Journal 8 Essay Example | Topics and Well Written Essays - 500 words

Journal 8 - Essay Example metaphor, irony, and oxymoron, that the political is also poetic, wherein the poetic confirms the death-denying ideologies of people through the oxymoron of a silent poet. â€Å"What He Thought† uses enjambment to depict that political actions are poetic, in the sense that they reflect the innermost emotions, which are present in Flight from Death: death anxiety and the need to safeguard death-denying ideologies. The studies in the film, which aim to prove the influence of death anxiety on human attitudes and behaviors, establish that, when reminded of their death, people tend to support more those who are similar to them. One of the enjambments in â€Å"What He Thought† helps American poets connect to Italian poets: â€Å"†¦Among Italian writers we/could recognize our counterparts: the academic,/the apologist, the arrogant, the amorous,/the brazen and the glib† (McHugh 11-14). The American poets are not comfortable with differences because they will fear the Italians as potential reminders of death, so they seek to find similarities between them as much as possible. Furthermore, identifying similarities should go beyond havi ng the same interest in literature, but also in politics, because politics is an important way of affirming life. McHugh’s inclusion of the German suggests historical differences between American and German politics: â€Å"where it must have been abandoned by/the German visitor (was there a bus of them?)†¦Ã¢â‚¬  (27-28). The enjambment suggests a tone of superiority against the Germans, as if a bus of them is an affront to a bus of Americans. These enjambments emphasize the need of poets to be related to fellow poets, or else they will feel conscious of linguistic, political, and cultural differences, differences that remind them of their deaths. Aside from enjambment, McHugh uses metaphors and irony to illustrate the clashes that arise from the interaction between different death-denying beliefs. The metaphor of God as something that is

Professional Athletes Essay Example for Free

Professional Athletes Essay Companies that use professional athlete have the right to use that endorsement at their discretion. This question is difficult to answer as a whole because there are so many factors that occur. When it comes to a contract or obligation the bylaws of such agreement can lend both parties to not fulfill the agreed terms. Most athletes are held to a standard that is based upon their role in their specific sport. The star or leader is usually held in higher regard than the 12th man on a team. With that said the argument for companies comes from a different perspective so its lends one to speak from both sides of the argument. I have to take the affirmative for the companies even though I believe in the marketability of the professional athlete. In the case of Micheal Phelps his ability to perform at a high level has led directly to the rebound of his image. Tiger Woods on the other had way more to lose at the time of his marital problems. In turn his on course performance has not been at the level in which we are use to seeing of him. He has no amassed the same fervor or attention for positivity as a Micheal Phelps. The bad play on the course as not lifted the stain of all the negative press that he garnered. Had he been even more successful on his playing field he more than likely would have been able to get companies to get back on the Tiger train. Companies, tend to use athletes that match their persona, the bigger the name the bigger the company. Image is so important to what a company is trying to convey about its product and service. Most companies have their values listed somewhere near their corporate profile. The two have to match. The values of a company must meet the value that is percieved the by the value of the product. The best and most current case of this is with Lance Armstrong, his Livestrong Foundation and Nike have distances themselves from Lance. He was a very visible and outspoken spokesman, he had a following  that added to his legend on an almost daily basis. The findings that there was unanimous evidence that he was using PEDs (Performance Enhancing Drugs) to win in his sport was detrimental to not only his incredibility but it clings to a company like Nike being a company built on the athletic prowess of athletes from a varied amount of sports. So as a company what do you do? You have no choice but to cut ties with this athlete not just because he lied but the implication can be made that Nike and its athletes also lie and use PEDs. You cant blame a company from wanting to distance its brand from that of a liar and cheater. In a different effect the Livestrong Foundation has a separate delimma to look at aside from the moral issue. They have a financial conundrum that affect the legacy of what Lance did for cancer and cancer research. The livestrong bands that are so popular in our community, were marketed to people on the basis that the proceeds from the sale of the bands go to the fight against cancer. People that associate Lances image struggle with his Foundation have become outraged. Here it is, this â€Å"winner† who was at the pinnacle of his sport lied on top of lying he cheated. He used his acclaim and sickness to capitalize on a disease and in turn not only made money for the foundation but also lined his pocket. The only recourse it seems the foundation had to take is to severe ties. Companies have a obligation to their shareholders, They have a obligation to their employees as well. The obligation to the shareholders and employees comes in the form of profit and money. Imagine if your brand is built on honesty and integrity. Your marketing and advertising say you are honest but your commercials have a Tiger Woods or Lance Armstrong there is a clear distinction that these two athletes have had trouble with honesty. The audience can then place your brand with dishonesty which can lead to losing business. As a bottom line all companies want to make money. You tend not to do things on a consistent level that contradict the reason why most businesses go into business, to make money! Performance is also a factor in whether a company will give an endorsement to an athletes. We are a culture that tends to use the what have you done for me lately concept when it comes to our professional athlete. Businesses also use this practice to capitalize  on the success and marketability of an athlete. If there was a ethical issue the easiest way for that athlete to get the endorsements back or to gain new is to win. Winning is the cure for any image problems because it covers up the moral and places emphasis on the practical. In the case of Peyton Manning, Buick comes to mind. He did not play in the NFL in the 2011 season. He suffered tremendous neck injuries that put his playing future in jeopardy. He lost several endorsement deals not because he had a moral issue, in fact he is one of the top professional athletes in the world when it comes to image. In 2012 he was picked up but another team and that team has been success, Buick looking for a spokesman to embody the brand of Buick they went with Manning. He was not high on their list they dropped Tiger and needed to find a spokesman that matched the brand. Companies have to make the decision to drop or keep an athlete based on so many factors. The need to satisfy the bottom line and the customer is always a hard task. The hardest part is picking the right spokesman that can push the brand, product or service. It is hard because these athletes have personal lives, these athletes are human, they make decisions at times without thinking about what company has paid them to speak about their product. The company has to make sure that they include language in the contract that can help the athlete make inclusive decisions. The moral clause is always a good way for a company to protect itself from the damage that can happen when favorable decisions are not made by an individual. It is up to the athlete to make sure he wants to keep the money and fame that can come from being on commercials and in ads by Fortune 500 companies. I feel as though they do not think about the overall consequences of their actions or how it may affect their decisions. This is where the company comes in and can make up for that. Its egoism from both sides. A athlete can act unbecoming and lose it all but due to great performances he can redeem his career. While the company can extend a 2nd chance allowing the athlete to be in the public eye again. Its a line that both have control over but in the world of business and sport the lines are so often blurred. In the end the companies have the right to giveth and the right to taketh away.

Neurotransmitter Serotonin Cause Depression Psychology Essay

Neurotransmitter Serotonin Cause Depression Psychology Essay According to the World Health Organization, about 121 million people across the globe suffer from depression and the WHO has ranked depression as fourth in a list of most urgent problems worldwide (2). It is the most prevalent psychiatric disorder and is responsible for nearly 850,000 deaths every year. Supporting this fact, statistics have revealed that the use of anti-depressants has soared over 400 percent in the past two decades (3). According to Kresser, a licensed acupuncturist and practitioner of integrative medicine, several chemically distinct anti-depressants marketed under trade names such as Prozac, Zoloft, and Paxil now enjoy immense popularity as anti-depressants (4). Amongst the four classes of anti-depressant medication, namely selective serotonin reuptake inhibitors (SSRIs), atypical depressants, tricyclic anti-depressants (TCAs) and monoamine oxidase inhibitors (MAOIs), SSRIs have been the most widely prescribed medication by physicians. In this essay, the terms S SRI and anti-depressant will be used interchangeably. The current model of SSRIs assumes that a low level of extracellular neurotransmitter, serotonin, is primarily responsible for depression. Serotonin in our body can be found in two places 80 percent of it in our gastrointestinal tract while the rest in our brain (5). The 80 percent of serotonin function as hormones and they play a role in muscular contractions whereas the 20 percent act as a neurotransmitter in our brain (6). In our brain there are many cells called neurons, which are separated by small gaps. Messages carried by neurotransmitters are delivered from one neuron to another across the gaps. These messages come in the form of chemical impulses, and contain information about mood, behaviour, body temperature, appetite and sleep. Once a neurotransmitter leaves the sending neuron, it will latch onto the receiving neuron and relay chemical impulses over. Then the neurotransmitter returns to its sending neuron to be re-used again this process is called reuptake. On the other hand, if there are inadequate amounts of neurotransmitters, the next impulse does not fire off and messages will not be relayed. (7) SSRIs work to block or slow down the reuptake of serotonin in particular, hence increasing the amount of extracellular serotonin. As a result, more serotonin are present in the gaps which will increase rate of successful transmission of impulses to the receiving neuron. SSRI is hence engineered on the belief that serotonin is the cause of depression. However ever since the advent of the drug and its side-effects exposed, drug researchers are compelled to re-investigate the efficacy of SSRIs, in which confounding results were revealed. The investigation into the serotonin-depression link will not only prevent doctors making inappropriate prescriptions that may not be in the best interest of their patients health, it also allows a clearer definition of the causes of depression. Ultimately, establishing the proper function of serotonin may lead to a ground-breaking change in the methodology of treating depression and related disorders in the psychiatric and pharmacology world. While most people concur with the belief that a deficiency of serotonin is related to depression, some argue that an imbalance in serotonin levels leads to depression. This imbalance theory arises because of the widespread notion that SSRIs are only effective for patients with moderate to severe depression while it is ineffective for mildly depressed patients. The basis of the debate surrounding the efficacy of SSRIs in fact boils down to a deeper problem whether or not the neurotransmitter, serotonin, is related to depression at all. Nevertheless, I oppose both claims of the serotonin-depression link and contest that there is no coherence between levels of serotonin and depression. Up till now, there have no substantial evidence that depression is caused by serotonin deficiency, neither is there one that shows that over stimulation of serotonin causes depression. Efficacy of SSRIs challenged by small drug-placebo difference Many studies have shown that the efficacy of SSRI drugs in the treatment of depression is challenged by low drug-placebo difference scores. Studies to investigate the efficacy of anti-depressants by giving placebos to a controlled group have revealed that the recovery rate of patients who took a glucose pill was equivalent to patients who consumed the anti-depression drug (8). A 2008 meta analysis of the efficacy of SSRIs that was published by the Food and Drug Administration (FDA), revealed that these anti-depressants have no clinically significant edge over all placebos. By this, it means that it did not meet the drug licensing authority, UK National Institute of Clinical Excellence (NICE) standards. As evident in the meta analysis, the placebo response groups account for up to 75 percent of all positive effects of anti-depressant medication (9) which shows that 3 in 4 of all patients who reported an increase in heightened emotional well-being were actually consuming sugar pills. O ther studies yielded similar results a study by Khan et al. found a 10 percent difference in level of symptoms when patients consume the inert placebos compared to the active drugs in two separate meta-analyses (10). As the drug-placebo difference is small, it can be seen that regardless of whether SSRI is administered or not, symptoms of depression are still greatly reduced. This implies that serotonin level may not be related to depression at all. Opponents argue that experiments to test the efficacy of SSRIs against inert placebos may not be accurate because the side effects of SSRIs are not mimicked. They claim that commonly known side effects of SSRIs, such as diarrhoea, nausea, dizziness, headaches or even gastrointestinal bleeding (11) may affect patients mood, which in turn underrate the impact of serotonin in lifting depression. This claim is however rejected by many scientific literatures which show counter-evidences. According to Joanna Moncrieff, the co-chair person of Critical Psychiatry Network, when she used active placebos to simulate the adverse-effects of SSRIs in anti-depressant drug trials, results revealed that differences between active placebo and SSRI were significantly small (12). To measure severity of depression before and after the drug trials, the conventional Hamilton Rating Scale of Depression (HRSD) was used. Since it did not meet NICE standards of an improvement in rating score of 3 points to be defined as clinically significant (8), the above studies involving inert and active placebos clearly show that no matter which placebo type was administered active or inert, drug versus placebo significance in anti-depressant efficacy is clinically insignificant. Whether or not the level of serotonin is increased, patients reported a reduction in symptoms of depression, therefore there is little evidence to say that a lack of this neurotransmitter causes depression. Another common belief by proponents of anti-depressants is that initial severity of depression is directly related to the effectiveness of SSRIs, that SSRIs work best for patients with very severe depression. It is thought that over stimulation of serotonin may cause further chemical imbalance in patients suffering from mild depression, hence rendering SSRIs ineffective (13). Thus in order to test this claim, Kirsch et al moved on to investigate whether initial severity of depression affects the efficacy of anti-depressants. He tested on the hypothesis that anti-depressants work only for people suffering from moderate to major depression. In this double-blinded study of 35 clinical trials involving 5,133 subjects, both drug administers and subjects were unknown to results of randomized medication (placebo or SSRI) to prevent sampling biasness and subjects severity of depression was measured by HRSD (14). The test was conducted to see if there is an improvement in the subjects depress ion, measured against their baseline severity and the final conclusion is as follows: patients with an initial moderate depression did not report a drug-placebo difference, patients with an initial severe depression reported a relatively small drug-placebo difference and only for patients situated at the upper end of very severe depression category did the drug-placebo difference fall into the clinically significant criterion by NICE standards (8). Although effectiveness of SSRIs may seem to improve with the severity of depression, further research has revealed a negative coherence between severity and placebo response. As highlighted from Figure 1, the drug-placebo difference reached clinical standards for people with a higher initial severity of depression. Further analysis shows that a higher drug-placebo difference is due to a decrease in improvement of the placebo group rather than due to the effects of SSRIs. Figure 1. Mean Standardized Improvement as a Function of Initial Severity and Treatment Group, Including Only Trials Whose Samples Had High Initial Severity graph.png Source: http://www.plosmedicine.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pmed.0050045.g003representation=PNG_M This implies that the increased benefit for extremely depressed patients seems attributable to a response-deficiency to placebos rather than a heightened response to SSRI medication. Therefore efficacy of SSRI does not increase with severity of depression and increasing amount of serotonin did not work for patients with all levels of depression. Since SSRIs are designed to alleviate depression by inhibiting the reuptake of serotonin in our brain cells, it shows that there is no relationship between extracellular serotonin and ones mood. Furthermore, it usually take weeks before effects of anti-depressants are expressed and can be measured by testing for serotonin levels in the blood, yet patients often report relief within hours or days of medication. Therefore this phenomenon demonstrates the lack of correlation between serotonin and depression and gives support to the placebo effect. The lack in correlation is further evidenced by the results of a Force Swim Test (FST). FST, also known as the behavioural despair test, is a conventional anti-depressant screening test which involves using rodents as test subjects. In this test, rats are dropped in an enclosed water cylinder and their movements observed. The struggling time of rats is measured based on the assumption that immobility of rats is directly proportional to their state of depression. For example depressed rats will cease trying and float in the cylinder, which is akin to despair, whereas non-depressed rats will continue to struggle in search of a way out (15). Although it is thought that SSRIs should extend struggling time of rats, final results were inconsistent hence inconclusive (16). The administration of SSRIs in rodents did not make them less susceptible to depression, displaying no direct relationship between serotonin and depression. Nonetheless, it should be noted that experiments done on mice ma y not be entirely accurate in predicting responses in humans (17). The bold assumption made by researchers The serotonin-depression link came about when scientists first discovered that in most depressed patients, the level of serotonin is comparably lower than that in non-depressed people. The amount of serotonin in a humans body was measured by comparing blood samples taken from depressed and healthy people. Subsequently the anti-depressant SSRI was invented, which targets the neurotransmitter serotonin and works to stimulate the production of it. This methodology then raises a few doubts. Firstly, the assumption that blood serotonin and brain serotonin are directly proportional can be contested as it is certainly impossible to measure the amount of serotonin in the brain. Patients who have high levels of serotonin in the blood may have low levels of serotonin in the brain and vice versa. As mentioned earlier, 80 percent of the humans body total serotonin is found in our bloodstream and the rest in the brain. While the level of blood serotonin can be measured, current biomedical technol ogy has yet to transcend the brain barrier. In all clinical trials involving SSRIs, the assumption made is that blood serotonin reflects brain serotonin, which is a very bold one to make. This then creates a paradox in research methodology: the reason for inventing SSRIs instead of feeding serotonin directly to a humans body is due to the blood-brain barrier. Orally ingested serotonin are ineffective as they do not pass through bloodstreams into the brain, that is the digestive system is unparallel to the central nervous system. Whereas SSRIs work because they merely seek to enhance an impulse that is already present, but too feeble to cross the gap. Yet scientists conveniently established a link between serotonin and depression by measuring serotonin in patients blood. It is reasonable to say that since blood serotonin is not proven to be a clear indication of brain serotonin, any positive outcomes of anti-depressant drug trials may not be due to the increase in brain serotonin bu t other unknown factors. This again shows a lack of tangible evidence between the neurotransmitter, serotonin, and depression. Secondly, in all probability that there is a direct attestation of serotonin deficiency in any mental disorder lacking, it is still unclear whether low levels of serotonin causes depression or depression causes a dip in serotonin. Evidences supporting the latter can be based on observations of non-depressed people with low amounts of serotonin. In a 1996 investigation of the biochemistry of depression, attempts made to induce depression by reducing serotonin levels yielded no consistent results (18). Similarly, researchers found that a surge in brain serotonin, arrived at by administering SSRIs, were ineffective at alleviating depression (19). Therefore there is little evidence to support serotonin as a mood chemical. Also problematic for the serotonin-depression claim is the expanding field of research comparing SSRIs to other anti-depression drugs that do not target serotonin specifically (20). For instance, the atypical anti-depressant buproprion (21) and St. Johns Wort (22), which do not alter the level of serotonin were proven to be just as effective as SSRIs in the treatment for depression. Therefore doubts about the serotonin-depression link are acknowledged by many researchers as well as by advocates of SSRIs (23). To supplement my stand, serotonin is not listed as the cause of depression disorder in the  Diagnostic and Statistical Manual of Mental Disorders (24). The American Psychiatric Press Textbook of Clinical Psychiatry (25) also reiterates that serotonin deficiency as an unconfirmed hypothesis (20). In short, there exists no rigorous corroboration of the serotonin theory, which may suggest the reliability of positive drug trials published by drug companies. Conclusion In addition to what textbooks have to say about serotonin, it is important to look at what not being said in scientific literature. There are numerous peer-reviewed articles supporting the disconnect between serotonin and depression however not a single one can be precisely cited to directly endorse claims of a serotonin deficiency in any mental disorders (20). Assuming that blood serotonin is a good measure for brain serotonin, abundant evidences of high placebo significance in anti-depressant drug trials, the rejection of the claim that efficacy of SSRIs depends on severity of depression, and an inconsistent Force Swim Test results indicate that serotonin may not be the cause of depression. No doubt there may be a positive outcomes from the drug trials, however because blood serotonin may not reflect brain serotonin, these outcomes coupled with the above mentioned proofs against the serotonin hypothesis strongly suggest that other factors are involved in depression. The incongruenc e between the scientific literature and the claims made by proponents are prominent, hence I stand for the fact that there is no direct correlation between serotonin level and depression.

Ernesto Guevara :: essays research papers

Ernesto Guevara Ernesto Guevara was born in l928. When he was two, he moved to Cordoba, Spain, because of asthma. As a young child, Guevara became interested in reading Marx, Engels, and Freud found in his father's library. As he grew up, he watched the Spanish refugees from the Spanish Civil War fight against the fascist dictator, Francisco Franco. Mr. Guevara was influenced by the war and refugees. He began to hate military politicians, the U.S. dollar, and parliamentary democracy. Ernesto's parents were both anti Franco activists. In Buenos Aires, Mr. Guevara went to medical school. He graduated in l953. After several years, Ernesto went to Guatemala writing articles on the Inca and Myan ruins. During his stay in Guatemala, he had the chance to become a government medical personnel. He refused this chance because he did not want to join the Communist party. Therefore, he was penniless for a number of years. Shortly thereafter, Guevara met one of Fidel Castro's lieutenants with whom he fled to Mexico City. In Mexico City, he also met Fidel Castro, and his brother Raul. In Fidel Castro, he saw a great Marxist leader that he was seeking. Guevara joined Castro followers at a farm where they were training for guerrilla war tactics. The tactics were those first used by Mao Tse-Tung. At this time, Ernesto Guevara first was nick named "Che", which is Italian for pal. The group invaded Cuba, where Che was commander of the revolutionary army. From then on, he was known as the most aggressive, clever and successful guerrilla officer. He also got the reputation for cold-blooded cruelty. One reason for this reputation was because of his orders to mass execute followers of the former Cuban president Batista. There after, Che Guevara was second only to Castro in the government of Cuba. As the years went on, Guevara ran the department of industry for Cuba. The government they formed was communist but very different from the then Russian government. Ernesto attacked the Russian style of Communism and said "It was tacit accomplice of imperialism." The Russians were not trading only with communists and they were not giving under developed countries aid. After April of l965, Guevara disappeared from the public eye. Castro dropped his association with Guevara because of Che's criticism. Che's plan at that time was to bring about Marxism by starting a world-wide revolution. He went around the world with forces (120 Cubans). In Congo, they attempted to accomplish one of these revolutions. It fell short when Belgian aid arrived to help the current government. Che had little help from the rebels of Congo and Ernesto Guevara :: essays research papers Ernesto Guevara Ernesto Guevara was born in l928. When he was two, he moved to Cordoba, Spain, because of asthma. As a young child, Guevara became interested in reading Marx, Engels, and Freud found in his father's library. As he grew up, he watched the Spanish refugees from the Spanish Civil War fight against the fascist dictator, Francisco Franco. Mr. Guevara was influenced by the war and refugees. He began to hate military politicians, the U.S. dollar, and parliamentary democracy. Ernesto's parents were both anti Franco activists. In Buenos Aires, Mr. Guevara went to medical school. He graduated in l953. After several years, Ernesto went to Guatemala writing articles on the Inca and Myan ruins. During his stay in Guatemala, he had the chance to become a government medical personnel. He refused this chance because he did not want to join the Communist party. Therefore, he was penniless for a number of years. Shortly thereafter, Guevara met one of Fidel Castro's lieutenants with whom he fled to Mexico City. In Mexico City, he also met Fidel Castro, and his brother Raul. In Fidel Castro, he saw a great Marxist leader that he was seeking. Guevara joined Castro followers at a farm where they were training for guerrilla war tactics. The tactics were those first used by Mao Tse-Tung. At this time, Ernesto Guevara first was nick named "Che", which is Italian for pal. The group invaded Cuba, where Che was commander of the revolutionary army. From then on, he was known as the most aggressive, clever and successful guerrilla officer. He also got the reputation for cold-blooded cruelty. One reason for this reputation was because of his orders to mass execute followers of the former Cuban president Batista. There after, Che Guevara was second only to Castro in the government of Cuba. As the years went on, Guevara ran the department of industry for Cuba. The government they formed was communist but very different from the then Russian government. Ernesto attacked the Russian style of Communism and said "It was tacit accomplice of imperialism." The Russians were not trading only with communists and they were not giving under developed countries aid. After April of l965, Guevara disappeared from the public eye. Castro dropped his association with Guevara because of Che's criticism. Che's plan at that time was to bring about Marxism by starting a world-wide revolution. He went around the world with forces (120 Cubans). In Congo, they attempted to accomplish one of these revolutions. It fell short when Belgian aid arrived to help the current government. Che had little help from the rebels of Congo and

Ordering System Essay

Automated store ordering has been offered as a potential solution to many store level problems: Automation could improve availability, decrease inventories, and reduce the time and labor required for ordering. However, despite the potential advantages, it seems that the majority of retailers have only just started to implement automated ordering systems at store level. Furthermore, very little published information can be found on store level processes, not to mention automated store ordering. Therefore, well-documented research on how and if conventional inventory management practices can be applied at store level operations should be extremely  engrossing both from academic and business viewpoints. This master’s thesis examines how automated store ordering could more efficiently be utilized to improve store operations and performance. The problem is approached first from the theoretical viewpoint: In the literature review, the retail supply chain and store level processes and performance are examined. Furthermore, inventory management and forecasting practices as well as their application in retailing are reviewed. The empirical work in the thesis consists of a part where survey material form the study â€Å"Logistics processes of European grocery retailers† is analyzed, and a case as well as a simulation study. The survey material provides information on how common ASO systems are and what kind of systems actually have been implemented; The case study offers the opportunity to explore the implementation of an ASO system in practice; And the simulations enable developing and testing ways in which the performance of ASO systems can be enhanced. Both the theoretical and empirical parts of the thesis present practical conclusions and results. The most important findings of the thesis are the following: – Many companies have just started to implement automated store ordering systems. The systems in use are typically fairly simple, and they are most often used for managing the normal material flow. Exception situations as well as more challenging product groups are still usually handled manually. – The performance of basic automated store ordering systems can be enhanced by taking into consideration special characteristics of store environment. In case of normal material flow, robust methods are needed to tackle weekday demand and varying replenishment intervals. This can be accomplished by applying material requirements planning logic in order determination. – For efficiently managing promotions with automated store ordering systems, it is important to improve flexibility and react to initial promotion demand. Key words: Automated store ordering, retail logistics, inventory management, retail store processes Language: English Acknowledgements ACKNOWLEDGEMENTS Special word of thanks to the people who have contributed to the completion of this thesis. First, I would like to thank my instructor, and friend, Johanna Smà ¥ros for her support, feedback and guidance. Without her deadlines, and understanding, this thesis would not exist. My appreciation goes to Professor Kari Tanskanen for his supervision and guidance, and to all the members of the Logistics Research Group for a wonderful and inspiring working environment. I would also like to thank the people in the case company, especially Aleksi. And most of all, I would like to thank those closest to me. My wonderful friends at Helsinki University of Technology have been a great cause of happiness and comfort during the last five years, and especially this spring. Finally, I am deeply grateful to my family: What allows me to risk getting shattered is the knowledge that you will be there to pick up the pieces.

Ray Percival

I think that Ray Percival's article, â€Å"Malthus and His Ghost: When He Formulated His Theory, Malthus Ignored the Ingenuity of Man† (August. 18), in which he attempts to silence the Reverend Thomas Robert Malthus and his pro-population-control fanatics, the neo-Malthusians is a work of art. Paul Ehrlich and the other nay-sayers portray man as a gluttonous consumer. Yet, by default, every healthy human being is born with two hands every stomach comes with two hands attached. As Ray Percival asserts, by producing more than he consumes man has worked his way up from the near-universal poverty that was his fate two centuries ago. In my opinion, only one argument in Percival's article needs to be revised. In his dismissal of Ehrlich's simple-minded declaration that â€Å"more people = more famine,† he suggests that there have been â€Å"at most 15 million famine deaths† in this century. In fact, there has been nearly twice that in China alone. Most of which occurred from 1959 to 1962, following the Great Leap Forward, a campaign undertaken by the Chinese communists between 1958 and early 1960 to organize its vast population, especially in large-scale rural communes, to address China's industrial and agricultural problems. It was the scheming of men, not the impulses of nature that led to mass starvation after the Great Leap Forward. This, of course, is a familiar story, told in the Ukrainian famine, the Cambodian famine. We live in an age in which governments, more specifically one-party Communalist rà ©gimes, deliberately cause famines. Percival's optimism about the ability of free human populations to feed them could not be more accurate: it takes significant malicious geniuses to create economic systems and policies which render people incapable of providing for their basic needs. The population-control advocates have come to treat their body of belief more like a religious system than a scientific theory. It is impossible to convince anyone operating within neo-Malthusian constraints of its falsity by rational or pragmatic argument otherwise. They are intensely hardened in their narrow-mindedness by the abundance of funds to which they have access, since they have managed to convince many governments and foundations that they hold the key to mankind's success as a species: reducing the numbers of living, breathing and loving human beings.