Luis Torres Essays - Music, Culture, African-American Culture, Fads

Luis Torres Dr. Ray Gehani Globalization and Outsourcing of U.S Industry 04/23/2017 Globalization and Outsourcing of Music in U.S Globalization of markets also means globalization of culture and Americanization. An example can be observed in the music industry. Since the creation of hip-hop in the 1980's, rap music has extended to other cultures around the globe. From South Africa to Japan, hip hop has made a universal impression. Many rap artists from the United States confess that a substantial amount of their music is actually purchased in other countries. So much so that, the overseas sales frequently surpass the amount of music bought domestically. This stimulates World Tours, touring places like Germany, Puerto Rico, and Australia. Around the world, various nationalities are also rapping to beats that reflect their culture. Punjabi MC is a DJ out of London of Indian descent who makes music with a different spin. His music often encompasses instruments and sounds that are reminiscent of India and Bollywood and has also collaborated with renowned American rappers such as Jay Z. Not only do American performers try to make it in the music business, brilliant men in Nigeria, Cuba, and Brazil have done so as well. "American hip hop music coursed the cultural corridors of the planet and has been captivated and reinvented around the globe", (Nawotka, 2004). Some claim that hip hop has become prevalent on a global scale because many people relate to the music. African-americans in New York shaped rap to what it is today, using it as a way to express their struggles at the time. Often rappers express their adversities, challenges, and issues with poverty. Rappers also oust their feelings about corruption, the government, and racial inequality. As a culturally oppressed people, other societies identify with these feelings of oppression expressed by African Americans. "Hip hop is something Americans take for grantednot so elsewhere, especially in the developing world, where it has come to represent the empowerment of the disenfranchisement of the American dream", (Nawotka, 2004). As a result, globalization and Americanization has impacted other countries across the world. Globalizing markets means that different cultures and societies will be oppressed and disenfranchised. Rappers in Nigeria also rap about their struggles with poverty. T hrough American hip hop, artist around the world use music as a way to express themselves, relating with the want for liberty and social equality. Americanization is an effect that is presently dispersing throughout the developed world. It is especially observed in music where most industrialized countries are moved and affected by the hip hop singularity. Although rap was created in America by Americans, many people around the globe have picked up on this art and changed the music to reflect their culture, or rap to an American beat in their native language.

Qué es el formulario de ESTA para viajar sin visa a USA

Quà © es el formulario de ESTA para viajar sin visa a USA El formulario de ESTA para viajar a Estados Unidos sin visa es una autorizacià ³n que deben solicitar los turistas o las personas de negocio de ciertos paà ­ses para ingresar al paà ­s por avià ³n o por barco de transporte. No es posible utilizar la ESTA si se llega en una embarcacià ³n o en avià ³n privado o de aerolà ­neas no autorizadas por el gobierno de Estados Unidos. En la actualidad de entre todos los paà ­ses en los que se habla espaà ±ol sà ³lo los espaà ±oles y chilenos pueden entrar en Estados Unidos sin visado. Aunque el gobierno de Washington est en conversaciones con algunos gobiernos latinoamericanos para extender este privilegio a argentinos, brasileà ±os y uruguayos. Quià ©nes pueden solicitar el formulario de ESTA para viajar sin visa Las personas que tengan un pasaporte de uno de los paà ­ses del Programa de Exencià ³n de Visas y que desean viajar a Estados Unidos como turistas o personas de negocios. Sin embargo, si se ha viajado a Irn, Iraq, Yemen, Siria, Libia o Somalia despuà ©s del 1 de marzo de 2011, no se puede solicitar la ESTA. Es necesario pedir una visa de turista. Si se solicita la ESTA y se obtiene, destacar que la estancia siempre debe ser por 90 dà ­as o menos. No se puede ampliar de ninguna manera sin salir del paà ­s. Las personas con visa de turista B1/B2 vigente pueden seguir utilizndola. Tambià ©n necesitan este tipo de visado los extranjeros que viajan a Estados Unidos en aviones privados. Por à ºltimo, entender que los extranjeros que residen legalmente en un paà ­s del Programa de Exencià ³n de Visas no pueden beneficiarse de este privilegio. Por ejemplo, en Espaà ±a vive un nà ºmero considerable de latinoamericanos. Ellos necesitan visa para viajar a Estados Unidos, a menos que se hayan naturalizado espaà ±oles y tenga, por lo tanto, pasaporte espaà ±ol. Cà ³mo se solicita la ESTA para viajar a USA El formulario de ESTA se solicita por internet en una direccià ³n oficial del gobierno americano. Es necesario tener a mano el pasaporte (sin expirar) y una tarjeta de crà ©dito VISA, MasterCard, Discover o American Expres. En los dos primeros casos tambià ©n se admiten las tarjetas de dà ©bito.Tambià ©n hay que tener una direccià ³n de correo electrà ³nica. Si no se tiene, crear una antes de iniciar la solicitud.La aplicacià ³n es sencilla y requiere, como media, unos quince minutos en completarse. Hay que pagar una tasa por la gestià ³n de cuatro dà ³lares americanos. Y si la solicitud es aprobada se cargarn otros 10 dà ³lares. Adems, es posible que la tarjeta de crà ©dito cobre una tasa por la gestià ³n.Antes de hacer el pago verificar que todos los datos son correctos. Ya que si se han cometido errores en cosas como la fecha en la que el pasaporte fue emitido o en la que expira y se detectan despuà ©s del pago ser necesario volver a comentar la aplicacià ³n del pri ncipio y habr que pagar de nuevo.La respuesta se sabe prcticamente al momento. Se recomienda imprimirla y anotar el nà ºmero de caso. Finalizar posteriormente la aplicacià ³n o hacer cambios no esenciales Es posible hacer cambios posteriores, por ejemplo, para completar el nombre de la aerolà ­nea, la ciudad desde la que se viaja o la direccià ³n en la que se va a estar en Estados Unidos, el nà ºmero de telà ©fono o la direccià ³n de correo electrà ³nico. En estos casos basta con introducir el nà ºmero de la aplicacià ³n o datos como el nà ºmero de pasaporte, nombre completo y paà ­s que ha emitido el pasaporte. Cul es la validez de la ESTA La autorizacià ³n para viajar es vlida por dos aà ±os o hasta la fecha de expiracià ³n del pasaporte, cualquiera que se produzca antes. Adems, es necesario aplicar por una ESTA nueva, aà ºn cuando su fecha està © vigente si han cambiado las circunstancias y la respuesta a alguna de las preguntas con opcià ³n de sà ­ o no del formulario ha cambiado. Por ejemplo, si se contestà ³ a una de ellas no y ahora la respuesta correcta es sà ­. (Sà ³lo a ese tipo de preguntas).   Si el formulario de ESTA expira mientras se est presente legalmente en Estados Unidos no es necesario aplicar por otra. Todo est bien. Quà © pasa con el I-94 Sà ³lo se llena el I-94W si se ingresa a EEUU por una frontera terrestre. El control de quien entra y quià ©n sale por aeropuertos y puertos se hace digitalmente. Ya no es necesario llenar el papelito con el que seguro estn familiarizados las personas que han viajado con anterioridad a Estados Unidos. Quà © pasa si la solicitud de la ESTA es denegada Aunque en la mayorà ­a de los casos la ESTA se concede, cuando esto no es asà ­ no es posible saber la razà ³n exacta de la denegacià ³n. Y esto es lo que hay que hacer si no se obtiene la autorizacià ³n electrà ³nica para viajar. Es fundamental no caer en la terrible tentacià ³n de solicitar una nueva autorizacià ³n para viajar cuando la primera es denegada y mentir para intentar conseguir asà ­ la ESTA. Lo ms probable es que el sistema informtico detecte el intento o, si no lo hace, que sà ­ se descubra cuando se llega a la Aduana americana y se tiene que pasar por el examen de un oficial de inmigracià ³n. Cuando un extranjero solicita de nuevo la ESTA y le agarran en una mentira  se puede convertir  en inelegible para entrar a Estados Unidos. Y lo ms probable es que nunca consiga viajar al paà ­s. Adems, es posible que aà ºn teniendo la ESTA la aerolà ­nea prohà ­ba embarcar.   A tener en cuenta Tener la ESTA no significa que se asegure poder entrar a Estados Unidos. La à ºltima palabra la tiene siempre el oficial de Inmigracià ³n en la Aduana. Para asegurarte de que conoces todo lo fundamental sobre la ESTA y sobre la estadà ­a en Estados Unidos cuando se tiene ese documento toma este test de respuestas mà ºltiples. Si sabes todas las respuestas seguro que te evitars problemas. Listado de paà ­ses y casos de doble nacionalidad Segà ºn las leyes de los Estados Unidos  ciudadanos de estos paà ­ses pueden viajar sin visa, sà ³lo con la ESTA. En el caso de doble nacionalidad es importante entender que si la visa se negà ³ con un pasaporte no es posible utilizar el otro para ingresar solo con la ESTA. Por ejemplo, un venezolano que solicità ³ la visa americana con ese pasaporte y su peticià ³n fue negada no puede utilizar el pasaporte portuguà ©s que tiene por ser hijo de portugueses para ingresar sin visa a los Estados Unidos. No se puede legalmente y adems hay que tener muy claro que esta trampa que se pretende hacer es fcil de descubrir ya que cuando se pidià ³ la visa se tomaron las huellas digitales y cuando se pretende ingresar a Estados Unidos, tambià ©n, y el sistema TEC hace una comparativa y el oficial migratorio identifica al ciudadano portuguà ©s como el venezolano al que se denegà ³ la visa.

Post-editing and Translation Management Essay Example | Topics and Well Written Essays - 500 words

Post-editing and Translation Management - Essay Example Current TM software enables profession or domain-based customization, which limits the scope of substitutions, allowed and, therefore, improves output, especially where formulaic or formal language is required. As such, it would be expected that TM in cases involving legal and official documents can produce more palatable output as compared to less standardized text and conversations. Output quality in TM can also be enhanced through human intervention, such as the unambiguous identification of words that can be considered proper names in the text, which enables more accurate translation (Somers, 2013). The TM process can be described in terms of decoding the source text’s meaning, as well as re-encoding in the target language supported by a complex cognitive operation. Post-editing refers to the process through which machine-generated translations are improved with little manual intervention or labor, and is closely linked to the concept of pre-editing. During translation of the text, it is possible to achieve best results through source text pre-editing, such as through controlled language principles, after which the machine output is post-edited (Somers, 2013). Post-editing is quite different from editing that refers to the improvement of text generated by humans, also known in translation as revision. Text that has been post-edited could be revised afterward in order to ensure that language choice are of the best quality. Post-editing generally involves correction of output from translation, specifically to ensure that the output is of high quality. The degree or extent of post-editing may differ, which is dictated by the translation management criteria, and may either be full post-editing or light post-editing. Light post-editing involves minim al human intervention and is mainly meant to ensure that the output is readable, in which case the post-editor expects that the client only needs the text for inbound reasons (Somers, 2013). Full post-editing, on the other hand, seeks to make a text more stylistically appropriate by achieving improved quality of text for outbound and inbound purposes.

To what extent is there a gap between sociological and cultural Essay

To what extent is there a gap between sociological and cultural studies of youth can these ever be bridged - Essay Example The United Nations (UNESCO) officially‘†¦ defines youth as people between the ages of 15 and 24 years inclusive’ (op. cit.). The popular view of youth as the period of rebelliousness is contrasted with childhood as one of acceptance of adult norms, and adulthood as the period of consolidation and conservatism. In Western societies it has been observed that increasingly, the years of childhood appear to shrink while the period of youth gets extended as the adoption of an adult identity becomes ever more delayed. Today young children are exposed to adult concerns through mass media and lose their childhood innocence much earlier than in previous epochs ‘There was now a sense that the end of childhood is happening quicker, and that the period of youth goes on longer‘(Report of the Workshop on Global Youth Media Culture -2004). The World Bank has concluded that on the whole, today’s youth (in industrially developed countries) as compared to their parents at a similar age, are: ‘†¦more likely †¦to be unemployed, ‘†¦ more likely than their parents to be living at home, †¦more likely †¦to be in full time education or training, †¦ less likely to be married’, and†¦Ã¢â‚¬â„¢less likely to have (had) their first child’ (h ttp://www.worldbank.org/devoutreach/spring02/article.asp.id=156). Human beings unlike other species in the animal kingdom do not merely live out their biological lifespan in a state of nature. Over millennia, they have built up civilizations with distinct cultures. Culture is all that which is transmitted from generation to generation in terms of language, norms, customs, practices, values and behaviours, which are essential to establish one‘s place in society as a contributing member. With scientific and technological advances in the West, resulting in the dominance of powerful multinational purveyors of popular culture such as

Criminal Procedure (Assignment 1) Assignment Example | Topics and Well Written Essays - 250 words

Criminal Procedure ( 1) - Assignment Example In general, then, due process affords a person with the right to a notice before trial, a right to an impartial trial and an impartial jury, a right to be heard in defense, and the taking of property and taxes, with prior notice, only for public purposes (Mount, 2010). In the case of Brown v. Mississippi, the fourteenth amendment due process rights were the basis for the court’s ruling in favor of the defendants (Justia, 2011). It was then established that testimony or evidence procured solely by means of violence and torture by the police cannot be considered valid, and is in violation of the due process rights of the fourteenth amendment (Justia, 2011). In Powell v. Alabama, the right to a counsel was discussed in relation to the accused, and it was established that the accused has the right to a counsel with sufficient time for advice and preparation, in accordance with the sixth amendment, which is in especial respect to the Federal courts, and the rights laid down in the fourteenth amendment (Justia,

Pathogenic Etiology of Atherosclerosis

Pathogenic Etiology of Atherosclerosis Atherosclerosis Heart Coronary Special Topics in Pathophysiology Introduction to the Components of the Cardiovascular System: To understand the basis of this paper, the pathophysiology of atherosclerosis, it is vital to appreciate the basic physiology of the heart, circulatory system, and most importantly, the coronary arteries. This fundamental comprehension will lay the foundation to better understand the devastation caused to the coronary arteries by the pathogenesis of atherosclerosis. This may also provide insight into prevention and treatment strategies to counteract the destructive mechanism of this disease. The heart is a very small, vitally important organ composed of four muscular chambers: the right and left atria, and the right and left ventricles. The atria have relatively thin muscular walls, allowing them to be highly distensible [1]; whereas the ventricles are of greater muscular thickness, which is vital for pumping the blood to the pulmonary and systemic circuits. A normal healthy heart has two main functions: to pump blood to the pulmonary circuit where the blood becomes oxygenated and to pump the oxygen-rich blood to the systemic circuit. The heart is essentially a small, muscular pump that is responsible for propelling deoxygenated blood to the lungs, while correspondingly pumping nutrient rich, oxygenated blood to the body. Once the blood leaves the left ventricle, it enters the aorta and corresponding network of arteries that constitute the circulatory system. Blood vessels are divided into four categories: arteries (take oxygenated blood away from the heart to the body), arterioles (branch out from the arteries leading into the capillaries), capillaries (smallest of blood vessels where gas and nutrient exchange occurs), and veins (carry deoxygenated blood from the body to the heart). Arteries and veins have different functions; however, they both are composed of three distinct layers: tunica intima, tunica media, and the tunica adventita [2]. The tunica intima is the innermost layer of any given blood vessel; it includes the endothelial lining and a layer of connective tissue containing variable amounts of elastic fibers [3]. The tunica media is the middle layer which contains concentric sheets of smooth muscle composed of elastin and collagen fibers [3]. It is this smooth muscle that when stimulated by the sympathetic nervous system either constricts, decreasing the diameter of the lumen (vasoconstriction), or it relaxes, increasing the diameter of the vessel lumen (vasodilation) [2]; the role of these vasoactivators will be discussed later in this paper. Lastly, the tunica adventitia is the outer most layer, which is composed of collagen and elastin fibers. Often, this outer layer is blended into adjacent tissues allowing the anchoring and stabilization of some vessels [2]. As the heart is an organ continuously doing work, the cardiac muscle cells are in need of a constant supply of oxygen and nutrients. It is the coronary circulation that is responsible for the blood supply to the cardiac tissues, via an extensive network of coronary arteries. Both the left and right coronary arteries originate from the base of the ascending aorta within the aortic sinus [1,3]. The autonomic nervous system (ANS) plays an important role as neurogenic stimuli have the ability to restrain the extent of coronary vasodilation. This neuromodulation governs the rate of release of vasoconstrictive norepinephrine (NE), which is increased by the adrenergic activation and angiotension II (AII) [1]. Other vasoconstrictors include ÃŽ ±1 and ÃŽ ±2 adrenergic activity, AII, and endothelin. Vasoconstrictive stimuli are also responsible for an increase in free cytosolic calcium in the vascular smooth muscle, resulting in the homeostasis of myocardial contraction [4]. Importantly, these vasoconstrictive adrenergic influences are opposed by vasodilatory influences such as ÃŽ ²-adrenergic vascular receptors and metabolic mechanisms such as nitric oxide (NO), adenosine (ATP) and the activation of vascular ATP dependent potassium channels (KATP) [1]. With this, there are three essential regulators of coronary tone: i) the metabolic vasodilatory system; ii) the neurogenic control system (more vasoconstrictive than vasodilatory); and iii) the vascular epithelium, which can be either vasodilatory by releasing NO or vasoconstrictive by releasing endothelin-1 [1, 4]. Thus, we must keep in mind that endothelin-1 is one of the more powerful vasoconstrictors, especially when endothelial damage is extensive [1, 4]. These vasoactive substances are activated by their respective and very different, signaling pathways; thus contributing to the complexities of atherosclerosis, making it a true multifactorial disease. As with other vessels within the body, when there is an increased demand for oxygen, vasodilation of the coronary arteries occurs. This vasodilation is usually mediated by the release of NO from healthy endothelium; in contrast, when the endothelium is damaged, it releases vasoconstrictive endothelin [1]. It is because of their vital importance that the coronary arteries have gained popular attention when they are partially or completely occluded by atherosclerotic plaques. These atherosclerotic plaques cause inadequate oxygen supply to the cardiac tissue resulting in tissue death (myocardial infarction), and various other forms of heart diseases [1]. Therefore without an adequate supply of oxygen and nutrients to the myocardial muscle, the heart will cease to function properly. This basic foundation will give us a better idea on how a healthy cardiovascular system functions. Therefore allowing us to understand the drastic effects a disease such as atherosclerosis can have on this system. The main focus of this paper will be on atherosclerosis; however other forms of heart disease will be discussed to solidify the idea of how destructive atherosclerosis can be. Thus, the remainder of this paper will focus on the cellular mechanisms behind atherosclerosis, along with old and new thoughts in regards to the etiology and treatment options for this type of heart disease. Their Underlying Relation of Atherosclerosis to Other Coronary Heart Diseases: Cardiovascular disease (CVD) has emerged as the dominant chronic disease in many parts of the world, and early in the 21st century it is predicted to become the main cause of disability and death worldwide [5]. CVD represents a very broad category of conditions that affect the heart and circulatory system. Common risk factors include: blood pressure (hypertension), total cholesterol (LDL and HDL), diabetes, obesity, left ventricular hypertrophy, and genetic predisposition [6]. The most prominent and worrisome of these diseases are those that contribute to coronary heart disease. The coronary heart diseases of interest include: ischemic heart disease, angina pectoris, myocardial infarction, and most importantly, atherosclerosis. As a result of these coronary heart diseases, cardiac output is often depressed and often increases the oxygen demand needed by the cardiac tissues. Therefore the effects of coronary heart disease cannot be taken lightly, as the effects can be highly variable, ranging from diffuse damage, to localized narrowing or stenosis of the coronary arteries [7]. Importantly, these coronary diseases have direct vasodilatory effects of the coronary circulation, acting by the formation of adenosine and NO, and the opening of the KATP channels; also the vascular endothelium is damaged, causing the vasodilatory stimuli to be overcome by the vasoconstrictors such as endothelin and AII [1]. By discussing these other forms of coronary heart disease, the reader will better understand the relationship between these diseases and atherosclerosis; allowing a better understanding of the importance for prevention and treatment strategies of coronary heart disease. Traditionally, it has been thought that the major cause of myocardial ischemia is the result of fixed vessel narrowing and abnormal vascular tone, caused by atherosclerosis-induced endothelial cell dysfunction [6]. This narrowing of the coronary arteries reduces the blood and oxygen flow to the myocardial tissues. It is the cessation of the myocardial blood flow due to atherosclerotic occlusions that results in the immediate physiological and metabolic changes. Unfortunately, the heart cannot increase oxygen extraction on demand, therefore any additional oxygen requirements are met by increasing the blood flow and autoregulation of the coronary vasculature [6]. This oxygen imbalance may also be an underlying cause for not only myocardial ischemia, but contractile cardiac dysfunction, arrhythmias, infarction, and sometimes death [5]. However, important to note is the heart’s unique ability to adapt to these sudden changes in coronary blood flow by correspondingly decreasing the rate of cardiac contraction [1,5]. Thus, the decreased work during ischemia proportionately decreases the oxygen demand and helps conserve the underperfused myocardium [1]; this protective mechanism prevents further damage and cell death due to decreased oxygen levels. Besides physiological factors, there are also metabolic changes that occur immediately after the initial onset of ischemia. The myocardial energy metabolism shifts from aerobic (mitochondrial) metabolism to anaerobic glycolysis within a few seconds [5]; simultaneously, the energy depletion causes the myocardial contraction to diminish, eventually ceasing altogether. Consequently, due to the inhibited mitochondrial metabolism, there is an increase in adenosine concentrations; which causes the adenosine to bind to the smooth muscle receptors, decreasing calcium entry into the cells, thus causing relaxation due to vasodilation [7,8]. Overall, the inability to meet the myocardial oxygen demand often results in severe, vice-like chest pain, or more commonly known as angina pectoris. Angina pectoris often is an associated symptom of myocardial ischemia and is the common medical term used to describe chest pain or discomfort due to coronary heart disease without myocardial necrosis. Interestingly, angina can also occur in people with valvular disease, hypertrophic cardiomyopathy, and uncontrolled high blood pressure (hypertension). Currently there are three major variations of angina pectoris. The first is known as stable angina, or more commonly, chronic stable angina. This form of angina is characterized by a fixed, obstructive atheromous plaque in one or more coronary arteries [1,7,9]. Patients who suffer from chronic stable angina usually have episodes of discomfort that are usually predictable. The discomfort is experienced shortly after over exertion and/or mental or emotional stress; these symptoms are usually relieved by rest, nitroglycerin, or a combination of both. Again, the major contributing factor in stable angina is due to the coronary vasoconstrict ion caused by atherosclerotic endothelial dysfunction [7]. A second form of angina is known as unstable angina. Unstable angina is characterized by unexpected chest pain which usually occurs at rest without any type of physical exertion. This chest pain is due to coronary artery stenosis caused by atherosclerotic plaque or the narrowing of the vessels obstructed by blood clots. Also other key factors in unstable angina include inflammation and infection [7,9]. The last form of angina is the variant angina, or more commonly known as Prinzmetal’s Angina [7]. This form of angina is manifested by episodes of focal coronary artery spasm in the absence of atherosclerotic lesions [7,9]. The coronary vasospasm alone reduces coronary oxygen supply and is thought to be caused in response to abnormal endothelial dependent vasodilators (Acetylcholine – ACh, and serotonin) [1,7]. These coronary spasms are often manifested by the coronary atheroma which damages the vascular endothelium, causing a decreased production of vasodilators (NO and prostaglandin – PGI2) and an increase in vasoconstrictive factors such as endothelin and AII [1]. Often when someone is diagnosed with either form of angina, they are usually monitored closely, as they are at an increased risk of a heart attack (myocardial infarction), cardiac arrest, or sudden cardiac death. A myocardial infarction (heart attack) is the resultant complication when the blood supply to part of the heart is interrupted. This ischemic oxygen shortage causes damage and sometimes death to the heart tissues. Important associated risk factors include: atherosclerosis, previous heart attack or stroke, smoking, high LDL and low HDL cholesterol levels, diabetes, obesity, and high blood pressure [10]. Often referred to as an acute myocardial infarction, it is part of the acute coronary syndromes which includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina [1,7,10]. As with angina, the pain experienced may result from the release of mediators such as adenosine and lactate from the ischemic myocardial cells onto the local nerve endings [7]. This ischemic persistence triggers a process called the ischemic cascade [5], which usually results in tissue death due to necrosis. Certain factors such as psychological stressors and physical exertion have been identified as major triggering factors involved with acute myocardial infarctions. Often these acute myocardial infarctions are brought on by the rupturing of atherosclerotic plaques, which then promote thrombus (blood clot) formation causing further occlusion of the arteries. This atherosclerotic blockage thus initiates myocardial necrosis, which in turn activates systemic responses to inflammation causing the release of cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFÃŽ ±) [7,10]. Damaged caused by myocardial necrosis includes: i) loss of critical amount of ATP, ii) membrane damag e induced metabolically or mechanically, iii) formation of free radicals, iv) calcium overload, and v) sodium pump inhibition [1]. Apart from damaging the myocardial tissue, an acute myocardial infarction can cause varying pathophysiological changes in other organ systems. Some of these changes include: decreased pulmonary function – gas exchange, ventilation, and distribution of perfusion, decreased vital capacity; reduction in hemoglobin’s affinity for oxygen, causes hyperglycemia and impaired glucose function, increases the plasma and urinary catecholamine levels (thus enhancing platelet aggregation), and also has been found to increase blood viscosity [5]. From the above evidence, we can see that coronary heart disease should not be looked at light heartedly. It is due to their similarity that the different coronary heart diseases can be diagnosed using a given set of molecular markers and other diagnostic tools. Serum cardiac markers have become widely used when it comes to diagnosing the extent and type of coronary heart disease a patient is symptomatic of. Also, these tests have allowed physicians to diagnose an additional one third of patients that do not exhibit all criteria of a given disease [5], thus preventing more premature deaths. The most common of these cardiac markers are myocardial bound creatine kinase (CK-MB), and cardiac troponin l and t (cTnl and cTnT). These markers are often found within a blood sample as levels start to rise between 3-8 hours and 3-4 hours respectively [7]. More recently, new ‘risk factor’ biomarkers such as C-reactive protein (CRP), myeloperoxidase (MPO) [11, 12], and lipoprotein-associated phospholipase A2 [12] are being studied more in depth as alternative cardiac markers. Although cardiac biomarkers are heavily used, the role of noninvasive technologies also plays a major role in diagnosing coronary heart disease. These noninvasive metho ds include electrocardiography, exercise stress testing, echocardiography, cardiovascular MRI, and CT imaging of the heart [5]. Some invasive, intravascular techniques include ultrasound, thermography, near infrared spectroscopy, cardiac catheterization, and cardiac angiography [12]. As coronary heart disease is the leading cause of hospitalization and death among today’s population, primary and secondary prevention strategies need to be considered with the utmost importance. Primary prevention generally means the effort set forth to modify risk factors and prevent their development delaying or preventing new onset coronary heart disease [13]. As for secondary prevention, this often refers to the therapy involved to reduce recurrent coronary heart disease events; thus secondary preventions are essentially treatment strategies. The most common and less intensive of these treatment strategies are that of the pharmaceutical therapies. Often, these drug regimes range from the daily aspirin intake to angiotension-converting enzyme inhibitors (ACEi), to ÃŽ ²-blockers and nitrates [12]. These drug therapies often lower the risk of recurrent cardiovascular events. Unfortunately daily drug regimes do not work for everyone. Some people have their coronary heart dise ase surgically corrected either by angioplasty (insertion of stent to keep the blocked vessel open) or by means of a more complex surgery consisting of a single to multiple coronary artery bypass. With everything considered, drug therapies and surgical correction are only a means of correcting the problem; patients are also encouraged to increase physical activity and change their daily dietary habits in becoming more successful in reducing risk of development or progression of coronary artery disease. These different forms of coronary heart disease are very closely related to one another, more importantly, closely related to atherosclerosis. As discussed previously, coronary heart diseases are characterized by the narrowing or stenosis of the coronary vessels, usually caused by the atherosclerotic plaque formation due to endothelial cell dysfunction. As a result, atherosclerosis is the underlying mechanism for ischemic heart disease, angina pectoris (stable, unstable, and variant), myocardial infarction and sudden cardiac death [12]. Therefore it is important to understand the cellular pathogenesis of atherosclerosis, which will lead to a better understanding resulting in better prevention and treatment strategies for all forms of atheroma induced coronary heart disease. Introduction to Atherosclerosis: Atherosclerosis, the primary etiology of cardiovascular disease, is characterized by intimal plaque that forms as a time-dependent response to arterial injury [14]. Atherosclerosis is a disease affecting the arterial blood vessels, which is commonly known as â€Å"hardening of the arteries.† This form of coronary heart disease is the principle source of both cerebral and myocardial infarction, gangrene of the extremities, and loss of function of both organs and tissues [15]; this disease is ultimately responsible for a majority of deaths in North America, Europe, and Japan [16]. The method of atherogenesis is not fully understood, however there are a number of current models that suggest that stressors corrupt the vascular integrity allowing the abnormal accumulation of lipids, cells and extracellular matrix within the arterial wall [7]. Due to its very slow progression, it is not surprising that atherosclerosis goes undetected and remains asymptomatic until the atheroma obstr ucts the blood flow within the artery [14,16]; hence atherosclerosis is often referred to as the â€Å"silent killer†. Often, the atherosclerotic plaque can be divided into three distinct components. The first being the atheroma, which is the nodular accumulation of the soft, flaky, and yellow material of the plaques, usually composed of macrophages closest to the lumen of the artery. The second component is the underlying areas of cholesterol crystals, and the third is the calcification at the outer base of the older/more advanced lesions [17]. Collectively, these components constitute the basis of the atherosclerotic plaques. These atherosclerotic plaques are responsible for the arterial narrowing (stenosis) or they may rupture and provoke thrombosis [7, 14, 15]; either way the atherosclerotic plaque causes an insufficient blood supply to the heart and other organs. As discussed previously, the atherosclerotic plaques lead to other major complications such as ischemia, angina pectoris, myocardial infarction, stroke, and causes impaired blood flow to the kidneys and lower extremities. Interestingly, arteries without many branches (internal mammary or radial arteries) tend not to develop atherosclerosis [5]. One of the most evidence-based hypotheses regarding atherogenesis is that of the response-to-injury hypothesis. This hypothesis suggests that the atherosclerotic lesions represent a specialized form of a protective, inflammatory, fibroproliferative response to various forms of insult to the arterial wall [15]. This seems to be a reoccurring theme, as now atherosclerosis is considered to be a form of chronic inflammation between modified lipoproteins, monocyte derived macrophages, T cells, and normal cellular elements of the arterial wall [16, 18]. As with other diseases, there are a number of physiological factors that increases one’s risk for developing atherosclerosis. These factors include: age, sex, diabetes or impaired glucose tolerance, hypertension, tobacco smoking, estrogen status, physical inactivity, metabolic syndrome, and dyslipidemia [7, 19]. The remainder of this paper will shift its focus to the pathogenesis of atherosclerosis including the ideas of endothelial dysfunction, lipoprotein entry and modification, recruitment of leukocytes, recruitment of smooth muscle; as well as other contributing factors such as dyslipidemia, hypertension, and diabetes. Also, the cellular complications of atherosclerosis will be discussed. Endothelial Dysfunction – Primary Initiation of Atherosclerosis: Healthy arteries are often responsive to various stimuli, including the shear stress of blood flow and various neurogenic signals. These endothelial cells secrete substances that modulate contraction and dilation of the smooth muscle cells of the underlying medial layer [7]. These healthy endothelial cells are also responsible for the inhibition of migration of smooth muscle cells to the intimal layer [20] and they also play an important role in immune responses. Normal functional characteristics of healthy endothelium includes: i) ability to act as a permeable barrier between the intravascular and tissue space, ii) ability to modify and transport lipoproteins into the vessel wall, iii) acts as a non-thrombogenic and non-leukocyte adherent surface, iv) acting as a source of vasoactive molecules, v) act as a source of growth regulatory molecules, and vi) a source of connective tissue matrix molecules [14, 15]. Overall, in a normal, healthy state, the endothelial layer provides a prote ctive, non-thrombogenic surface with homeostatic vasodilatory and anti-inflammatory properties [7]. It is widely known that the endothelium is responsible for the synthesis and release of several vasodilators such as: NO, endothelium derived hyperpolarizing factors (EDHFs), endothelial derived relaxing factors (EDRFs), and prostacyclin (PGI2) [7, 20]. These vasodilators utilize a G-coupled signaling pathway, where NO diffuses from the endothelium to the vascular smooth muscle where it activates guanylyl cyclase (G-cyclase) [7]. The G-cyclase in turn forms cyclic guanosine monophosphate (cGMP) from cGTP; an increase in cGMP results in smooth muscle relaxation which subsequently involves a reduction of cytosolic Ca2+. Aside from these anti-thrombic substances, the endothelium also produces prothrombic molecules including endothelin-1 and other endothelium derived contracting factors (EDFCs) [20]. Importantly, the endothelium derived NO not only modulates the tone of the underlying vascular smooth muscle, but is also responsible for the inhibition of several proatherogenic processes. These processes include smooth muscle proliferation and recruitment, platelet aggregation, oxidation of low density lipoproteins (LDLs), monocyte and leukocyte recruitment, platelet adhesion, and the synthesis of inflammatory cytokines [20]. Therefore, relating back to the response-to-injury hypothesis, loss of these endothelial functions promotes endothelial dysfunction, thus acting as the primary event in atherogenesis. Endothelial dysfunction is considered to be an initiating event which leads to the pathogenesis of atherosclerosis. For this reason endothelial dysfunction has been shown to be of prognostic significance in predicting such vascular events as heart attacks or strokes [21]. It has been established that endothelial cell dysfunction is characterized by alterations in vascular permeability and inadequate production of NO [4, 22, 23]; thus predisposing the endothelium to the development of atheromas. Interestingly, in response to initial atheroma formation, the arteries often dilate, causing outward remodeling of the vessel for this accommodation [4]; however if this remodeling is insufficient, the blood flow is impaired, thus causing ischemia [4]. Several physical and chemical factors are responsible for affecting normal endothelial function. Some common factors discussed previously include diabetes, hypertension, hypercholesterolemia, smoking, age, diet, and physical inactivity. However, more importantly are the physiological factors: i) impairment of the permeable barrier, ii) release of inflammatory cytokines, iii) increase transcription of cell-surface adhesion molecules, iv) altered release of vasoactive substances (PGI2 and NO), and v) interference with normal anti-thrombotic properties [7]. Commonly, endothelial dysfunction is characterized by the reduction of vasodilators NO and PGI2, and the increase of various endothelial derived contracting factors [23, 24]. This impairment may also predispose the vessels to vasospasm [22]. This decrease in NO bioavailability is thought to cause a decreased level of expression of endothelial cell NO synthetase (eNOS) [21], thus reducing the likelihood of vasodilation from occurring. Apart from its vasodilatory role, NO is also responsible for resisting inflammatory activation of endothelial functions such as expression of the adhesion molecule VCAM-1 [5]. NO has also appeared to exert anti-inflammatory action at the level of gene expression by interfering with nuclear factor kappa B (NFÃŽ ºB), which is important in regulating numerous genes involved in inflammatory responses [5]; these inflammatory responses will be discussed later on. The other common vasodilator, PGI2 is also reduced during endothelial dysfunction. PGI2 is a major product of vascular cyclooxygenase (COX) and is considered a potent inhibitor of platelet aggregation [20]. Like NO, PGI2 is an endothelial derived product which is often produced in response to shear stress (commonly caused by blood flow) and hypoxia [20]. By understanding the other roles NO and PGI2 play within the endothelium, we can see that a decrease in one or the other ultimately leads to dysfunction and disruption of the endothelium. As a result of vasodilator reduction, the endothelium often synthesizes and releases EDCFs causing endothelial constriction. The major constrictors include superoxide anions (which act by scavenging NO – thus further reducing NO levels), thromboxane A2, endothelin-1, AII, and ÃŽ ±-adrenergic factors [20]. Unlike the vasodilators, the vasoconstrictors utilize two signaling pathways. The ÃŽ ± 1-adrenergic receptor signaling pathways utilize the same G-coupled pathway as the vasodilators (discussed previously) however instead of cGMP; it ut ilizes cyclic adenosine monophosphate (cAMP) [1]. The other constrictors including thromboxane A2, endothelin-1 and AII utilize the cAMP-dependent protein kinase pathway; where the activated kinase acts as a trigger for various physiological effects, including increased contractile activity on the arterioles [1]. The overall progression of atherosclerotic plaque formation is best illustrated in Figure 1, which showcases multiple events that are simultaneously triggered by endothelial dysfunction. Apart from the imbalance of vasoactivators, endothelial dysfunction is responsible for initiating two other separate pathways that also participate in the progression of plaque formation and growth. Lipoprotein entry is the next initial stage in atherogenesis. This is then followed by the modification and entry of lipoproteins, the recruitment of leukocytes, and the migration and proliferation of smooth muscle cells. Overall this â€Å"evolutionary† process best represents the formation of atherosclerotic plaques within the vessels. Lipoprotein Entry and Modification: Lipid accumulation is another major manifestation of the vascular response to injury, and is accelerated by the entry and modification of lipoproteins. Lipoproteins are composed of both lipids and proteins, and help transport water-insoluble fats throughout the bloodstream [7, 25]. The lipid core is surrounded by hydrophilic phospholipids, free cholesterol and apoliporoteins; where the protein portion has a charged group, aimed outwards to attack water molecules, thus making the lipoproteins soluble in the plasma of the blood [26, 27]. In total, there are five major classes of lipoproteins: the chylomicrons, very low density lipoproteins (VLDLs), intermediate low density lipoproteins (ILDLs), low density lipoproteins (LDLs), and the high density lipoproteins (HDLs). The chylomicrons provide the primary means of transport of dietary lipids, while the VLDLs, ILDLs, LDLs, and HDLs function to transport endogenous lipids [16, 25]. Of the lipoproteins, the LDLs are of most interest. Inter estingly high LDL levels often correlate closely with atherosclerosis development, whereas high HDL levels protect against atherosclerosis; the HDL protection is thought to be related to its ability to transport lipids away from the peripheral tissues back to the liver for disposal [7]. A key component to the accumulation of lipids is due to the endothelial dysfunction, which causes a loss of selective permeability and barrier function. This ineffective permeability allows for the entry of LDLs into the intima lining of the vessels [7, 16]. The highly elevated circulating levels of LDLs are colloquially referred to as having hyperlipidemia, hypercholesterolemia, or dyslipidemia [7, 25-27]. In either case, once the LDL has entered the intima of the vessel, the LDL starts accumulating in the subendothelial space by binding to components of the extracellular matrix, the proteoglycans; lipolytic and lysosomal enzymes also play a role in lipid accumulation [27]. Importantly, statins lower circulating cholesterol levels by indirectly inhibiting HMG CoA-reductase (rate limiting enzyme required for endogenous cholesterol biosynthesis [16]. This results in the decrease of intracellular cholesterol levels, which leads to the activation of SREBP, upregulation of LDL receptors, and the clearance from plasma degradation of LDL; thus reducing circulating LDL levels [16]. When the lipid accumulation increases the residence time that the LDL occupies within the vessel wall, it allows more time for lipoprotein modification [7]; which appears to play a key role in the continued progression of the atherosclerotic plaque. Often, endothelial cell dysfunction leads to the altered expression of lipoprotein receptors used to internalize and modify various lipoproteins [14]. These changes usually occur via oxidative modifications. The oxidative modification hypothesis (figure 2) focuses on the concept that LDLs in their native state are often not atherogenic [27]. It is believed, however, that LDLs are modified chemically by the endothelial cells [26] and are readily internalized by macrophages (formation of the foam cell) via the ‘scavenger-receptor’ pathway [27]. Essentially the â€Å"trapped† LDL within the subendothelial space is oxidized by the resident vascular smooth muscle cells, endothelial cells, and macrophages. As a result t

To Kill A Mockingbird Essays: Great Courage -- Kill Mockingbird essays

Courage in To Kill A Mockingbird Courage is shown within the characters of To Kill A Mockingbird in several situations. The characters are challenged to face danger or pain without fear. The courage they display gives them strength and deepens their self-understanding as the novel progresses. Early in the novel, Scout illustrates the courage she embodies. On her first day of school, Scout acts as an ambassador for the entire class. She takes the duty of informing Miss Caroline of Walter Cunningham's situation. Miss Caroline had just scolded Scout for her ability to read, however, Scout still feels the classes' need for leadership. Most children at her age would fear speaking to the teacher is such a bold fashion. Scout shows advanced maturity for her age, and this allows her to successfully act upon her courage, rather than suppressing its existence. Walter Cunningham, himself, was shy and fearful of speaking to the teacher. Scout over came the petty fears that plagued the remainder of the class, and acted out of Walter's best interest. Her courage spoke in Walter's absence, and inability to express his monetary situation. Jem is faced with a courageous situation in regards to the Radley house. His courage stems from fear of receiving a whipping from Atticus, and more important, his disapproval. Jem is willing to risk his life in order to save his father from showing disappointment. The threat of Mr. Radley waiting for the intruder with his gun instils fear within Jem. However, Jem overcomes this fear in order to sustain Atticus' faith. Being the only and eldest son places pressure upon Jem to set an e... ...re you begin but you begin anyway and you see it through no matter what. You rarely win, but sometimes you do." (112). Within all the examples of courage there is not a situation when the courage did not stem from a need within the character. Courage is the inner desire to succeed and to do what is righteous, no matter what humiliation or consequences that plague you because of your decision. Scout, Jem, Atticus, Calpurnia and Mrs. Dubose understood the risks they faced but continued with their actions because it was moral. They did not all enter their personal situation expecting to win. Scout still faced further scolding from Miss Caroline. Jem eventually told his father what he had done to the Radley's. There were winners and losers but they do not regret the courage they showed for the sake of good intentions.