Criminal Procedure Sample Essay

Criminal Procedure Sample EssayA criminal procedure sample essay is an essay that is taken from real life cases. The purpose of this is to allow a student to see how the real law works. It will provide a better understanding of what the judge or attorney is looking for in a case. This type of essay can also be used to teach students about the law.This type of essay is also used to demonstrate the workings of the judicial system. A student should understand what is going on in a case to fully understand what the judge or attorney is looking for. Without being familiar with this type of writing, a student will not be able to fully grasp all the rules of the court.Students must understand the importance of the facts and good information when creating these type of essays. Students should make sure they gather good information before writing the paper. A good way to know if a particular source is good is to use the research tools.Good research can be done by using a research tool such as the internet. There are many sources of information. Students should find the one that is reliable and learn about the topic thoroughly. From there, they can then search for facts.The students should also consider the methods they would use in a real case. They should use the same method they would use in a court case to make their essay a successful one. Not every court uses the same method, so students should consider this. All students should understand the legal process and the way things work.All material needs to be kept accurate and not leave anything out. When writing a paper on a case, it is important to give the reader the information they need. It is not possible to give every detail in a class.A good reference is always provided to help the student understand the way a case works. The professor provides a concise way to explain something. This helps the student to understand the process better.Using a criminal procedure sample essay is a great way to educate a student a bout the law. It helps to provide the students with a specific way a case works. If a student is unsure of how something works, they should consider finding a good resource.

Current Concept And Machanisms In The Pathogenesis Of Atherosclerosis Essay Example

Current Concept And Machanisms In The Pathogenesis Of Atherosclerosis Paper Atherosclerosis is the leading cause of death and disability in the developed world. Despite our familiarity with the disease, some of its fundamental characteristics remain poorly recognized and understood. Although many generalized or systemic risk factors predispose to its development, atherosclerosis affects various regions of the circulation preferentially and yields distinct clinical manifestations depending on the particular circulatory bed affected. Atherosclerosis of the coronary arteries commonly causes myocardial infarction and angina pectoris. Atherosclerosis of the arteries supplying the central nervous system frequently provokes strokes and transient cerebral ischemia. In the peripheral circulation, atherosclerosis causes intermittent claudication and gangrene and can jeopardize limb viability. Involvement of the splanchnic circulation can cause mesenteric ischemia. Atherosclerosis can affect the kidneys either directly (e. g. , renal artery stenosis) or as a frequent site of atheroembolic disease. Even with in a given arterial bed, atherosclerosis tends to occur focally, typically in certain predisposed regions. In the coronary circulation, for example, the proximal left anterior descending coronary artery exhibits a particular predilection for developing atherosclerotic occlusive disease. Likewise atherosclerosis preferentially affects the proximal portions of the renal arteries and in the extracranial circulation to the brain, the carotid bifurcation. We will write a custom essay sample on Current Concept And Machanisms In The Pathogenesis Of Atherosclerosis specifically for you for only $16.38 $13.9/page Order now We will write a custom essay sample on Current Concept And Machanisms In The Pathogenesis Of Atherosclerosis specifically for you FOR ONLY $16.38 $13.9/page Hire Writer We will write a custom essay sample on Current Concept And Machanisms In The Pathogenesis Of Atherosclerosis specifically for you FOR ONLY $16.38 $13.9/page Hire Writer Indeed, atherosclerosis lesions often form at branching points of arteries, regions of disturbed blood flow. Not all manifestations of atherosclerosis result from stenotic, occlusive disease. Ectasia and development of aneurismal disease, for example, frequently occur in the aorta. The mechanisms that underlie this discontinuous anatomic distribution of atherosclerosis remain uncertain. (Rodney A. White, White A. , Ramadan Shaafi, White A. White, 1989) Atherosclerosis manifests itself focally not only in space, as just described, but in time as well. Atherogenesis in humans typically occurs over a period of many years, usually many decades. Growth of atherosclerotic plaques probably does not occur in a smooth linear fashion, but rather discontinuously, with periods of relative quiescence punctuated by periods of rapid evolution. After a generally prolonged silent period, atherosclerosis may become clinically manifest. The clinical expressions of atherosclerosis may be chronic, as in the development of stable, effort-induced angina pectoris or of predictable and reproducible intermittent claudication. Alternatively, a much more dramatic acute clinical event such as myocardial infarction, a cerebrovascular accident, or sudden cardiac death may first herald the presence of atherosclerosis. Other individuals may never experience clinical manifestations of arterial disease despite the presence of widespread atherosclerosis demonstrated post mortem. INITIATION OF ATHEROSCLEROSIS FATTY STREAK FORMATION An integrated view of experimental results in animal and study of human atherosclerosis suggests that the fatty streak represents the initial lesion of atherosclerosis. The formation of these early lesions of atherosclerosis most often seems to arise from focal increases in the content of lipo-protein within regions of the intima. These accumulations of lipoprotein particles may not result simply from an increased permeability or leakiness of the over lining endothelium. Rather this lipoprotein may collect in the intima of arteries because they bind to constituent of the extracellular matrix, increasing the residence time of the lipid- rich particles within the arterial wall. Lipoproteins that accumulate in the extra cellular space of the intima of arteries often associate with proteoglycan molecules of the arterial extracellular matrix, an interaction that may promote the retention of lipoproteins by binding them and slowing their egress from the intima. (James S. C. Gilchrist, Paramjit S. (EDT) Tappia, Thomas (EDT) Netticadan, 2003) Lipoprotein particles in the extracellular space of the intima particularly those born to matrix macromolecules, may undergo chemical modification. Accumulating evidence supports a pathogenic role for such modifications of lipoproteins in atherogenesis. Two types of such alterations in lipoproteins bear particular interest in the context of understanding how risk factors actually promote atherogenesis: oxidation and nonenzymatic glycation. Lipoprotein Oxidation Lipoprotein sequested from plasma antioxidants in the extracellular space of the intima become susceptible to oxidative modification. Oxidatively modified low density lipoprotein (LDL), rather than being defined homogerous entity, actually comprises a variable and incompletely defined mixture. Both the lipid and protein moieties of these particles cab participate in oxidative modification. Modifications of the lipids may include formation of hydroperoxides, lysophospholipids, oxysterols, and aldehydic breakdown products of fatty acids. Modifications of the apoprotein moieties may include breaks in the peptide backbone as well as derivatization of certain amino acid residues. A more recently recognized modification may result from local hypochlorous acid production by inflammatory cells within the plaques, giving rise to chlorinated species such as chlorotyrosyl moieties. Considerable evidence supports the presence of such oxidation products in atherosclerotic lesions. Nonenzymatic Glycation In diabetic patients with sustained hyperglycemia, nonenzymatic glycation of apolipoproteins and other arterial proteins likely occurs that may alter their function and propensity to accelerate atherogenesis. A good deal of experimental work suggests that both oxidatively modified and glycated lipoproteins or their constituents can contribute to many of the subsequent cellular events of lesion development. LEUKOCYTE RECRUITMENT After the accumulation of extracellular lipids, recruitment of leukocyte occurs as a second step in the formation of the fatty streak. The white blood cells types typically found in the evolving atheroma include primarily cells of the mononuclear lineage; monocytes and lymphocytes. A number of adhesion molecules or receptor for leukocyte expressed on the surface of the arterial endothelial cell likely participitate in the recruitment of leukocyte to the nascent fatty streak. Constituent of oxidatively modified LDL can augment expression of leukocyte adhesion molecule. This example of illustrate how the accumulation of lipoprotein in the arterial intima may link mechanistically with leukocyte recruitment and subsequent events in the lesion formation. (Pierre-Jean Touboul, J. R. Crouse, 1997) Laminar shear forces such as those encountered in most regions of normal artery can also suppress of the expression of leukocyte adhesion, example branch points often have disturbed laminar flow. Ordered laminar shear of normal blood flow augments the production of nitric oxide by endothelial cells. This molecule in addition to its vasodilator properties can act at the low levels constitutively produced by arterial endothelium as a local anti-inflammatory autacoid, for example limiting local adhesion molecule expression. These examples indicate how hemodynamic forces may influence the cellular that underlie atherosclerotic lesion initiation and provide a potential explanation for the local distribution of atherosclerotic lesions at certain sites predetermined by altered flow pattern. Once adherent to the surface of the surface of the arterial endothelial cell via interaction with adhesion receptors, the monocytes and lymphocytes penetrates the endothelial layer and take out residence in the intima in addition to products of modified lipoprotein, cytokines can regulate the expression of adhesion molecules involved in the leukocyte recruitment. For example, the cytokines interlukin one (IL-1) or tumor necrosis factor alpha (TNF-alpha) induce or augment the expression of leukocyte adhesion molecules on endothelial cells. Because modified lipoprotein can induce cytokines release from vascular wall cells, this pathway may provide an additional link between accumulation and modification of lipoprotein and leukocyte recruitment. The directed migration of leukocyte into the arterial wall may also result from the action of modified lipoprotein. For example, oxidized LDL may promote the chemotaxis of leukocyte. Also, oxidatively modified lipoprotein can elicit the production by vascular wall cells of chemoattractant cytokines such as monocytes chemoattractant protein-1. (Frank Kessel, Patricia L. Rosenfield, Norman B. Anderson, 2003) FOAM CELL FORMATION Once resident within the intima the mononuclear phagocyte differentiate into macrophages and transform into lipid-laden foam cells. The conversion of mononuclear phagocytes into foam cells requires the uptake of lipoprotein particles by receptomediated endocytosis. One might suppose that the well recognized classical receptor for LDL mediated the lipid uptake. Patients or animals lacking effective LDL receptors due to genetic alterations however have abundant arterial lesions and extraarterial xanthomata rich in macrophage derived foam cells. Also the exogenous cholesterol suppresses expression of the LDL receptor, such that under hypercholesterolemic conditions the level of this cell surface receptor for LDL decreased. Candidates for alternative receptors that can mediate lipid-loading of foam cells include a growing number of macrophage scavenger receptors, which preferentially endocytose modified lipoproteins and other receptors for oxidized LDL or beta-VLDL (very low density lipoprotein) a type of lipoprotein commonly encountered in certain hypercholerterolemic states. By ingesting lipids from the extracellular space the mononuclear phagocytes bearing such scavenger receptors may remove lipoproteins from the developing lesion. Some lipid loaded macrophages may leave the artery wall, functioning to clear lipid from the artery. Lipid accumulation and hence propensity to form atheroma, ensues if the amount of lipid entering the artery wall exceeds that exported by mononuclear phagocytes or other pathways. Macrophages may thus play a vital role in the dynamic economy of lipid accumulation in the arterial wall during atherogenesis. Some lipid laden foam cells within the expanding intimal lesion perish. Some foam cells may die as a result of programmed cell death known as apoptosis. This death of mononuclear phagocytes results in formation of the lipid rich center often called necrotic core, of more complicated atherosclerotic plaques. (Shari R. Waldstein, Merrill E Elias, 2001) Macrophages taking up modified lipoproteins much like intrinsic vascular wall cells may elaborate cytokines and growth factors that can further signal some of the cellular events in lesion complication. A number of growth factors or cytokines elaborated by mononuclear phagocytes can stimulate smooth-muscle cell proliferation and production of extracellular matrix, which accumulates in atherosclerotic plaques. Cytokines found in the plaque including IL-1 or TNF – alpha can induce local production of growth factors such as forms of platelet derived growth factor (PDGF), fibroblast growth factor and others that may contribute to plaque evolution and complication. Other cytokines, notably interferon gamma (IFN-gamma) derived from activated T cells within lesions can inhibit smooth muscle proliferation and synthesis of interstitial forms of collagen. These examples illustrate how atherogenesis likely depends on a complex balance between mediators that can promote lesion formation and other pathways that can mitigate the atherogenic process. (Aron Wolfe Siegman, Timothy W. Smith, 1994) FACTORS THAT MODULATE INHIBITATION OF ATHEROMA Elaboration of small molecules by activated mononuclear phagocytes and vascular wall cells in the evolving lesion may also modulate atherogenesis. Notably reactive oxygen species can modulate growth of smooth muscle cells, activate inflammatory gene expression via the nuclear factor kappa beta (NFk beta) transcriptional control system and annihilate NO radicals, decreasing the effect of this endogenous vasodilator. However macrophage in the lesion may be activated to express the inducible form of the enzyme that can synthesize NO, known as inducible NO synthase. This high capacity form of the enzyme can produce relatively large, potentially cytotoxic amounts of No radicals. While at the low concentrations of NO produced by the constitutive NO synthase in endothelial cells, this radical may produce beneficial effects; when overproduced by activated phagocytes, however it may prove deleterious. Export by phagocytes may constitute one response to local lipid overload in the evolving lesion. Another mechanism, reverse cholesterol transport mediated by high density lipoproteins (HDL), may provide an independent pathway for lipid removal from atheroma. This transfer of cholesterol from the cell to HDL particle involves specialized cell surface molecules such as the ATP binding cassette transporter (ABCA1) (the gene mutated in tangier disease, a condition characterized by very low HDL levels) and a family of scavenger receptors (the B family). Such reverse cholesterol transport explains part of HDL’s antiatherogenic action. (Richard O. Cannon, Julio A. Panza, 1999) Although clear evidence supports lipoprotein disorder as predisposing factors for atheroma formation, other etiologies may contribute to or modulate atherogenesis. For example hypertension constitutes an independent risk factor for coronary events. Male gender and the postmenopausal state also augment the risk of developing coronary artery disease. Premenopausal women have increased HDL levels compared to age matched men. However a favorable lipoprotein pattern only partially accounts for the protection against atherosclerosis conferred by the premenopausal state. Although laboratory studies suggest that estrogens have direct beneficial effects on the arterial wall, clinical trials have not shown that estrogen replacement therapy prevents recurrent myocardial infarction in postmenopausal women. Indeed treatment with a combination of estrogen and progesterone appears to augment cardiovascular events in women with or without prior myocardial infarction. (Susan Wilansky, James T. Willerson, 2002) Diabetes mellitus aggravates atherogenesis. In addition to the well known microvascular complications of diabetes, macrovascular disease such as atherosclerosis causes a great deal of excess mortality in the diabetic population. Diabetes associated dyslipidemias strongly promote atherogenesis. In particular the constellation of insulin resistance, high triglycerides and low HDL often in association with the central adiposity and hypertension frequently seen in type 2 diabetic patients, seems to accelerate atherogenesis potently. As noted above hyperglycemia may promote the nonenzymatic glycation of LDL, LDL modified in this manner, like oxidatively modified LDL, may signal many of the initial events in atherogenesis. Triglyceriderich lipoprotein particles often elevated in poorly controlled diabetic patients also accentuate atherogenesis. Lp(a) (often pronounced lipoprotein little a to distinguish it from apolipoprotein AI and others found in HDL) provides a potential link between hemostasis and blood lipids. The Lp(a) particle consists of an apoprotein (a) molecule bound by a sulfhydryl link to the apolipoprotein B moiety of an LDL particle. Apoprotein (a) has homology with plasminogen and may inhibit fibrinolysis by competing with plasminogen. Other risk factors for atherosclerosis related to blood clotting include elevated levels of fibrinogen or of the inhibitor of fibrinolysis, plasminogen – activator inhibitor 1 (PAI-1). Another nonlipid risk factor for coronary events, elevated levels of homocysteine, may act by promoting thrombosis, although the pathophysiology of this association is uncertain at present. Although individuals with marked elevations of Lp(a) or homocysteine do appear to have heightened risk of coronary thrombosis, in the population at large these factors show a much weaker correlation with vascular events than LDL, HDL, or the global inflammatory marker C-reactive protein (CRP). (Philip M. McCabe, Neil Schneiderman, Tiffany Field, A. Rodney Wellens, 2002) The relationship between tobacco use and atherosclerosis also remains poorly understood. The rapid reduction in risk for cardiac events after cessation of cigarette smoking implies that tobacco may promote thrombosis or some other determinant of plaque stability as well as contribute to the evolution of the atherosclerotic lesion itself. For example tobacco smokers have elevated fibrinogen levels a variable associated with increased atherosclerosis and acute cardiovascular events. INFLAMMATION In other situations, antecedent inflammatory states may predispose toward atherosclerosis. For example Kawasaki disease in childhood may promote developments of vascular lesions in the arteries of adults. Infectious agents continue to be proposed as instigators or potentiators of atherogenesis. However in humans atherogenic role for vital or microbial pathogens remains speculative. In some patients immune or autoimmune reactions may contribute to atherogenesis. In the particular example of the accelerated form of coronary arteriopathy that plagues heart transplant recipients, immunologic factors may contribute importantly to the pathogenesis. (James Shepherd, Sheperd and Gaw, Allan Gaw, 2001) Known monogenic defects in lipoprotein metabolism account for only a fraction of the familial risk for coronary artery disease. Thus other as yet undefined and perhaps multiple genetic factors may contribute to coronary risk. Mechanisms of disease susceptibility involving the arterial wall might account for some of the genetic predisposition to atherosclerosis unexplained by lipoprotein disorders. Application of molecular genetic techniques may identify new polymorphisms linked to coronary risk and may eventually shed light on new pathophysiologic mechanisms. For example some data suggest a link between certain alleles of the genes encoding angiotensin converting enzyme, the cytokine lymphotoxin, or PAI-1 with increased risk of myocardial infarction. Application of genomic technologies may aid identification of modifier genes that modulate individual responses to established risk factors. Large studies currently in progress should clarify these and other potential genetic factors that influence atherosclerosis. REFERENCES: Aron Wolfe Siegman, Timothy W. Smith, 1994. Anger, Hostility, and the Heart; Lawrence Erlbaum Associates Frank Kessel, Patricia L. Rosenfield, Norman B. Anderson, 2003. Expanding the Boundaries of Health and Social Science: Case Studies in Interdisciplinary Innovation; Oxford University Press James Shepherd, Sheperd and Gaw, Allan Gaw, 2001. Lipids and Atherosclerosis; Taylor Francis James S. C. Gilchrist, Paramjit S. (EDT) Tappia, Thomas (EDT) Netticadan, 2003. Biochemistry of Diabetes and Atherosclerosis; Springer Philip M. McCabe, Neil Schneiderman, Tiffany Field, A. Rodney Wellens, 2002. Stress, Coping, and Cardiovascular Disease; Lawrence Erlbaum Associates Pierre-Jean Touboul, J. R. Crouse, 1997. Intima-Media Thickness and Atherosclerosis: Predicting the Risk? ; Taylor Francis Richard O. Cannon, Julio A. Panza, 1999. Endothelium, Nitric Oxide, and Atherosclerosis: From Basic Mechanisms to Clinical Implications; Blackwell Publishing Rodney A. White, White A. , Ramadan Shaafi, White A. White, 1989. Atherosclerosis and Arteriosclerosis: human pathology and experimental animal methods and models; CRC Press Shari R. Waldstein, Merrill E Elias, 2001. Neuropsychology of Cardiovascular Disease; Lawrence Erlbaum Associates Susan Wilansky, James T. Willerson, 2002. Heart Disease in Women; Churchill Livingstone

The Leader of South Africa essays

The Leader of South Africa essays To be a great leader there are a lot of things that one needs to possess. Having business skills along with political and civic means are some of the ways to be established as a leader. Taking control and guiding your people through trials and tribulations shows many characteristics of leading. For South Africa that leader was a man named Rolihlahla Dalibhunga Mandela also known as Nelson Mandela. Based on his life and his political attributes Mandela was a hero to a near falling country. Mandela once stated that The struggle is my life, and he was not kidding everything that he tried or did accomplish in his life took a struggle to get it done and in the right way, the Mandela way. Mandela was born in the Transkei province in Eastern Cape pf South Africa. His father Hendry Mphakanyiswa Gadca was the chief of the Mvezo. Mandela was the first member of his family to attend school while at school he was given his English name of Nelson by his teacher. At the age of 10 his father died and he then began to attend a Wesleyan mission school. At the age of 16 he began to go to Clarkebury Boarding Institute; he completed his junior certificate in 2 years instead of the 3. Around the 1940s Mandela started his BA degree at Fort Hare University where he met and became life long friends with Oliver Tambo. After being asked to leave Fort Hare for political reasons, he moves to Johannesburg where he completed his degree with the University of South Africa (UNISA), he then received his law degree at Wits University. In 1944 he helped found the African National Congress Youth League (ANCYL), whose program of action was adopted by the ANC in 1949. Mandela than began to travel around the country organizing resistance. Following him founding the youth league he was suspended and during that time he created the M Plan where the ANC branches were broken down into underground cells. By 1952 Mandela and ...

Personal Reflection Paper Essay Example | Topics and Well Written Essays - 1000 words - 1

Personal Reflection Paper - Essay Example I was able to change my thinking from having goals of childish nature to a more mature outlook on life. The activity gave me an opportunity to compare my life goals with those of my classmates. This is critical in terms of comparing me with other like-minded and equally intellectual formidable classmates. This comparison showed me that despite my ambitious nature in terms of my life goals, there are others who are more ambitious and aggressive. It was a revelation and a challenge for me to work harder and be more ambitious in order to compete on the same level with my intellectual equals. As the exercise proceeded, I was able to reevaluate my life goals and coalesce them with a more realistic and tangible future. The defining moment for the entire exercise was the peer review section where classmates were tasked with evaluating each other’s life goals. The result of this activity was that my teammates gave me the second highest score in the entire class. It was a defining moment for me in terms of not just my self-esteem but also my general outlook on life. This event truly gave me an opportunity to evaluate and reevaluate my life goals. This activity also helped me to distinguish between the tangible life goals and what is pure fantasy. The score given to me by my classmates was evidence of the progress I am making in terms of fulfillment of my life goals. I honestly feel that I am making huge strides in the right direction, and I have a more confident approach to life and achievement. A bulk of this is fully attributed to the activity presented to us by the professor. My book club facilitation focused on chapter 6 of the book titled, "Becoming a leader" by Benis. The title of the chapter was effectively dubbed leaders perspective and desire. This activity was rather significant because I had never thought of myself as a leader. The activity was a revelation into my potential as a

R Sennett The Corrosion of Character. The personal consequences of Essay

R Sennett The Corrosion of Character. The personal consequences of work in the new capitalism. Norton 1999 - Essay Example There is no argument that change is sometimes good although often it disrupts people’s lives and may be traumatic. The bone of contention with sociologist Richard Sennett is that change and especially technological advances is the root cause of worker’s woes and the source of injuries to and corrosion of character. It has transformed the capitalist economy into a new form of â€Å"flexible capitalism† or what Sennett calls â€Å"New Economy† which is less concerned about interpersonal relationships. In Sennetts words it is â€Å"a regime which provides human beings no deep reasons to care about one another† (1999, 148). It has brought about new ways or working such as flexibility whereby jobs are replaced with projects and also involves reengineering, de-layering, downsizing; teamwork, decentralization and control; flextime; illegible work; disposablw workers and new work ethic not based on hard work like the earlier protestant ethic promoted by Max Weber. This in turn according to Sennett has brought injuries to employees as well as corroded their character as now they are unable to make a coherent narrative of their lives or build their identity around work. This essay will explore Sennett’s work The Corrosion of Character: The personal Consequences of Work in the New Capitalism to gain an insight as to how new ways of working injures and corrodes character and, whether it has made employees disposable and precarious workers and causes and consequences of such work in the modern corporation. The world of work is characterised by change. Sociologists like Jean Jacques Rousseau, Thomas Hobbes and John Locke give detailed accounts of how modern states and institutions emerged from state of nature to civilisation. In the state of nature, men hunted and gathered fruits for their sustenance. They then developed crude tools to skin animals and also for farming. With bountiful harvest and domestication of

Organizational Planning Verizon Wireless Essay Example for Free

Organizational Planning Verizon Wireless Essay Organizational Planning: SWOT Analysis for Verizon Wireless Before planning can begin, a framework should be built to guide the decision making process by identifying what the overall goal is to be. At Verizon Wireless, the mission statement, or credo, is broken into 5 sections that are the pathway for leadership within the company, as well as for internal stakeholders, to ensure the success of the company. Verizon Wireless identifies strengths as being a high quality provider of communications services, being committed to customers through teamwork, and acknowledging that just being the biggest is not the same as being the best. By identifying weaknesses such as being reactive to competitor offerings, pricing structure of plans, and the perceived lack of a global presence, reviewing the credo can initiate change to address these weaknesses and create opportunities from them. Identifying the opportunities of network infrastructure growth, simplification of pricing plans for both businesses and consumers, and providing varied equipment pricing options allow the company to address some of the weaknesses. Threats are identified as competition from other providers, market penetration for services, and proposed regulations from the F.C.C. with regard to net neutrality. As a whole, these identified areas provide the roadmap to achieve success for both the internal and external stakeholders. When setting a long term goal, or strategic plan, the credo is consulted to ensure that the areas identified in the SWOT are being addressed. With a strategic plan in place, Verizon Wireless can set long term goals on how they plan to broaden their strengths, lessen their weaknesses, capitalize on their opportunities and minimize the threats. One of these strategic plans in place is to grow market share by gaining additional customers. Long term growth of customers is fundamental to the longevity of the company. Without new customers the company becomes stale and profits may fall. Both the internal and external stakeholders would be unhappy if Verizon Wireless did not provide a value to them either  monetarily or through the service itself. Review and confirmation of programs being offered to customers is constantly being revised as changes within the marketplace dictate. This long term strategic planning will be fluid as the needs of the customer change. An operational plan has a shorter time line to achieve the goal. The target of initiating new growth through new products and service can be accomplished through the Verizon Wireless Partner Program. The adoption of new technology and integration of devices ensure Verizon Wireless to achieves this goal going forward by partnering with companies to provide equipment and services. According to Partnerships Verizon (n.d.), Verizon’s award-winning Partner Program focuses on better serving the needs of customers by enabling them to simplify how they consume communications and IT services in a way that best meets their needs, while giving them access to the full Verizon portfolio. Whether teaming with Verizon directly, indirectly through program members, or as a hybrid, customers can take advantage of Verizon’s next-generation services portfolio.† (2). These types of partnerships build from the commitment that Verizon Wireless has stated, â€Å"We hold ourselves to a very high standard of performance. We prize innovative ideas and the teamwork it takes to make them happen. We never stop asking ourselves how we can make the customer experience better, and every day we find new answers.† (Commitment Values, n.d.) In this operational plan, the internal stakeholder is satisfied because the company is initiating new growth, and the external stakeholder is satisfied because the new products and services are providing additional revenue. With both strategic and operational plans in place, Verizon Wireless is poised to achieve success in both the near term as well as far into the future. Reference Verizon Wireless. (n.d.). Commitment Values. Retrieved 2/28/15 from http://verizonwireless.com/about/commitment-values Verizon Wireless. (n.d.). Partnerships Verizon. Retrieved 2/28/15, from http://www.verizon.com/about/our-company/partnerships/ (2)

the simpsons :: essays research papers fc

When Matt Groening and James L. Brooks created The Simpsons, a cartoon, family, they had no idea that it would become as big as it has now. There are many reasons the show has become very popular with the American public. Dumb and simple humor makes in enjoyable for people on all levels, and for the more sophisticated audience, there is some political satire in the show. It all started 1987, when Groening and Brooks created short cartoons for the Tracey Ullman show. If you were to compare these shorts to today’s show, there is a major difference in the quality of the show and the plots. This is due to better technology, more money, and a change in the things that can be said on television. (Groening) The show features five main characters. As stated by the show’s title, they are the Simpson family. The father, Homer, has had a very eventful life. Even though he is not very smart, he has led a life that is envied by many in Springfield. His job is the Nuclear Safety Inspector at the Springfield Power Plant. He has met presidents Gerry Ford, George Bush, and Bill Clinton, been an astronaut, and met bands such as the Who, the Smashing Pumpkins, U2, the Red Hot Chili Peppers, and REM, been a professional baseball mascot and numerous other jobs. His wife Marge has not led as an exciting life as Homer. She spends most of her time taking care of their three children, Bart, Lisa, and Maggie, and playing second fiddle in many of Homer’s adventures. Bart has become a 1990’s version of Dennis the Menace. He carries a slingshot in his back pocket and likes to cause havoc for his teachers and his father. Lisa is the brightest of the children. She has straight A’s i n the second grade, plays first chair saxophone, but is more like her mother, not getting involved in many adventures. Maggie is the baby and is mostly there to complete the family. (Holtz) The first full length episode was on December 17, 1989. This was the Christmas special entitled â€Å"Simpsons’ Roasting on an Open Fire.† The plot of this episode is that Bart gets a tattoo and Marge has to spend the family’s Christmas money getting it removed. She planned on having Homer’s Christmas bonus to buy presents with but he finds out that bonuses won’t be given out that year.