Book Review Ghosts from the Nursery

Book Review Ghosts from the Nursery Ghosts from the Nursery: Tracing the Roots of Violence written by Robin Karr-Morse and Meredith S. Wiley offers the reader an in-depth look at child abuse and neglect. Karr-Morse and Wiley (1997) discuss the effects of abuse and neglect, looking specifically at violence in children. The book follows a young man, 19 year old Jeffery, who is on death row for committing a murder when he was 16 years old. Jeffery serves as a beautiful case study for the authors and readers to analyze and apply theories to. By looking at Jeffery and other children who kill, Karr-Morse and Wiley(1997) begin to discover the truths about the delicate and important years of infancy and early childhood. The authors look at child development and behavior particularly from conception to age two. With development and behavior in mind, they investigate the effects that abuse and neglect have on childrens trust, empathy, conscience, and learning during these pivotal years. Throughout the journey of this book, the reader learns a plethora of interesting facts about human development and how it is influenced by abuse and neglect. Throughout the chapters the readers are also given an opportunity to see the implications of such behavior with real life cases and studies. By taking the time to read Ghosts from the Nursery, one will not only have a better understanding of infancy and early child development but also understand why negative experiences affect children as they do and what it means for society as a whole. Upon the completion of this text the reader will have an appreciation for quality parenting and know the devastating effects abuse and neglect have on children and its influence in creating violent children. Critique This text offers knowledgeable contributions to the readers understanding of infancy and early childhood abuse and neglect. Karr-Morse and Wiley (1997) do an excellent job of explaining why the interaction of biological variables with environment variables results in pro-social or antisocial outcomes (81). Examples of this interaction are presented in every chapter with different situations and scenarios. The reader will quickly deduct that this is the most important connection to make and that children reflect what they have absorbed biologically and socially (Karr-Morse Wiley, 1997, 183). The text does a great job assessing a number of issues related to child abuse and neglect including but not limited to early brain anatomy and development, exposure to drugs in the womb, the interaction of parenting and temperament, and the impact of early trauma, head injuries, and emotional deprivation. Each chapter within this text takes a profound look at these issues and how they relate back to childhood violence. Along with providing new and essential knowledge, each chapter is opened by reconnecting with the case study of Jeffery and providing the reader with a personal account of the implications of the issues being discussed. By reading each section carefully and deliberately the reader begins to understand all the variables involved in producing a violent child and the impact these variables have on the way the child processes information, or does not process information as it may be. Along with presenting valuable information to the reader and deepening the readers understanding of the child abuse and neglect, the text does have its downfalls. While reading, one will observe that ideas are repeated too often causing the reader to begin skimming the material. The authors have a tendency to be repetitious in their writing to a point that it hurts the overall affect of the book. Karr-Morse and Wiley also like to provide in depth explanations which detract from the main point they are trying to convey by shifting the focus to a minute fact, thus losing their readers attention. Along with in depth explanations, Karr-Morse and Wiley have a tendency to include too many supporting facts. Though interesting, the facts tend to distract the reader from the main arguments the authors are attempting to make. With these three issues in mind, the overall book is difficult to get through and a relatively slow read. With shorter, more to the point chapters, the authors may have b een able to retain their readers attention for longer amount of time. These improvements would also place more emphasis on the purpose of each chapter and how it influences the making of a violent child, rather than emphasizing the supporting facts. Overall, this text is very educational and a valued contribution to any mandated reporters collection of knowledge. It is suggested however, that Ghosts from the Nursery be read like a textbook and not like a book one would read before bed. With the knowledge of the writing style the authors express themselves in, one can successfully navigate their way through this book and come out the other side with considerably more knowledge in the field of child abuse and neglect. Implications There are numerous implications for anyone, particularly a teacher, after reading Ghosts from the Nursery by Robin Karr-Morse and Meredith Wiley. First and foremost, one must begin to understand the pervasive effects of child abuse and neglect and how important those first two years of life are on development. Abuse and neglect have many faces, some of which are well hidden from the publics eye. As a teacher, especially in preschool, it is imperative to be sensitive to these issues and the repercussions if not detected and treated. As an elementary or preschool teacher, one will be able to assess a childs basic physical, social, emotional and intellectual development in comparison to the childs peers and determine whether the child is on track or not. It is during the preschool years and prior that developmental delays as a result of abuse or neglect will begin to show up in the child. This information may contribute to the teachers inclination that abuse is or is not occurring. It is essential to know that abuse and/or neglect from the time the child is inside the mothers womb to present day can display itself throughout various times in the childs development, and in any one of the developmental domains. This text specifically assists the reader in their quest to better identify and understand the less obvious forms of abuse and neglect and comprehend what it means particularly for a childs social/emotional development. Looking more closely at the disruptive behavior disorders chapter in the text is also beneficial to an individual entering the education field. Children who have such disorders will become obvious during the early school years as they are overwhelming our preschools and child care centers. With children who have disruptive behavior disorders their parents often feel exhausted and angry, their feelings of affection stretched thin or greatly compromised (Karr-Morse Wiley, 1997, 104), placing the child at a higher risk for being abused or neglected and later developing oppositional defiant disorder or conduct disorder. Some of these children may be experiencing abuse at home, or come to school out of chaotic and neglectful circumstances that leave them physically and emotionally malnourished (Karr-Morse Wiley, 1997, 105). For a teacher, seeing a child who has a disruptive behavior disorder may be a warning flag to keep an eye on the child and family and offer them additional resources to ease any additional stress they may be experiencing. Consequently, from reading this text, one will have a thorough understanding of how child abuse and neglect affects a childs development and what that will look like in the childs behavior. For anyone entering the education field whether it be in the public school district or in a childcare center, those individuals will find themselves mandatory reporters of child abuse and neglect. By reading this text, and having a solid foundation of what abuse and neglect look like, one will have the knowledge to better be able to advocate for a childs needs when necessary.

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

Psychedelic Music, Its Origins, and Its Effects on Music Today Essay

Psychedelic Music, Its Origins and Its Effects on Music Today Psychedelia in music has been around for a long time and has changed much of the popular music of today. The dictionary definition of psychedelic is, â€Å"of or noting a mental state characterized by a profound sense of intensified sensory perception, sometimes accompanied by severe perceptual distortion and hallucinations and by extreme feelings of either euphoria or despair.† It started in the 1960’s with the discovery of LSD and use of other psychedelic drugs. Psychedelia did not only affect music, it affected people, cities, and the way people think. LSD, which was the catalyst for psychedelic music, was discovered on April 16, 1943, by Albert Hofmann. For months he had been studying ergot, a fungus that grows on rye, and synthesizing lysergic acid for possible use to help migraines. On his twenty-fifth try, he made LSD-25, and after his work he began to feel dizzy. He assumed he had the flu, so he went home. â€Å"I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with intense kaleidoscopic play of colors,† Hofmann wrote in his biography LSD, My Problem Child. â€Å"After some two hours, this condition faded away.† He then knew that it was not the flu that made him dizzy, so he tried LSD again and got the same results. After this, he and his staff began to use LSD on themselves and soon LSD was used in psychotherapy. Now that LSD was created, psychedelic music would soon follow (DeRogatis 2-4). The birth date of psychedelic rock music, as far as it can be known, was in 1966. Many bands started making songs with psychedelic references. In May of 1966, the Beach Boys released Pet Sounds, which was inspired by their experimentation... ... constantly-changing names, but ravers do not care. Ravers do not focus on the performing artist like at rock concerts, they just listen to the beat of the music, and dance (DeRogatis 431-439). Psychedelic music has expanded people’s minds since the 1960’s. It has given people a way to express themselves, and it has helped people to relate to each other. Psychedelic music revolutionized the way music is recorded, played, and listened to. Without psychedelic music, modern music would not be the same. Works Cited â€Å"Jimi Hendrix Biography.† Biography. 2006. 6 May 2007 search/article.do?id=9334756>. DeRogatis, Jim. Turn On Your Mind. Milwaukee: Hal Leonard Corporation, 1996. Scaruffi, Piero. â€Å"The History of Rock Music: 1966-1969.† History of Rock Music. 2002. 6 May 2007

The Madonnas of Echo Park by Brando Skyhorse :: Immigration, Immigrants

â€Å"Remember, remember always, that all of us, and you and I especially, are descended from immigrants and revolutionists.† -- President Franklin D. Roosevelt Throughout the course of my life, I have always encountered individuals wanting to better their economic situation especially those within my community. Those who come from impoverished communities in other countries risk their lives and lifetime savings to come to the United States hoping that one day they will regain everything that they lost. Their only motivation to come to this country is to be able to provide their family with basic necessities and in order to do this, they must work two or more jobs that pay at minimum wage and are taken for granted. However, many individuals do not see this side of the story and categorize immigrants as unambitious people. In order to be completely aware of what immigrants truly go through and how they succeed in life, one must be willing to place themselves in their shoes and hear his/her story. We must acknowledge that the hands of these people work in back breaking jobs in order to sustain their families. While some Americans may be agains t immigrants arriving to the United States in search of a better life and the American Dream, in The Madonnas of Echo Park, Brando Skyhorse further reveals that immigrants are exploited as cheap labor, and although they contribute greatly to the everyday function of American industry, they are quite invisible. Mexican immigrants in the United States are willing to work hard and long hours throughout the day regardless of the amount of sleep or rest they may get. Conversely, this is not how Efren Mendoza, a public city bus driver, views Mexicans and he believes they are not motivated to achieve things in life. One would assume that he would understand how difficult it is for immigrants to assimilate in a new foreign country without knowing anyone or anything here, but he is not on their side and it is somewhat hypocritical of him because he himself is Mexican. It is as though Efren sees his own people as invisible individuals because he does not acknowledge all their hard work and sacrifices they may have gone through in order to arrive in the United States. He further proves his insincerity when he mentions that the â€Å"new wetbacks [are] picky about what jobs they’ll do [and that they] half-ass [the] work† that they are given to do (77).

Death of a Salesman Essay -- essays papers

Death of a Salesman In the play Death of a Salesman by Arthur Miller, Willy is both sympathized with and looked down upon throughout the story. Willy is a very complex character with problems and faults that gain both sympathy and also turn the reader off to him. Willy Loman is both the protagonist and the antagonist, gaining sympathy from the reader only to lose it moments later. The play begins with Willy as the antagonist, fighting with his wife Linda and a generally mean person. He insults his sons and scolds Linda for buying the wrong cheese. Willy shows his biggest personality flaws early on in the story; contradicting his own thoughts, being verbally abusive, and showing his over developed sense of pride. Willy loses the readers sympathy again in a flashback early on in the play when he goes off on a rant about the money he owes for things, almost blaming Linda for their hardship. During a conversation with Happy, Willy again loses his temper and yells at Happy for trying to be nice and saying "Pop, I told you I'm gonna retire you for life"(I,1300). As that is going on the next door neighbor, Charley, comes over because of the noise and strikes up a conversation with Willy. The two are playing cards and shooting the breeze when Willy once again starts with the insults, calling Charley ignorant, and telling him hes disgusting, as if to boost his own con fidence or make himself seem smarter or better than Charley. Soon after his arguement with Charley, Willy is in a flashback ordering Happy and Biif to steal lumber from a nearby building project, teaching his boys to steal to impress his brother Ben. Willy and Biff then get into an arguement over Biff's lack of effort in getting a job and keeping it, and about ... ...is off in his own little world almost ignoring Biff. The reader sympathizes with Willy due to his clouded mind, yet is turned away by his arrogance and showmanship attitude. In the begining of the story Willy is scolding his wife and bad mouthing his sons one moment, then the next hes saying how great his children are and telling his wife how much he loves her. Willy sends the audience on a roller coaster throughout the entire play, gaining sympathy and pity one minute, while the next turning the reader's sympathy and pity elsewhere. Willy Loman is both the protagonist and the antagonist, gaining sympathy from the reader only to lose it moments later. He is his own worst enemy, causing his life to be much harder than it needs to be. If only Willy had realized his faults and accepted life as it is, perhaps the reader would have been his sympathizer the entire play.

Coffee from Ampalaya Seeds

COFFEE FROM AMPALAYA SEEDS (Momordica Charantia) TABLE OF CONTENTS A. Background Of The Study3 B. Statement Of The Problem And Objectives Of The Study4 C. Significance Of The Study6 D. Scope And Limitations6 E. Operational Definition Of Terms7 Chapter II8 Review Of Related Literature8 Chapter III11 Methodology11 A. Research Design11 B. Type Of Study12 C. Independent And Dependent Variable12 D. Treatments Of The Study13 E. Subjects / Samples13 F. Replications Per Treatment14 G. Methodology Proper14 H. Statistical Treatment For Data Analysis17 Chapter IV18Results And Discussions18 Chapter V30 Summary, Conclusion And Recommendations30 Appendix32 Appendix A32 Appendix B34 BIBLIOGRAPHY36 References36 CHAPTER I Introduction A. Background Of The Study Coffee alternatives have been famous since the last two decades due to economic crisis and experimentations for health and medical benefits. Any seeds that are edible when powdered can be used as an alternative source for coffee. The differenc e of the generic coffee from the seeds of the coffee plant from those of the alternatives is that it has a good amount of caffeine content.The similarity you can find in the alternatives and those of the original is that seeds contain carbohydrates which cause the aroma in roasted coffee [4, 5, and 6]. Ampalaya, on the other hand, is a crawling vine that grows mostly on tropical countries like the Philippines. It is said to be rich in iron, potassium, beta-carotene and other nutrients. It is also famous in treating diabetes because of its properties like polypeptide-P; a plant insulin that can lower blood sugar levels.Many researches on agricultural food chemistry convey that it provides nutritionally significant amounts of nutrients, minerals and amino acids that are needed for life [1, 2, and 3]. Ampalaya seeds when used as an alternative coffee will act as a stimulant, an herbal drink and at the same time can increase its additional properties like source for insulin and other nu trients found on Momordica charantia. Ampalaya seeds when used as dry powders have clearly demonstrated hypoglycemic activity [3].The researchers decided to process Ampalaya seeds the same routine on how the coffee bean is processed into a drinking beverage and test its sensory qualities using sampling techniques. B. Statement Of The Problem And Objectives Of The Study Main Problem * Can Ampalaya Seeds (Momordica charantia) be made into coffee? Sub-Problems * Does the coffee out of Ampalaya (Momordica Charantia) Seeds have a good quality in terms of taste? color? odor? texture? * What are the sensory qualities of the different treatments in terms of taste? color? odor? texture? * Which of the groups/set-ups are acceptable in terms of its overall acceptability?A. Control (Pure Ampalaya Coffee) B. Control (Pure Commercial Coffee) C. Treatment A (75% Ampalaya Coffee, 25% Commercial Coffee) D. Treatment B (50% Ampalaya Coffee, 50% Commercial Coffee) E. Treatment C (25% Ampalaya Coffee, 75% Commercial Coffee) General Objectives * This study primarily aims to determine if Ampalaya Seeds (Momordica charantia) can be made into coffee. Specific Objectives * To determine the quality of coffee out of Ampalaya (Momordica charantia) Seeds in terms of taste, color, odor and texture. * To identify the sensory qualities of the different treatments in terms of taste, color, odor and texture. To determine which of the groups/set-ups are acceptable in terms of its overall acceptability. A. Control (Pure Ampalaya Coffee) B. Control (Pure Commercial Coffee) C. Treatment A (75% Ampalaya Coffee, 25% Commercial Coffee) D. Treatment B (50% Ampalaya Coffee, 50% Commercial Coffee) E. Treatment C (25% Ampalaya Coffee, 75% Commercial Coffee) C. Significance Of The Study This research can play a significant role in replacing the generic coffee’s market cost for affordability and its medical benefits for various types of diseases/sickness like diabetes and anemia.It can also conserve unused or to-be-thrown away seeds of Ampalaya and use it for a better cause. According to the study of YumikoYasui, its seeds have linoleic acid that can  prevent coloncancer. It also contains polypeptide-P;a plant insulin that helps diabetic patients. D. Scope And Limitations This research will be conducted on July–August 2012 at Paraiso Cmpd. Baybay City, Leyte. This study focuses on how to make Ampalaya (Momordica charantia) seeds into coffee. The whole fruit is not included in making the product, only the seeds are used to make coffee.The researchers are not focusing on the nutrient values that they can get in the Ampalaya (Momordica charantia) seeds nor will they include it in their research. Instead, the researchers are focusing in making coffee out of Ampalaya (Momordica charantia) seeds and in the sensory qualities (taste, color, and odor) of Ampalaya (Momordica charantia) coffeein comparison to the commercial coffee. E. Operational Definition Of Terms * Momordica charantia * scientific name of the Ampalaya or Bitter Melon * polypeptide-P * a plant insulin found only in the Ampalaya * potentiate insulin is an alternative cancer treatment using insulin to administer low-dose chemotherapy or mandelonitrite * caffeine * is a bitter, white crystalline xanthine alkaloid that acts as a stimulant drug and a reversible acetylcholihesterase inhibitor * is found in varying quantities in the seeds, leaves, and fruits of some plants, where it acts as a natural pesticide that paralyzes and kills certain insects feeding on the plants * Coffea Arabica * is a species of coffea originally indigenous to the mountains of Yemen in the Arabian * Coffea canephora is a variety of coffea which has its origin in central and western sub-Saharan Africa * Hemileia vastatrix * severe symptoms of leaf rust * is a fungus of the order uredenales that causes coffee rust, a disease that is devastating to coffee plantations Chapter II Review Of Related Literature Coffee altern atives can be a solution to the serious need for a very economical, nutritious and medicinal coffee. It is very economical in the sense that its cost would be near to costless. It is nutritious that it has additional properties, vitamins and minerals that is very essential in the body’s growth and development.It is medicinal in a way that the coffee can cure several diseases more than ordinary commercial coffees can [7]. Ampalaya seeds are a good alternative for making coffee because it has more similar properties to coffee beans like carbohydrate and its bitterness. It is also good for dysmenorrhea and amenorrhea, provides daily need of iron in the body, and is good for people with diabetes. Ampalaya powdered seeds contain iron and folic acid which helps in the production of red blood cells and formation of myoglobin and hemoglobin.It is also rich in antioxidants that helps flushing out harmful toxins in the body and regulates the blood flow well. It also has been found out that this alternative may discourage people to use commercial coffee that has no nutritional value compared to coffee made from Ampalaya seeds [3, 7, and 8]. In the study conducted by Ma. Liza Lamanilao and Venus Sejalbo, entitled â€Å"Make/Making Ampalaya Seed Coffee and Polvoron†, in which their main objective is to make coffee and polvoron from unused ampalaya seeds that are being thrown away.They also specifically aims to develop this research to answer the serious need for a very economical, nutritious and a medicinal coffee. During the experiment in making coffee, they collected ampalaya seeds, remove the shells, toasted the seeds until the seeds will turn brown and finally, pound them to produce fine powdered coffee and a caffeine free coffee. They also make nutritious polvoron by toasting again the granules together with milk and sugar. After the experiment, they have found out the nutritional value we could get in Ampalaya Seeds.It contains iron and folic acid or Vi tamin B12 which helped the production of red blood cells and formation of myoglobin and hemoglobin. They also found out that Ampalaya Seeds is good for dysmenorrheal and amenorrhea and it provides the daily need of iron in the body and good for diabetics. It has been found out that the discovery may discourage the people to use the commercial coffee that has no nutritive value compared to coffee made from ampalaya seeds. Ampalaya Seeds is also a good substitute in making coffee based on nutritive value present in seeds. (http://www. foodrecap. net/recipe/ampaya-coffee-pulvoron/)In the research entitled â€Å"Coffee, Decaffeinated Coffee and Tea Consumption in Relation to Incident Type 2 Diabetes Mellitus† which was conducted by Rachel Huxley, Dphil, et al. The study primarily aims to identify the relation between the Coffee, Decaffeinated Coffee, and Tea Consumption and the Incident of Type 2 Diabetes Mellitus. The data from 18 studies with information on 457 922 participants reported on the association between coffee consumption and diabetes. Six (N=225,516) and 7 studies (N=286,701) also reported estimates of the association between decaffeinated coffee and tea with diabetes respectively.The putative protective effects of these beverages warrant further investigation in randomized trials. There was inverse log-linear relationship between coffee consumption and subsequent risk of diabetes such that every additional cup of coffee consumed in a day was associated with a 7% reduction in the excess risk of diabetes relative risk, 0. 93 (95% confidence interval, 0. 91-0. 95) after adjustment for potential confounders. Based on the results, the researchers owe to the presence of of small study bias represented an overestimate of the true magnitude of the association.The researchers concluded that high intakes of coffee, decaffeinated coffee and tea consumption can reduce risk of diabetes. (http://archinte. jamanetwork. com/article. aspx? articleid=773949#) A ccording to Rachel Huxley, DPhil and colleagues in the Archives of Internal Medicine during December 14, 2009 they conducted a study about â€Å"Every Cup of Coffee per Day Lowers Risk of Type 2 Diabetes by 7%†. This study was conducted at the George Institute for International Health, University of Sydney, Australia. The researchers stated that there are several studies to prove that drinking coffee may lower the risk of developing type 2 Diabetes.During the study, the researchers resolved information from 18 studies on coffee and diabetes. They also analyzed another 13 studies that includes data on decaffeinated coffee, tea drinking and diabetes. When all the information, from each study was combined, they out that each additional cup of coffee drunk per day was accompanied with a 7% lower risk of diabetes. People who drunk three to four cups of coffee per day had about a 25% lower risk than those who didn’t drank two r fewer cups per day while people who drank decaf feinated coffee more than three to four cups per day had about a ne-third lower risk of having type 2 diabetes. The study shows that if tea drinkers drank more than three to four cups of tea per day had about one-fifth lower risk of diabetes. In a nutshell, the results shows that people who drank more cups of coffee, whether it’s decaffeinated or regular or tea will have a lower risk of developing type 2 diabetes. Therefore, the researchers conclude that they will advise the patients who are most at risk for diabetes mellitus should increase to consume a coffee and tea in addition to increase their levels of weight loss and physical activity. (http://diabetes. webmd. om/news/20091214/coffee-tea-may-stall-diabetes) Chapter III Methodology A. Research Design The researchers will gather unused Ampalaya seeds from clean market sites and homes. They will wash and dry it up under the heat of the sun for 2-3 sunny days. Then, they will peel off its seed coat, roast it for 25 minutes and grind it to powder form. After it is powdered, it will be brewed and distributed to different controls and treatments. Then it will be ready for sensory evaluations for different sampling techniques and rate its acceptability. Problem Can Ampalaya seeds (Momordica charantia) be made into coffee?Hypothesis Ho: There is no difference between the commercial coffee and the Ampalaya seeds made into coffee. HA: There is a significant difference between the commercial coffee and the Ampalaya seeds made into coffee. B. Type Of Study This research study is quasi-experimental which focuses in making coffee from Ampalaya seeds. C. Independent And Dependent Variable The independent variable in this study is the Ampalaya seeds (Momordica charantia) coffee and the dependent variable is the sensory qualities of coffee (taste, color, odor, and texture). D. Treatments Of The Study + Control| – Control| TreatmentA| TreatmentB| TreatmentC| Ampalaya coffee (tsp. )| 1| None| ? | ? | ? | Comm ercial coffee (tsp. )| None| 1| ? | ? | ? | Sugar (tsp. )| ? | ? | ? | ? | ? | Water (cup)| 1| 1| 1| 1| 1| Table 1- Different Treatments of Powdered Ampalaya Seeds This study has 2 treatments for control set-up (positive control – 100% Ampalaya coffee, negative control – 100% commercial coffee) and 3 treatments for the quasi-experimental set-up (TA – 75% Ampalaya coffee, 25% commercial coffee; TB – 50% Ampalaya coffee, 50% commercial coffee; TC – 25% Ampalaya coffee, 75% commercial coffee).E. Subjects / Samples This research study involves ESEP curriculum students from Grade 7 to 4th year. The researchers take only 30 respondents / samples from the whole population of ESEP curriculum. F. Replications Per Treatment There were 5 treatments in this study (positive and negative control, treatment A, B, and C) and in every treatment, there were 30 replicates. G. Methodology Proper Table 2 – Process Flow Of The Conducted Study Preparation of Ingre dients and Materials and Roasting of Seeds for 25 Minutes Heat the frying pan in preparation for the roasting of seeds.Then, prepare the bowl and the mortar and pestle. Wash the seeds until it is free from dirt and other physical elements aside from the seeds. Lastly, prepare the heater for the boiling of hot water and the 5 plastic cups. Then, roast the washed, dried seeds in the pan for 25 minutes. Then cool it off. Drying of Ampalaya Seeds and Removing of Seed Coat The researchers will prepare the seeds which were gathered on the cleaner side of the market and will not be used by the vendors. The researchers wash the seeds, put it in a plate and placed it under the heat of the sun for 2 to 3 sunny days.Then, peel of the seed coat of the seeds with bare hands. Grinding of Seeds After the seeds were cooled off, place the roasted seeds in the mortar then grind it using the pestle until all of the seeds are powdered. Treatment Distribution for Ampalaya and Commercial Coffee In each o f the grouped teacups for the five samples, each teacup is distributed based on the data in Table 1. Sensory Evaluation The researchers conducted the evaluation through sensory qualities (taste, color, odor, and texture) and its acceptability. The treatments A to E are presented to the respondents for the evaluation based on the data on Table 3.Image 1Sample Questionnaire H. Statistical Treatment For Data Analysis The researchers used Chi-square Test in order to find the significant differences between treatments. They also used the mean in order to compute the average rating of sensory qualities (taste, color, odor, and texture) in every treatment. Chapter IV Results And Discussions This research study primarily aims to determine if Ampalaya Seeds (Momordica charantia) can be made into coffee. Based on our experiment, researchers can answer their objectives. The data gathered were tabulated and evaluated as shown below.Graph 1 – Total Respondents Per Rating Of Overall accept ability For The Positive Control This graph is skewed to the left. That means that the respondents rate the pure Ampalaya coffee a little bit lowly. On the brighter side, the majority was clustered in the average part of the graph hence; it can be treated as acceptable. Rating| Sensory Qualities| | Taste| Color| Odor| Texture| 1| 1| 0| 6| 4| 2| 8| 18| 3| 14| 3| 2| 8| 12| 2| 4| 17| 4| 7| 7| 5| 12| 0| 2| 3| | 30. 33| 37. 33| 10. 33| 15. 67| Table 3 – Total Respondents Per Rating Per Sensory Quality Of The Positive ControlGraph 2 – Total Respondents Per Rating Per Sensory Quality Of The Positive Control The table and graph above shows the relationship of the number of respondents and the rating they rate based on the coffee of the positive control. The graph conveys that the curve of the taste have the best rating results and color shows a more degrading result compared to the other variables. The solution performing the Chi-square Test of the Positive Control values for each of the sensory quality can be found at Appendix A. Comparing these results, we can evaluate: With the total number of respondents, n = 30, total data groups for the rating, k = 5, ? 0. 05, and d. f. = k – 1 = 5 – 1 = 4, then the x? 0. 05= 9. 49. * Since x? taste(30. 33) ? 0. 05(9. 49), then the rating distribution for the taste is significantly different to each other. The curve of the taste variable is positively skewed in which the respondents have taken the liking to the taste of the Ampalaya coffee. * Since x? color(10. 33) ? 0. 05(9. 49), then the rating distribution for the color is significantly different to each other. The curve of the color variable is negatively skewed in which the respondents may not have taken the liking to the color of the Ampalaya coffee. Since x? odor(37. 33) ? 0. 05(9. 49), then the rating distribution for the color is significantly different to each other. The curve of the odor variable is concentrated more on the average side of the rating. Maybe the Ampalaya coffee is more of an odorless beverage because unlike the commercial coffee, it has an aroma because of carbohydrates which may be a little bit of lacking on the Ampalaya seeds. * Since x? texture(15. 67) ? 0. 05(9. 49), then the rating distribution for the texture is significantly different to each other. The curve of the texture variable is negatively skewed.Maybe the physical appearance of the ground Ampalaya coffee powder is a lot different than the commercial coffee because of the differences of the type of fruit they produce, in which the coffee is a berry fruits so its color is a lot concentrated compared to the gourd family of Ampalaya which has a larger fruit. Rating| Taste| | + Control| – Control| Ta| Tb| Tc| 1| 1| 4| 0| 2| 1| 2| 8| 7| 9| 8| 12| 3| 2| 2| 6| 5| 4| 4| 17| 7| 8| 9| 8| 5| 2| 10| 7| 6| 5| Mean| 3. 37| 3. 4| 3. 43| 3. 30| 3. 13| Table 4 – Total Respondents Per Rating Per Treatment For The Taste Graph [ 3 ] â€⠀œ Mean Rating For The Taste Per TreatmentGraph 4 – Mean Rating For The Taste Per Treatment The graph above shows that the treatment that garnered the highest rating for the taste is TA, coffee of 75% Ampalaya coffee and 25% of the commercial coffee. Though the results were quite unexpected, the nearness of the rating between the pure commercial coffee and pure Ampalaya coffee is the most focused in this study so, we can say that Ampalaya coffee can be an alternative to a commercial coffee on the basis of its taste. Rating| Color| | + Control| – Control| Ta| Tb| Tc| 1| 0| 0| 1| 1| 0| 2| 18| 7| 10| 6| 11| 3| 8| 8| 9| 12| 7| 4| 4| 13| 10| 9| 12| | 0| 2| 0| 2| 0| Mean| 2. 53| 3. 33| 2. 93| 3. 17| 3. 03| Table 5 – Total Respondents Per Rating Per Treatment For The Color Graph 4 – Mean Rating For The Color Per Treatment The graph above shows that the treatment that garnered the highest rating for the color is the negative control, 100% commercial coffee. Thoug h the results were quite expected, it means that the Ampalaya coffee can always be distinguished visually from the commercial coffee. Rating| Odor| | + Control| – Control| Ta| Tb| Tc| 1| 6| 0| 5| 6| 3| 2| 3| 1| 9| 5| 7| 3| 12| 6| 8| 10| 10| 4| 7| 15| 8| 3| 7| 5| 2| 8| 0| 6| 3| Mean| 2. 87| 4. 00| 2. 3| 2. 93| 3. 00| Table 6 – Total Respondents Per Rating Per Treatment For The Odor Graph 5 – Mean Rating For The Odor Per Treatment The graph above shows that the treatment that garnered the highest rating for the odor is the negative control, 100% commercial coffee. If the graph is analyzed, you can hypothesize that an amount of the Ampalaya coffee can greatly diminish the good aroma the commercial coffee currently has. Rating| Texture| | + Control| – Control| Ta| Tb| Tc| 1| 4| 1| 7| 2| 1| 2| 14| 3| 8| 4| 5| 3| 2| 0| 5| 7| 7| 4| 7| 12| 9| 14| 11| 5| 3| 13| 1| 3| 6| Mean| 2. 70| 4. 17| 2. 63| 3. 40| 3. 53|Table 7 – Total Respondents Per Rating Per Treat ment For The Texture Graph 6 – Mean Rating For The Texture Per Treatment The graph above shows that the treatment that garnered the highest rating for the texture is still the negative control, 100% commercial coffee. Though the results are quite expected, if the graph is analyzed, there is a really much big difference on the texture dealt on the brewing of an Ampalaya coffee and those results are not quite on the liking of the respondents, hence this data might become one of the reasons on why Ampalaya seeds might not be a good alternative of the commercial coffee.But on the other hand, it might become another beverage like a medicinal tea. Rating| Control| Quasi-experimental| | + Control| – Control| TA| TB| TC| 1| 4| 2| 6| 5| 5| 2| 12| 4| 9| 5| 6| 3| 10| 9| 9| 12| 8| 4| 3| 14| 4| 5| 10| 5| 1| 1| 2| 3| 1| Table 8-Total Respondents Per Rating Per Treatment For Overall Acceptability Graph 7- Total Respondents Per Rating Per Treatment For Overall Acceptability With all t he results obtained, expectedly, the commercial coffee achieved the highest overall acceptability among the different treatments.If the curves are trend lined, Graph 8 – Trend Lines For The Total Respondents Per Rating Per Treatment For Overall Acceptability In this graph, it is clearly shown that the positive control has the lowest slope among the treatments, hence; Ampalaya seeds may not be a good alternative for the commercial coffee on the basis of overall acceptability of the respondents. Chapter V Summary, Conclusion And Recommendations SUMMARY Coffee alternatives have been famous last two decades due to economic crisis and experimentations for health and medical benefits.Ampalaya is a crawling vine that grows mostly on tropical countries like Philippines. It is said to be rich in iron, potassium, beta-carotene and other nutrients. Any seeds that are edible when powdered can be used as an alternative source for coffee. The general objective of the study is to determine if Ampalaya (Momordica Charantia) seeds can be made into coffee. This research can play a significant role in replacing the generic coffee’s market cost to affordability and medical benefits. It can also conserve unused or to-be-thrown away seeds of Ampalaya.The researchers focus in making coffee out of Ampalaya (Momordica Charantia) seeds and in the sensory qualities (taste, color, odor and texture) of Ampalaya coffee in comparison to commercial coffee. First, the researchers gathered unused Ampalaya seeds from clean market sites and homes. They will wash and dry it up under the heat of the sun for 2-3 sunny days. Then, they will peel off its seed coat, roast it for 25 minutes and grind it to powder form. After it is powdered, it will be brewed and distributed to different controls and treatments.Then it will be ready for sensory evaluation for different sampling technique and rate its acceptability. CONCLUSION Therefore the researchers conclude that: * The overall acceptabi lity of Ampalaya coffee is slightly acceptable. * There are significant difference in every treatment in terms of taste, color, odor and texture. In taste, the positive control (Ampalaya Coffee) got the highest mean rating among the 5 treatments while in color, odor and texture the negative control (Commercial Coffee) got the highest mean rating. * In overall acceptability of groups or set-ups, the negative control is the highest among the 5 treatments.RECOMMENDATIONS If the researchers were given a chance to remake this research, the researchers should gather the Ampalaya seeds at the same plantation, same stem and at the same age. After the researchers have gathered the seed, it should be simultaneously placed it in a plate and dried under the heat of the sun for 2-3 days. The Ampalaya seeds should also be roasted together for 25 minutes. And the researchers hoped that they have a machine in grinding the Ampalaya seeds so that the Ampalaya coffee will have a tiny particle. Appendi x Appendix A Taste x2=i=0n(fo-fe)2fe x2=1-626+8-626+2-626+(17-6)26+(2-6)26 2=(-5)26+(2)26+(-4)26+(11)26+(-4)26 x2=25+4+16+121+166 x2=30. 33 Color x2=i=0n(fo-fe)2fe x2=(0-6)26+(18-6)26+(8-6)26+(4-6)26+(0-6)26 x2=(-6)26+(12)26+(2)26+(-2)26+(-6)26 x2=36+144+4+4+366 x2=37. 33 Odor x2=i=0n(fo-fe)2fe x2=(6-6)26+(3-6)26+(12-6)26+(7-6)26+(2-6)26 x2=(0)26+(-3)26+(6)26+(1)26+(-4)26 x2=0+9+36+1+166 x2=10. 33 Texture x2=i=0n(fo-fe)2fe x2=(4-6)26+(14-6)26+(2-6)26+(7-6)26+(3-6)26 x2=(4)26+(64)26+(16)26+(1)26+(9)26 x2=4+64+16+1+96 x2=15. 67 Appendix B Taste + Control X= i=0nXin X= 10130 X=3. 37 – Control X= i=0nXin X= 10230 X=3. 40 Treatment A X= i=0nXin X= 10330 X=3. 3 Treatment B X= i=0nXin X= 9930 X=3. 30 Treatment C X= i=0nXin X= 9430 X=3. 13 Color + Control X= i=0nXin X= 7630 X=2. 53 – Control X= i=0nXin X= 10030 X=3. 33 Treatment A X= i=0nXin X= 8830 X=2. 93 Treatment B X= i=0nXin X= 9530 X=3. 17 Treatment C X= i=0nXin X= 9130 X=3. 03 Odor + Control X= i=0nXin X= 8630 X=2. 87 à ¢â‚¬â€œ Control X= i=0nXin X= 12030 X=4. 00 Treatment A X= i=0nXin X= 7930 X=2. 63 Treatment B X= i=0nXin X= 8830 X=2. 93 Treatment C X= i=0nXin X= 9030 X=3. 00 Texture + Control X= i=0nXin X= 8130 X=2. 70 – Control X= i=0nXin X= 12530 X=4. 17 Treatment A X= i=0nXin X= 7930X=2. 63 Treatment B X= i=0nXin X= 10230 X=3. 40 Treatment C X= i=0nXin X= 10630 X=3. 53 BIBLIOGRAPHY * Lamanilao, Ma. Liza and Sejalbo, Venus. â€Å"Make/Making Ampalaya Seed Coffee and Polvoron†, <http://www. foodrecap. net/recipe/ampaya-coffee-pulvoron/>. * Huxley, Rachel and Dphil, et al. â€Å"Coffee, Decaffeinated Coffee and Tea Consumption in Relation to Incident Type 2 Diabetes Mellitus† <http://archinte. jamanetwork. com/article. aspx? articleid=773949#>. * Huxley, Rachel, DPhil. â€Å"Every Cup of Coffee per Day Lowers Risk of Type 2 Diabetes by 7%† <http://diabetes. webmd. om/news/20091214/coffee-tea-may-stall-diabetes>. References [1] http://www. charantia. com/about-ampalaya/ [2] http://www. livestrong. com/article/292220-properties-of-ampalaya-sticky-extract/#ixzz1zWJX6zfP [3] http://www. agribusinessweek. com/ampalaya-bitter-gourd-natural-weapon-against-disease/ [4] http://en. wikipedia. org/wiki/Coffee [5] http://en. wikipedia. org/wiki/Health_effects_of_coffee [6] http://www. blurtit. com/q709932. html [7] http://www. foodrecap. net/recipe/ampaya-coffee-pulvoron/ [8] http://diabetes. webmd. com/news/20091214/coffee-tea-may-stall-diabetes

Does FIFA Do Enough To Prevent Racism In Football

Racism; hatred or intolerance of another race or other races is unfortunately a very frequent occurrence around the world. Starting very early on, the belief that someone’s race is superior and has the right to rule others still takes place even to this day. Football, is a sport which should bring countries and races together to compete against each other. But this is not the case, the degree of Racism in football is simply unacceptable. From League 2 in England, to the FIFA World Cup it takes place on the pitch, in the stands and even on the internet.Many various organisations have attempted to prevent Racism in Football, including; Fà ©dà ©ration Internationale de Football Association (FIFA) & Union of European Football Associations (UEFA). But are they doing enough? The most recent incident was on the 24th July 2013 where AC Milan left back Kevin Constant kicked the ball into the crowd and left the pitch after racist abuse was being chanted from the stands of the Sassuolo supporters while he was preparing to take a throw in. Constant's actions emulate those of Boateng’s where a similar scene occurred however the whole team walked off the pitch instead of the one player.While Boateng had plenty of support, it seemed that AC were much less supportive of Constant's decision to exit the pitch. The club said in a statement: â€Å"This was not a decision he should have taken upon himself to make. † After the situation had been reviewed by the FIGC (Italian Football Federation) Sassoulo were fined 30,000 euros for their fans actions, I fully support the decision to punish the club but aren’t others to blame for Constant’s decision to leave the pitch? Is this really going to stop the Racist remarks? The answer is absolutely not.FIGC’s solution did not directly affect the fans and therefore these scenes will undoubtedly keep occurring. Situations like this should be dealt with in the equitable way to abrogate Racism in foot ball and not just result in a careless fine. However this isn’t the worst part of the story. Constant was fined with 3,000 euros for is actions. This is an absolutely appalling decision, and could perhaps encourage supporters to carry on with racist remarks towards the players. Kevin Constant had every right to exit the pitch in the manor he did.On the other hand, FIFA -along with its employees and the football community- have showed that they’re currently unquestionably attempting to stop Racism in football and inside civilisation in general. FIFA has begun and presented events such as the FIFA Conference on Racism in Football, UN Anti-Racism Conference, and established its very first Anti-Discrimination Day on 7 July 2002. But this isn’t enough, FIFA have thought of many methods, but haven’t executed enough hands on tasks to cause any great effect. For example, the FIFA Disciplinary code was taken into place a few years ago.The code shows what happens i f the FIFA Statues -basic laws for world football- are violated. It applies to everyone involved in the football match being played but is everyone being caught out? Not everyone can be dealt with at one time, especially when multiple people join in Racist chants. Therefore I don’t see the Disciplinary Code as being an effective method to eliminate Racism from Football. UEFA work very closely with FARE (Football Against Racism In Europe) and give them a lot of aid in promotion, finance etc.I personally feel that have a much more effective method of preventing Racism. I feel this way because annually at 40 UEFA club competition matches, players are accompanied onto the field by children wearing Unite Against Racism T-shirts, while team captains wear matching armbands. I support this form of preventing racism because fans respect their club’s players and if they see the players supporting the fight against racism then they might think twice about shouting abuse at a play er with a different colour of skin. This method is also incredibly cheap and extremely effective.Considering the millions of pounds some of these respected organisations will have, purchasing t-shirts and armbands should not affect them financially in any way. There are multiple Racist incidents in Football and Kevin Constant’s wasn’t the worst. Standard Liege player Onyewu, stated that Anderlecht’s Jelle Van Damme called him a â€Å"dirty ape† under his breath during the first leg of a play off match. Onyewu alerted the white referee but no action was taken and he was ignored. Although this isn’t the worst of what happened on that match day.When Onyewu arrived at the stadium he was punched and shouted at by the opposition fans. These fans were unpunished and allowed to enter the stadium with nothing said. This is just one of many racist incidents in football which haven’t been dealt with correctly, the referee blatantly showed he was simply uninterested in Onyewu’s complaint. I believe that the referee should receive a long match ban and fine for his actions as he should have been one of the first to report the incident. As for the fans who physically attacked Onyewu, they deserved a permanent ban from going to any future matches.I personally feel that FIFA, FIGC, UEFA and all other major Football related organisations should work together to fight racism and not just focus on their own ways of preventing it. Every match should be promoting the act against racism, tickets, programmes and all forms of merchandise should have ‘Say No To Racism printed on them. Furthermore the punishments for violating the FIFA Disciplinary code should be stricter, fans should have a very long –or possibly life- ban from going to matches if caught and players, managers, match officials should be treated in the same manor along with a minimum fine of 40,000 pounds.