatty acids and phospholipids. But further modification like fusion of lipoproteins, proteolysis, lipolytic degradation and glycation are well known [25]. Such modified lipoproteins or particles of the modification process have inflammatory potential and trigger a local inflammatory response responsible for signaling subsequent steps in the atherogenesis. It includes a further increased endothelial dysfunction, which may cause a vicious circle of LDL accumulation, and activation of various cell types [24, 26, 27]. (3) Migration of Monocytes and Transformation into Macrophages/Foam Cells More important, the inflammatory response induces migration of leukocytes such as monocytes or lymphocytes into the lesion. Leukocytes are attracted by chemoattractant factors including modified lipoprotein particles themselves and chemoattractant cytokines depicted by the smaller spheres, such as the chemokine monocyte chemoattractant protein-1, interleukin 1 (IL-1) or tumor necrosis factor alpha (TNF-ÃŽ ±) produced by vascular wall cells in response to the inflammatory process [REF]. The activated arterial endothelial cells express a number of adhesion molecules and receptors on their surface, which participate in the recruitment of leukocytes from the blood to the nascent lesion [REF]. Macrophages are a key player in atherogenesis [27]. They develop from recruited monocytes, which migrated as described above into the lesion. In the mediator stimulated process of maturation, those macrophages become lipid-laden foam cells by uptake of lipoprotein particles through receptor-mediated endocytosis [REF]. The accumulation of lipid in the macrophages results in the apoptosis and necrosis, which lead first to a boosted expression and secretion of inflammatory cytokines and second to a release of their lipid excess into a necrotic lipid-core [REF]. Macrophages further produce enzymes, such as metalloproteinases, that degrade the extracellular matrix and lead to instability of plaques [REF]. (4) Adhesion of platelets and Release of SMC activating factors The inflammatory process, especially triggered by the necrosis of the foam cells, microscopic breaches in endothelial integrity may occur. Platelets adhere to such sites of limited endothelial denudation owing to exposure of the thrombogenic extracellular matrix of the underlying basement membrane and form microthrombi. Although most of the arterial mural microthrombi resolve without any clinical manifestation, they lead indirectly to lesion progression by pro-fibrotic stimulation [REF]. The platelets, activated by adhesion, release numerous factors that promote a fibrotic response, including platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), insulin-like growth factor 1 (IGF-1), and transforming growth factor alpha (TGF-ÃŽ ±) [28-30]. Thrombin itself generates fibrin that has a pro-fibrotic stimulus [28]. (5) Migration and Proliferation of SMCs The pro-fibrotic response includes first the migration of SMC from the media of the arterial wall, through the internal elastic membrane, and the accumulation within the expanding intima of the arterial wall. Second, stimulate the proliferation of SMC, which is responsible to form the bulk of the advanced lesion. Another part of the advanced lesions is an increased extracellular matrix. TGF-ÃŽ ± and other mediators stimulate the interstitial collagen production by SMC. These mediators may arise not only from neighboring endothelial cells or leukocytes (a paracrine pathway) but also from the same cell that responds to the factor (an autocrine pathway). Together, these alterations in smooth-muscle cells, signaled by these mediators acting at short distances, can accelerate transformation of the early lesion (fatty streak) into a more fibrous SMC and extracellular matrix-rich plaque. (6) Enhanced accumulation of lipids, collagen and proteoglycans The formation of a complex atherosclerotic lesion is characteristic by an extent remodeling process. Further foam cells within the expanding intimal lesion perish, while they phagocytose more and more lipids. The fibrotic cap between the so arisen lipid-rich necrotic core and the vascular lumen may vary in thickness and allows the classification of â€Å"thin cap fibroatheroma†, which correlates with a higher risk for acute luminal thrombosis [REF]. The production of extracellular matrix, as well plaque evolution and complication can be stimulated by diverse growth factors or cytokines like IL-1 or TNF-ÃŽ ±, and can be inhibited by other cytokines (e.g. interferon alpha (IFN-ÃŽ ±)) [REF]. As atherosclerotic plaques advance, they show intimal arterial calcification [REF]. The same proteins, which can be found in bone, are also localize in atherosclerotic lesions, e.g., osteocalcin, osteopontin, and bone morphogenetic proteins [31]. Both, passive and active models are discussed for the development calcification [32]. SMC can, promoted by several cytokines (e.g. transcription core binding factor ÃŽ ±1), acquire osteoblast-like characteristics and secrete bone matrix [33]. These examples illustrate how the pathogenesis of atherosclerosis involves a complex mix of mediators that in the balance determines the characteristics of particular lesions [REF]. 3.1.1.2 The Role of Inflammation The role of inflammation is central, while those inflammatory mechanisms mediate initiation, progression, and the complications of atherosclerotic lesions [26, 34]. Through the inflammatory process, arterial endothelial cells begin to express on their surface selective adhesion molecules that bind various classes of leukocytes, especially monocyte and T lymphocyte which are found in early human and experimental atheroma [REF]. After monocytes adhere to the endothelium, they can first migrate in the intima, largely stimulated by chemokines; and second transform into macrophages and avidly engulf lipoproteins, largely oxidized LDL [REF]. Although the phagocytosis of potentially harmful lipid particles by macrophages and subsequently the transformation into foam cells has an initially protective, this process involves further expression and secretion of inflammatory chemokines like Interleukin (IL)-1, Monocyte Chemotactic Protein (MCP)-1 or Tumor Necrosis Factor (TNF)-ÃŽ ±. Those enhanc e the inflammatory reaction and enable the further migration of leukocytes into the lesion [REF]. Macrophages also produce toxic oxygen species that cause additional oxidation of the LDL in the lesions, and they elaborate growth factors that may contribute to SMC proliferation [REF]. Similary, T lymphocytes (both CD4+ and CD8+) are also recruited to the intima by chemo-attractants. Cross-talk between macrophages and T cells induces a chronic inflammatory state regarding cellular and humoral immune activation characteristics. This state of a chronic inflammation leads also to the next observed steps in the development and progression of atherosclerosis. Thus, it stimulates the migration and proliferation of smooth muscle cells (SMC), as well the proliferation of vascular endothelial cells in the lesion. Through fibrogenic mediators, released from activated leukocytes and intrinsic arterial cells, the replication of SMCs is getting enhanced and contributes to elaboration by these cells of a dense extracellular matrix characteristic of the more advanced atherosclerotic lesion. 3.1.1.3 Vasa Vasorum and Neo-Angiogenesis The vasa vasorum of the aorta is as a plexus in the wall of artery of microvessels, which are functional endarteries [35, 36]. They either originate from major branches, originate from the main lumen of the aorta or drain in concomitant veins [37]. These vessels allow the humoral communication between intravascular lumen, vessel wall and adventitial layer of large arteries including oxygen and nutrients supply [REF]. Several studies demonstrated that hypoxia [38], cytokines (e.g. vascular endothelial growth factor) [39, 40], pro-angiogenic factors (e.g. hypertension or hypercholesterolemia) stimulate the growth of the vasa vasorum [41]. Those increased microvascular network may contribute to inflammation and lesion complications in several ways. First, the vasa vasorum provides an abundant surface area for leukocytes trafficking and may serve as the portal of entry and exit of white blood cells from the established atheroma. Microvessels in the plaques may also furnish foci for intraplaque hemorrhage. Like the neovessels in the diabetic retina, microvessels in the atheroma may be friable and prone to rupture and can produce focal hemorrhage. Such a vascular leak leads to thrombosis in situ and thrombin generation from prothrombin. In addition to its role in blood coagulation, thrombin can modulate many aspects of vascular cell function, as described above. Atherosclerotic plaques often contain fibrin and hemosiderin, an indication that episodes of intraplaque hemorrhage contribute to plaque complications. Multiple and often competing signals regulate these various cellular events. Increasingly, we appreciate links between atherogenic risk factors, inflammation, and the altered behavior of intrinsic vascular wall cells and infiltrating leukocytes that underlie the complex pathogenesis of these lesions. The present data indicate that vasa vasorum neoangiogenesis and atherosclerosis are seemingly inseparably linked, triggered and perpetuated by inflammatory reactions within the vascular wall. 3.1.1.4 Risk Factors for Development of Atherosclerosis Local shear stress In the coronary circulation, for example, the proximal left anterior descending coronary artery exhibits a particular predilection for developing atherosclerotic disease. Likewise, atherosclerosis preferentially affects the proximal portions of the renal arteries and, in the extracranial circulation to the brain, the carotid bifurcation. Indeed, atherosclerotic lesions often form at branching points of arteries, regions of disturbed blood flow. Age, Gender, HTN, HLP, DM, Smoking, Race/Ethnicity, 3.1.1.5 Atherosclerosis of the Aorta In the characteristic distribution of atherosclerotic plaques in humans the abdominal aorta (Fig. 11-8) is usually much more involved than the thoracic aorta, and lesions tend to be much more prominent around the origins (ostia) of major branches. In descending order (after the lower abdominal aorta), the most heavily involved vessels are the coronary arteries, the popliteal arteries, the internal carotid arteries, and the vessels of the circle of Willis. Vessels of the upper extremities are usually spared, as are the mesenteric and renal arteries, except at their ostia. Nevertheless, in an individual case, the severity of atherosclerosis in one artery does not predict the severity in another. In an individual, and indeed within a particular artery, lesions at various stages often coexist. 2009_Dijk_The natural history of aortic atherosclerosis_A systematic histopathological evaluation of the peri-renal region.pdf 3.1.2 Peripheral Arterial Disease Peripheral Arterial Disease (PAD) is caused by atherosclerosis and represents the most common cause of lower extremity ischemic syndromes in developed countries [42]. Symptoms of PAD are variable including pain, ache, hair loss, thickened nails, smooth and shiny skin, reduced skin temperature, cramp, muscle atrophy, or a sense of fatigue in the muscles. Because of the variability of symptoms, the diagnosis of PDA is frequently missed [43]. In addition, the major part of patients with PAD is asymptomatic [REF]. Beside these diagnostic challenges, PAD affects a large and increasing numbers of patients worldwide. Round 30 million people are diseased in worldwide, but of those only 10 million patients are presenting with symptoms [44]. Further, the prevalence is increasing with age [6, 45], while the prevalence is 10% at the age of 60 years [46]. Association to mortality!!! 3.1.2.1 Pathogenesis of Peripheral Artery Disease The leading cause of PAD is atherosclerosis, especially in older patients (>40 years) and at the lower extremities [42]. Other, but rare causes of PAD include embolism, vasculitis, fibromuscular dysplasia, entrapment, and trauma. Atherosclerotic lesions, which are segmental and cause stenosis, are usually localized to large and medium-sized vessels. The pathology of these lesions is based on atherosclerotic plaques development, as described above (xxx). The primary sites of involvement are the abdominal aorta and iliac arteries (30% of symptomatic patients), the femoral and popliteal arteries (80-90%), and the more distal arteries (40-50%) [REF]. Atherosclerotic lesions have been predominantly observed at arterial branch points. These may be explained by altered shear stress [REF]. However, the involvement of the distal and smaller arteries is more common in elderly individuals and patients with diabetes mellitus [REF]. 3.1.2.2 Risk Factors for Peripheral Arterial Disease While atherosclerosis is the major underlying condition of PAD, the risk factors for PAD are essentially the same as those for other form of atherosclerosis (like e.g. CAD), see Table 1 [47-50]. However, the risk factors smoking and diabetes may have even greater effect for PAD as compared for CAD [51]. Risk Factors Increased risk for PAD Hypercholesterolemia 1- to 2-fold (low) Homocysteinemia 1- to 3-fold (moderate) Hypertension 1- to 3-fold (moderate) Smoking (current and past) 2- to 4-fold (high) Diabetes mellitus 2- to 4-fold (high) Table 1: Risk Factors for Peripheral Arterial Disease 3.1.2.3 Clinical Presentation of Peripheral Artery Disease PAD affects more often the lower extremities (xx times more often than upper extremities) [REF]. The most common symptom of PAD is intermittent claudication, which is defined as presence of pain, ache, cramp, numbness, or a sense of fatigue in the muscles. Those symptoms occur during exercise and are relieved by rest, as result of the increased muscle ischemia during exercise caused by obstruction to arterial flow. Patients with PAD in the lower extremities resulting in ischemia may range in presentation from no symptoms to limb-threatening gangrene. Two major classifications based on the clinical presentations are established, the Fontaine and the Rutherford classification. While the more simple Fontaine classification consists of four stages (Table 2) [52], the Rutherford classification has four grades (0-III) and seven categories (0-6). Asymptomatic patients are classified into Rutherford category 0. Any patient with claudicants are stratified into Rutherford grade I and divided into three categories based on the severity of the symptoms. If patients have pain at rest, they belong to Rutherford grade II and category 4. Any patient with tissue loss are classified into Rutherford grade III and categories 5 and 6, based on the significance of the tissue loss [4]. These two clinical classifications can be translated into each other according to Table 2. Fontaine Classification Rutherford Classification Stage Clinical Grade Category Clinical I Asymptomatic 0 0 Asymptomatic IIa Mild claudication I 1 Mild claudication IIb Moderate to severe claudication I 2 Moderate claudication I 3 Severe claudication III Ischemic rest pain II 4 Ischemic rest pain IV Ulceration or gangrene III 5 Minor tissue loss III 6 Major tissue loss Table 2: Classification of Peripheral Arterial Disease based on the Fontaine Classification in Comparison the Rutherford Classification In the Framingham Offspring Study, the prevalence of PAD was determined in 1554 males and 1759 females from 1995 to 1998.55 The mean age was 59 years. PAD, defined as an ankle-brachial (blood pressure) index (ABI) of ABI Severity of PAD The physician also queried the participant about symptoms of intermittent claudication using a standardized questionnaire [53]. 3.2 Local Adipose Tissue Depots 3.2.1 Variability of Adipose Tissue 3.2.1.1 Anatomy and Morphology SACK: Epicardial, mesenteric, and omental fat all share the same origin from the splanchnopleuric mesoderm associated with the gut.11 Pericardial fat (pericardial adipose tissue [PAT]) is defined as epicardial fat in all these possible locations plus paracardial fat.14 Paracardial fat is situated on the external surface of the parietal pericardium within the mediastinum and has alternatively been termed mediastinal fat.15 Paracardial fat originates from the primitive thoracic mesenchyme, which splits to form the parietal (fibrous) pericardium and the outer thoracic wall.16 Epicardial adipose tissue is supplied by branches of the coronary arteries, whereas paracardial fat is supplied from different sources including the pericardiacophrenic artery, a branch of the internal mammary.17 Lipolysis and lipogenesis have not been measured directly in human epicardial fat. Based on approximately 2-fold higher rates of lipolysis and lipogenesis in guineapig epicardial fat than other fat depots, Marchington et al18,19 proposed that EAT serves to capture and store intravascular free fatty acid (FFA) to protect cardiomyocytes from exposure to excessive coronary arterial FFA concentrations during increased energy intake and, at other times, to release FFA as an immediate ATP source for the myocardium during periods of need. Epicardial fat and the myocardium are contiguous. Islands of mature adipocytes are more frequ ent within the subepicardial myocardium of the RV than the LV13 and may act as more readily available, direct sources of FFA for cardiomyocytes. The thickness of the wall of the right atrium is about 2 mm; the left atrium, 3 to 5 mm; the RV, 3 to 5 mm; and the LV, 13 to 15 mm.20 Possibly, FFAs could diffusebidirectionally in interstitial fluid across concentration gradients from epicardial fat into the atrial and RV walls where EAT predominates and vice versa, but this process in the LV wall can be questioned because the diffusion distance is much longer. Peri-vascular adipose tissue is defined as any adipocytes, which are located close to the vascular wall and has the possibility to secret their biomarkers into the vasa vasora of the wall (see 3.2.1.2). 3.2.1.2 Secretion of Biomarkers by Adipose Tissue Adipose tissue is known to have more functions than lipid storing. Adipose tissue secrets biomarkers and serves as an endocrine organ. Beside hormones, it secrets also different inflammatory cytokines and chemokines. The amount of adipose tissue were associated to xxx, xxx, xxx (FRAMINGHAM?!). Especially peri-vascular adipose tissue like epicardial or visceral adipose tissue demonstrated higher expression of inflammatory biomarkers compared to other adipose tissue depots in the body [REF]. Beside the systemic effect of the secreted cytokines and chemokines, also a local effect/paracrine is hypothesied. Biomarkers secreted of peri-vascular adipose tissue reach over the vasa vasora of the major arteries their adventitia, media, and intima. Therefore it might be involved in the inflammatory process of atherosclerotic plaque. Further, a local effect can be thought by direct diffusion. 3.2.2 Association of Adipose Tissue to Cardiovascular Disease 3.2.2.1 Atherosclerosis 3.2.2.2 Peripheral Arterial Disease 3.2.3 In-Vivo Assessmentof Adipose Tissue 3.2.3.1 Traditional Measures * BMI and WC [54] 3.2.3.2 Imaging-based Assessment * dual energy X-ray absorptiometry (DXA) [55] * magnetic resonance imaging (MRI) [56, 57] * ultrasound [58] * multi-detector computed tomography (MDCT) [59, 60] 3.3 Framingham Heart Study 3.3.1 Historical Origin of the Framingham Heart Study Infectious diseases were prior to World War II the major burden for public health. But through a greater microbiological knowledge and improved sanitation, the morbidity and mortality of infectious disease decreased continuously. When penicillin was introduced in 1942, a dramatic reduction was made in the prevalence and incidence of infectious diseases, especially by controlling tuberculosis and pneumococcal pneumonia [REF]. Replacing infectious diseases, public health was challenged by a mounting epidemic of CVD starting in the 1940s. With World War II over the alarming rise of CVD became increasingly evident. In the United States, 30% of all men developed CVD before reaching the age sixty. The prevalence of CVD was twice of cancer by 1950 and had become the leading cause of death [REF]. Even so the available statistic data from around the world was often crude and inaccurate, it clearly demonstrated a worldwide atherosclerotic CVD problem. Furthermore there was no known treatment to prolong life and to reduce mortality. Added to these distresses was the fact that little was known about etiology, pathogenesis and epidemiology of CVD. The big gap between the enormous public health burden of CVD on the one site and the little understanding of this disease on the other site increased drastically the need for action. At this time, some believed a primary preventative approach was more promising than a search for cures [Dawber, Thomas R. (1980), The Framingham Study: The Epidemiology of Atherosclerotic Disease, Cambridge, Mass.: Harvard University Press.], while the secrets of the etiology of CVD and subsequently for treatment were not being uncovered by basic laboratory and clinical research. Some of these prevention-minded individuals occupied positions of influence and were able to translate their beliefs into actions. The key was to develop a preventive approach, where first of all the characteristics of the host and environment, which lead to the early appearance of the disease, had to be determined. In particular, preventable or modifiable predisposing factors had to be identified. If a practical preventive approach was developed, the hope was that doctors and public health officials would adopt it and so have a widespread impact on the reduction of CVD-based morbidity and mortality. Accordingly to the preventive approach, the Framingham Heart Study was designed given the charge to identify these modifiable characteristics of host and environment for CVD. 3.3.2 Initiation of the Framingham Heart Study By the mid 1940s several striking studies were conducted with an examples epidemiological approach in the fields of nutritional imbalance, metabolic disorders, occupational hazards, accidents, cancer and rheumatic fever under principle investigators (PI) Drs. Dawber, Meadors and Moore [REF, Dawber, Meadors and Moore 1951]. In common, an association between the circumstances and the disease could be identified with-out knowledge of the precise etiology. One of those studies was performed by Dr. John Snow in 1936. He demonstrated that cut-ting off the water supply from contaminated wells, despite incomplete knowledge of the pathogenesis of the disease, stopped cholera. He observed on the one hand the source of the water supply and on the other hand the time and place where the disease occurred. He sufficiently pinpointed based on his observations the major environmental factor for cholera. Further investi

Emerson and Thoreau as Prophets of Eco-wisdom :: Biography Biographies Essays

Emerson and Thoreau as Prophets of Eco-wisdom  Ã‚  Ã‚   The major premise of transcendental eco-wisdom is that connection with nature is essential for a person's intellectual, aesthetic, and moral health and growth. One must see and experience nature intimately, whether defined as the "not-me" or as landscape, to participate in the unity of Spirit underlying its visible processes. This connectedness is the basis of the self-reliance which determines how a person lives with integrity in nature and society. Granted, the concept of self-reliance apparently devalues social concerns, including the global commitment and cooperation needed to bring about the kinds of changes that would reverse the climatic greenhouse effect, for example. Indeed, Emerson's ideas have been unfairly appropriated to justify the capitalistic exploitative excesses and insensitivity to social problems and long-term consequences that lie at the root of many of our environmental problems. However, we cannot fault Emerson and Thoreau for not imagining our current dependen ce on technology, the complexity of a largely urban economy or the ties of a global community. Yet even the notion of a self-contained Concord or Walden Pond, which might seem naive and outdated, is reflected in current ideas about eco- regionalism. By accounting for what they could not have known of our present condition, we can still find fruitful ways of understanding where humans, singly and as a species, should fit into nature. Emerson's greatest gift was lessons in seeing in and through nature and extracting symbolic meaning, yet his own intimate encounters with the nature around him were relatively rare and indirect, with few concrete traces in his writings except as occasional metaphors. He wanted his revelations from nature to be abstract and come by surprise, as did the famed mystical encounter at the beginning of his book Nature: "Crossing a bare common, in snow puddles, at twilight, under a clouded sky, without having in my thoughts any occurrence of special good fortune, I have enjoyed a perfect exhilaration. I am glad to the brink of fear." In such an experience, even the self is absorbed by a greater power: "I become a transparent eye-ball; I am nothing; I see all; the currents of the Universal Being circulate through me." The metaphor may be unfortunate, but not his faith that a single person could perceive unspeakable meanings through experiencing nature, even if only indirectly. Such possibilit ies impelled Thoreau and countless others since to mine the details and processes of nature that Emerson had generalized, looking for embedded revelations and sharing in nature's "ecstasy.

Paleolithic, Neolithic, and Mesolithic Art Essay

The earth and the sky factor into Paleolithic, Neolithic, and Mesolithic art and monuments. Paleolithic means Old Stone Age and the art was mainly consisted of paintings in their caves and Venus figurines. Neolithic means New Stone Age and the art was consisted of the Stonehenge, figures, and pottery. Mesolithic means Middle Stone Age and the art consisted of some pottery, hand tools, and some figurines. In the Old Stone Age, (Paleolithic) their art was consisted of mainly paintings on cave walls. People painted animals because that was what they would see in the dark due to the prolonged time of being in darkness in the caves. They didn’t see much sunlight. As time went on, mathematical aspects started to rise from observational astronomy. Some cave paintings became known as an understanding of the path the moon takes around the sun. This is known as the ecliptic. The ecliptic lead to the discovery of the zodiac. Stars, moons, and planets in the Paleolithic culture are not the stars, moons and planets of modern time that we know. They are those whose habitat is the Milky Way and the celestial sphere now. Many of these paintings reflected images that were seen in the night sky. Such as the Bison that were painted in cave walls which is known as the Taurus in the zodiac sign today. The significance of their art was the astronomy and mathematical connections they made and how it created what we now know as the zodiac. The New Stone Age began to connect with the earth and the sun more by the use of famous monuments. In the New Stone Age (Neolithic) the people built villages that were built for family, life, and worship. They worshipped many gods, but their beliefs were strongly based on nature. They also built many walls that were used as a defense. The monuments they built was their main form art that had connection s to the earth and the sun. They created a giant stone monument that was known as Stonehenge. It was made out of earth, timber, and stones. By viewing this monument, it was observed that the Neolithic people had knowledge in architecture, mathematics, and astrology. The Stonehenge was created as an astrological observatory. It is known for this because of the rising and setting of the sun on the summer and winter solstice that can be seen through the monument. It was also considered to possibly have been used as an astronomical calendar. The significance of this monument is how these people had the mathematical and astronomy knowledge to build this in a way to be able to witness amazing views in the sky that come every year. The Middle Stone (Mesolithic) art consisted of mostly pottery and hand tools. During the Middle Stone age, the Mesolithic people made many hand tools because they began to gain more knowledge to be able to farm and capture animals more effectively. They created carved-engraved bone plates. These engraved or painted plates of stones were marked with dots. These dots were considered to be accurate lunar observations. The interpretation of the markings on many artefacts were considered to be marks that correlate with lunar or s olar motion. This showed that the Mesolithic people had some astronomical skills. The significance of these findings show that over time people were gaining skills on astronomy and were creating their observations through the use of art. Over time art has changed dramatically. It started off as just paintings on cave walls and lead to massive monuments that are still standing today. There is significance behind all of the art since the Stone Age times. These people from the stone ages used art to express their knowledge in mathematics and astronomy. They used it to better understand the earth, the sky, the sun, and the stars. They not knowingly created what is today the zodiac and proved they didn’t need any technology to create an astrological observatory.

Holden in “Catcher in the rye ” by J.R Salinger Essay

Holden is a complex person with many conflicting characteristics. He has many ambitions and desires for his life but he is faced with the basic conflict in the story, corruption. This corruption is what drives him and at the same time restricts him Holden’s being surrounded by corruption disgusts him. There are a few main instances in which Holden encounters corruption directly. One type is Stradlater, the ‘secret slob’or Ernie, who ‘performs for the people’. Two that affect Holden very much is his brother D.B. ‘selling out’ to the movies and Pheobe eventually having to grow up. This corruption is very evident in Holden’s life and situation. Corruption is what Holden wants to avoid but can not because he wants to grow up and act like an adult. Drinking, ordering the prostitute, and using money are all things that grownups do but Holden yet still wants to remain innocent. Theses are few of the obvious ironies of Holden’s pers onality. Holden’s utter hate for the fact that we have to grow up and how he ties adulthood with corruption just shows how he has a large problem determining illusion from reality. He doesn’t understand that to grow does not mean to become corrupt but to become wiser through experience. These experiences are what frighten Holden because this boy of sixteen has already been involved in many of the pleasures and problems that come from these experiences. Holden’s ‘catcher in the rye’ analogy shows how he wants to save the children from this corruption but he never will. Holden wants to be the great savior of a helpless cause and does not realize he has fallen into the evil hands of corruption. Holden idolizes Allie is little brother who died. The reason for this idolization is that Allie will never become corrupt. He will always be in Holden’s mind a little boy not affected by the dirty hands of society. Pheobe, on the other hand, will have to enter the world sooner or later and then she too will become corrupt. D.B., though, has already submitted to that corruption by ‘selling out’ to the movies. Holden realizes that D.B. has given his story to the movie business and does not like it because he wanted his brother to continue wr iting the little stories he loved so much. Pheobe, diametrically, has not yet been absorbed by society but is on her way and Holden nor anyone else can stop her. Holden finds corruption in almost everything he sees but does not yet even realize that he too is part of that corrupt world the minute he stopped being a child and wanting to be an adult. By doing many of the things he does he displays a desire to grow up, to act mature, to ultimately blend in with society but he is restricted by his ideals of innocence. The way he orders his drinks, dances with the two ladies in the hotel, and sends his money frivolously shows how Holden has accepted the reality of being an adult but can not come to terms with the fact that all children will also enter Holden’s corrupt society. Holden’s basic description of a corrupt person is a phoney. This characterization is often harsh and unjust to many of the people he attributes this characteristic to. But there are people that Holden does like other than Pheobe and Allie. James Castle, Jane Gallager, the two nuns he spoke to in the coffee shop, and the little child on the curb of the road are a few. James Castle is someone that Holden could possible identify with. He dies because of a refusal to take something back; something that was true. In respect to Jane Gallager Holden could possible be in love with her but does not ask her in fear of her saying ‘no’ but if she says ‘yes’ he would not be able to come through a attribute of adulthood Holden has yet to acquire. Holden has yet to acquire many different aspects of adulthood. This is what keeps his personality in a state of ambiguity. No one knows whether Holden wants to become an adult or stay a child. In my opinion, he wants to continue his life as an adult but a child at heart and mind. By doing this he destroys many incorrupt things that he has yet to experience. Holden’s whole life revolves around the battle of corruption and innocence. This battle, through Holden’s eyes, is one of adulthood verses childhood. this battle is an impossible one an until Holden realizes this he will never leave his land of illusion and adjust to the world.