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Mad Cow Disease: Governmental and Media Culpability, 2002.
A discussion of the discovery of mad cow disease, to the present, and the role the media/government has played in control, prevention, and the dissemination of information.
2,000 words (approx. 8.0 pages), 8 sources, MLA, $ 63.95
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Abstract
Examines the treatment of Mad-cow disease in the media, and by the government.
Discusses the following topics
Bovine Spongiform Encephalopathy and Scrapie
What Transmissible Spongiform Encephalopathies Do
Two Theories on the Action of Transmissible Spongiform Encephalopathies
British Government Admits Mad Cow Disease Exists (1987)
Testing Results by the British government MAFF
Culpability of the British Medical Society
The Spread of CJD
Steps Taken by the British Government
From the Paper
"Where the industry has gone wrong is in listening to the PR people. The mad-cow epidemic is not an information management issue?it is a disease that will not go away.? These words are from an interview with Dr. Pringle, a member of the Sperling Biomedical Foundation, and the founder of www.mad-cow.org. I believe that they highlight what has been fundamentally wrong about the treatment of mad-cow disease by the British government and the British media. Several grave errors have been made about the treatment of this issue, and they continue to have repercussions today, as we explore America?s mad-cow incidents, and rising problems in Europe, Asia, and South America. At the time this paper was written, mad cow disease had been confirmed in domestic cattle in Belgium, France, Ireland, Liechtenstein, Luxembourg, the Netherlands, Portugal, Switzerland, Spain and Germany."
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Mad Cow Disease and McDonald's, 2002.
A look at the efforts made by McDonald's to educate the public on the dangers of Mad Cow Disease .
1,150 words (approx. 4.6 pages), 5 sources, $ 44.95
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Abstract
This paper assesses the issue of advertising safety precautions for Mad Cow Disease from the position of a campaign manager for McDonald's customer service division. This paper will take the position that the public would remain loyal to McDonald's after efforts are made to educate them concerning mad cow disease.
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Mad Cow Disease, 2004.
An analysis of anticipated increases in business stock prices due to impact of mad cow disease on U.S. cattle.
1,816 words (approx. 7.3 pages), 5 sources, MLA, $ 58.95
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Abstract
The paper intrinsically studies the consequential affect and aftermath of ?mad cow disease?, which has led to the introduction of substitutes like pork and other meats in the market. It further studies the changing trends that many of these companies have incorporated in attempt to sustain and raise their profits from these substitutes. It looks at how studies show that integrating certain changes to the companies marketing mechanism and strategies on the eve of ?mad cow disease? have been successful, not only to replenish the sales figures, but also in incurring profits.
From the Paper
"The Other areas where consolidation occurred were the packing and retail industries. In an attempt to regain their market hold various leading food giants are vying to increase their sales and are introducing new trends. The four major companies, which followed the same suit, were Smithfield Foods, IBP, Swift (Conagra) and Excel (Cargill). In 1998, the four-firm concentration level was 56.3% of the packing sector. They contributed to the slaughter of more than half of the nation's hogs. Now Smithfield is the world's largest pork producer and kills an estimated 20% of the United States' hog supply. It considered itself as an integrated food company. Eventually owned the third largest hog producing firm in the US and also had been tightly coordinating with other large producers."
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Mad Cow Disease, 2004.
This paper discusses mad cow disease, a virulent cattle disease, which led to the destruction of 180,000 livestock in the United Kingdom and other European countries and plunged other major cattle-producing nations into a global panic.
1,500 words (approx. 6.0 pages), 8 sources, MLA, $ 49.95
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Abstract
This paper explains that mad cow disease is bovine spongiform encephalopathy, or BSE, a fatal brain disorder in cattle caused by a still-unknown agent. The author points out that U.K. reports also listed other animals as having been infected by TSEs, including domestic cats, mice, hamsters, goats, mink, monkeys, pigs, and some exotic species of the cat family. The paper reports that there is also suspicion that mad cow can be spread through human blood; therefore, the American Red Cross bans blood donations from people who have lived abroad, especially from those who spent as few as three months in the UK between 1980 and 1996.
From the Paper
"The disease spread to cattle in other countries through infected animal feed UK exported to them within that decade. These countries in Europe alone included Belgium, Canada, the Czech Republic, Denmark, France, Germany, Greece, Ireland, Italy, Luxembourg, Liechtenstein, the Netherlands, Portugal, Spain and Switzerland (Lohn), which were reported to have at least one infected cow each. The UK also supplied animal feed to South Africa and non-European countries at that time, extending the reach Mad Cow beyond Europe and making it a global health scare."
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Mad Cow Disease, 2007.
An analysis of the epidemiology, pathophysiology and prevention for Mad Cow Disease (known as Creutzfeldt-Jakob disease in humans).
1,445 words (approx. 5.8 pages), 10 sources, MLA, $ 47.95
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Abstract
This paper discusses Mad Cow Disease, otherwise known as Bovine Spongiform Encephalopathy or as Creutzfeldt-Jakob disease in humans. It discusses the history, background and pathophysiology of the disease. It then goes on to describe prevention and treatment options for the disease, concluding that there are no effective treatments available. The paper concludes by discussing nursing and collaborative care for patients with the disease.
Table of Contents:
Epidemiology
Pathophysiology
Prevention and Treatment
Differences in Classic CJD and Variant CJD
Nursing and Collaborative Care
From the Paper
"Variant CJD has a median age at death of 28 years. The duration of the illness is approximately 13-14 months. Some of the clinical signs and symptoms include: prominent psychiatric/behavioral symptoms, painful dyesthesiasis; and delayed neurologic signs. The "Pulvinar sign" on an MRI is present in greater than 75% of most of the Variant CJD. The presence of "florid plaques" on neuropathology is usually in large numbers and easily detected. The agent is readily detected in the lymphoid tissue. There is a marked accumulation of protease-resistance prion protein noted in the brain. This is why the Variant CJD is much more easily detected because it shows up on more tests."
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U.S. Fast Food and Mad Cow Disease, 2004.
Examines mad cow disease and how fast food companies are responding.
690 words (approx. 2.8 pages), 2 sources, APA, $ 23.95
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Abstract
This paper examines a 2004 Wall Street Journal article on mad cow disease, and how companies, especially fast food companies, are responding to the possibility of tainted meat. It uses the example of McDonald's.
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Mad Cow Disease, 2006.
An overview of this brain disease which affects cattle and humans.
857 words (approx. 3.4 pages), 4 sources, MLA, $ 30.95
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Abstract
Mad Cow Disease is a brain disease of cattle, which was first identified in the United Kingdom in the mid-1980s. Although not as widespread as some other livestock diseases, such as hoof-and mouth-disease, the Mad Cow Disease has attracted a lot of publicity because of its apparent apparent ability to transmit to humans, the fact that there is no known cure for the disease and the horrifying nature of the brain decay it causes. This paper explains the cause of the disease, how it affects the organisms, how it is transmitted from one organism to another, and the ways in which it could be transmitted to humans. The paper also discusses the human equivalents of the disease.
Paper Outline:
Cause of the Disease
How the Disease Affects the Organism
How is the Disease Transmitted from one Organism to Another
The Ways in Which it Could be Transmitted from Cows to Humans
Human Equivalents of the Disease
Works Cited
From the Paper
"This theory about the spread of disease is based on the observation that incidences of the disease have mostly been found in the UK where feeding of meat and bone meal to cattle was most common. Although other European countries also fed meat and bone meals to cattle as a protein supplement, the British laws about high temperature sterilization of the protein meal were relatively lax in order to keep meat prices competitive."
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Mad Cow Disease, 2005.
An overview of the causes, treatment and prevention of Bovine Spongiform Encephalopathy (BSE).
1,438 words (approx. 5.8 pages), 7 sources, MLA, $ 47.95
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Abstract
This paper examines how Bovine Spongiform Encephalopathy (BSE) is a neuro degenerative disease in a class of diseases known as Transmissible Spongiform Encephalopathies (TSE's). It looks at how BSE is caused by prions, which are related to several other TSE's and how it has been a major concern with the economy and human and animal health worldwide together with political policies. It also explores how testing, diagnosis and prevention of BSE and other TSE's are still under investigation.
From the Paper
"vCJD also affects humans, but differs from CJD. Symptoms include depression, mood swings, anxiety, withdrawal, hallucinations, delusions, parasthesia ("pins and needles"), headaches, cold extremities, lack of coordination, loss of memory, loss of concentration, inability to talk or move, and results in death after 7-24 months, averaging 14 months.(7) It affects people ages 8-14.(7) 156 confirmed or probable cases have been reported worldwide as of April 2004. 146 of these cases were reported in Great Britain, 6 in France, and one in each Italy, Ireland, United States, and Canada. (7)Treatment for this disease includes chlorpromazine and quainacrine, but only experimentally."
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Mad Cow Disease, 1996.
Bovine spongiform encephalopathy. Causes, symptoms, effects on humans, British govt. & public reaction to outbreak, economics.
1,350 words (approx. 5.4 pages), 7 sources, $ 47.95
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From the Paper
"Many people claim that they want less government. In the case of Great Britain's problems with "mad cow disease" this is exactly what they got. Yet few people can be pleased. On March 20, 1996, the United Kingdom Health Minister announced that ten relatively young people had died of a very rare brain disease, Creutzfeldt-Jakob disease (CJD), that generally attacks only a very few elderly people. The minister reported that "the most likely explanation at present is that these cases are linked to exposure to bovine spongiform encephalopathy (BSE) or mad cow disease (Bonte-Friedheim A10). This is tragic and alarming but it is also outrageous. BSE has been a serious problem for Britain for a long time yet "for a decade [the Conservative government] has dismissed concerns raised by some scientists that humans could contract the disease by eating the meat of diseased..."
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Prion Disease in Humans, 2005.
An overview of Mad Cow Disease and how it has benefited the medical world.
1,636 words (approx. 6.5 pages), 5 sources, APA, $ 53.95
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Abstract
Ever since Mad Cow Disease sparked terror in international headlines, the public has been concerned about eating beef. Mad Cow Disease is not, however, the first or only prion-caused disease. Several others, including Creutzfeldt-Jakob Disease (CJD) and kuru in humans and a host of agricultural animal disorders join Mad Cow in both cause and effects, the major effect being horror. This paper argues that, while the presence on the planet of a disease that literally lays waste to human brain tissue is frightening, there are two probabilities that can be seen as reasons not to be terrified. Instead, people could be hopeful that research sparked by the publicity surrounding Mad Cow Disease will eventually bring answers to such sociologically and medically devastating diseases as Alzheimer's Disease, and other lesser known but just as deadly diseases such as Lou Gehrig's Disease. The paper shows that these two probabilities are first, that prion-caused diseases are much less prevalent than media hype would indicate and, second, that a cure or vaccination is relatively certain to be discovered in the near to medium term.
Paper Outline:
Introduction
Methods
Discussion
Conclusion
References
From the Paper
"Questions have arisen regarding why these particles are not attacked by the body's defense mechanisms, and the answer, Mahy noted, is that they are so odd, they are simply not recognized and therefore cannot be neutralized. Prions contain no nucleic acid and are therefore extremely " extremely resistant to inactivation by chemical or physical interventions that would inactivate viruses" (Mahy 1998) because there is no vector through which to deliver the 'poison'. Even more so than viruses, then, it is reasonable to wonder whether prions are, in fact, alive. And if they are not alive, then how can they infect an organism? Do they replicate like bacteria and viruses, or what?"
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| Term Paper # 75067 |
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Non-Governmental Organizations and Inter-Governmental Organizations, 2003.
An analysis of the role of non-governmental organizations and inter-governmental organizations in post-conflict reconstruction of developing nations.
1,965 words (approx. 7.9 pages), 40 sources, APA, $ 62.95
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Abstract
This paper provides an overview of non-governmental and inter-governmental agencies, followed by an analysis of the different issues that can adversely affect the post-conflict reconstruction process. A summary of the research and relevant findings are provided in the conclusion.
From the Paper
"Conflicts among people represent one of the main problems around the world today. People continue to become embroiled in violent confrontations practically everywhere because of religious, racial or political differences. Often the parties in conflict are unable to resolve these fundamental differences, and the governments involved are either unable or unwilling to assist in the process. It is vitally important, therefore, that appropriate nongovernmental organizations and intergovernmental organizations understand the processes involved and the effects of their activities on the people they are trying to help."
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Minamata Disease.
This paper discusses Minamata Disease, a serious neurological disorder, and the first in which environmental pollution was transferred to food.
1,285 words (approx. 5.1 pages), 6 sources, MLA, $ 43.95
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Abstract
This paper explains that Minamata Disease, a poisoning disease of the central nervous system caused by methylmercury compound, which is discharged from factory effluent, polluting the environment and then, through the food-chain, accumulated in fish and shellfish. The author points out that, at first the Japanese government denied the relationship of the factory discharge and the illness, putting the needs of the factory above the well-being of its citizens and environment; but in 1969, well after the polluting production process had been shut down, the area was designated a protected marine area by the government, requiring that no waste-water containing methylmercury be released into it. The paper relates that the Japanese government has taken measures to prevent this from happening again; compensation settlements have been reached, and today, the national government is the body that certifies a person as being afflicted by the disorder.
Table of Contents
Introduction
Discovering Minamata Disease
A Deadly Disease
Significant First
Understanding the Disease
Governmental Involvement
Political Settlements
Continuing Lawsuit
The Disease Today
Conclusion
From the Paper
"The first case of Minameta Disease was reported in 1956, "in Minamata City located on the Yatsushiro Sea coast in Kumamoto Prefecture, in a patient suffering from neurological symptoms of unknown cause." This case led Minameta City to immediately develop the Committee on Unknown Disease to take measures against the patients and investigate to find the cause. The investigation was conducted mainly by Kumamoto University, and in November 1956, the university reported that the disease is a certain type of heavy metal poisoning transmitted via fish and shellfish. Since knowledge and experience about environmental pollution were not enough at that time and technology for analysis of very small amounts of chemical substances was insufficient, a great deal of time was required until the cause was made clear."
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Causes of Alzheimer's Disease, 2000.
A scientific paper on Alzheimer's disease. A discussion of the disease and an in depth look at its causes.
2,070 words (approx. 8.3 pages), 25 sources, $ 65.95
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Abstract
This review of Alzheimer?s disease (AD) focuses on the various causes of the disease. It is a compilation of material gathered from various scientific journals. The review begins by giving an introduction of AD followed by a discussion of various factors believed to cause AD, such as: amyloid plaques, neurofibrillary tangles, apolipoprotein E, and genetic factors. The author concludes by stressing the need for more research into the causes of AD.
Introduction
Overview of Alzheimer?s Disease
Pathological Causes of Alzheimer?s Disease
Amyloid Plaques
Neurofibrillary Tangles
Genetic Factors in the Development of Alzheimer?s Disease
Chromosome 19 and Apolipoprotein E
Other Genetic Factors
Presenilin
Conclusion
From the Paper
"Alzheimer?s disease (AD) is a neurodegenerative disorder characterized by progressive memory loss and dementia. The precise mechanisms that cause AD are still unknown, however, certain factors that predispose individuals to Alzheimer?s disease have been identified. Although no definitive cause has yet been discovered, this article reviews current research into various possible causes of AD, including the pathological causes, such as amyloid plaques and neurofibrillary tangles. Also the genetic factors that cause AD, such as apolipoprotein E (apoE) and presenilin gene."
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Alzheimer's Disease, 2006.
A review of Alzheimer's disease, discussing the history, symptoms, treatments and issues related to the disease.
2,171 words (approx. 8.7 pages), 9 sources, MLA, $ 67.95
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Abstract
This paper takes an in-depth look at Alzheimer's disease, a degenerative brain disorder that was first identified in 1906 by Alois Alzheimer. This disease represents the single most prevalent form of brain disorders and is also the leading cause of dementia, affecting approximately 4.5 million people in the Untied States. The paper provides a brief overview of the disease, the symptoms, the diagnostic procedures and the treatment methods in order for us to gain a better understanding of this degenerative brain disorder.
Outline:
Introduction
Alzheimer's Disease
Early and Late onset Alzheimer's Disease
Symptoms of the Disease
Memory Loss and Language Disorder
Depression
Dyspraxia and Agnosia
Diagnosis
Tests for Cognitive Impairment
Positron Emission Topography
Major Causes of Alzheimer's Disease
Amyloid Plaques
NeuroFibrillary Tangles
Metal ions
Treatment Methods
Restoring Cholinergic Transmission
Anti-inflammatory Drugs
Conclusion
From the Paper
"Considerable reduction in cholinergic transmission is one of the primary causes for the loss of memory and other associated symptoms of Alzheimer's disease and other kinds of dementia. Hence pharmacological treatment for AD mainly revolves around rectifying this circulatory deficit within the brain. Compounds designed to enhance cholinergic transmission constitute an important part of the treatment plan. Acetylcholine the neurotransmitter of the brain is considerably broken down in-patients suffering from AD and other dementias. The underlying mechanism of the neurotransmitter can be simplified as follows. An electrical impulse generated passes along the nerve and when it reaches the end it triggers the release of chemical messengers known as neurotransmitters, which in turn diffuse along the synaptic cleft and react with the specific receptor sites on the organ. Activation at the receptor junction initiates a series of chemical reactions resulting in a specific biological response. "
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