What are the arguments for and against the dropping of the atomic Essay

What are the arguments for and against the dropping of the atomic bombs on Japan Was this decision justified What alternatives existed - Essay Example Did President Truman authorize the bombing solely as a means to put an end to a bloody, prolonged conflict and to ultimately save both American and Japanese lives due to an impending invasion on Japan’s homeland or was the decision based on assuring that the Soviet Union would not have a say in post-war Asia is it had in post-war Europe? Finally, even if it is assumed that the first bomb dropped on Hiroshima was necessary and justifiable, was the second bomb on Nagasaki justifiable as well? While the battles for the Philippines and Okinawa were taking place, President Truman, who had become president following the death of Roosevelt, was considering an invasion of the Japanese mainland. By now, the U.S. Navy had ships stationed just off the Japanese coast while its submarines were deployed in the Sea of Japan. Because the battles at Iwo Jima and Okinawa were very fierce, it was estimated that half a million to a million soldiers would be killed if the scheduled November 1, 1945 invasion of Japan occurred (â€Å"Decision to Drop†, 2003). In addition, President Truman was contemplating that if the Japanese would quickly surrender prior to the Soviet Union becoming involved in the war, set for August 15, Russia could not demand a part in the post-war settlement. When America unleashed the atomic bomb on Japan, the act infuriated the Soviet Union because it wanted its say just as it had in the carving up of Eastern Europe. This was the beginning of the Cold War betw een the Soviet Union and the U.S. (Lewis, 2002). The war in the Pacific theater culminated in the dropping of two atomic bombs in 1945 on cities in Japan affecting surrender (Goldstein & Dillon, 1981). On the clear morning of August 6, the first atomic bomb, nicknamed Little Boy, was dropped on the city of Hiroshima† (â€Å"Atomic Bomb†, 2007). The blast leveled more than half of that city. Seventy

Impact of Frailty on Depression

Impact of Frailty on Depression Background With increasing life expectancy, diseases associated with old age have increased in growing proportion in recent decades. (1) The integration of frailty measures in clinical practice is crucial for the development of interventions against age-related conditions (in particular, disability) in older persons. Multiple instruments have been developed over the last years in order to capture this geriatric multidimensional syndrome characterized by decreased reserve and diminished resistance to stressors and render it objectively measurable. (2) Frailty is not uncommon to the medical contemporary research nowadays. Several possible definitions were given by different researchers in the past to define frailty. One and commonly used definition of physical frailty was given by Fried et al, Frailty was defined as a clinical syndrome in which three or more of the following criteria were present; unintentional weight loss (10lbs in past year), self-reported exhaustion, weakness (grip strength), slow walking speed, and low physical activity. (3) Frailty in older people was again classified into prefrail those having one or two criteria given by Fried et al, and frail elderly having three or more criteria as per Fried et al definition. Medical Syndrome like frailty, keeps older adults at increased risk of adverse health outcomes when exposed to a stressor. (4)   Stressors lead to decline across multiple physiological systems incrementally and are associated with greater depressive symptoms and disability. (5) Depression is not a normal part of ageing process (6) and is a potentially life-threatening disorder that affects hundreds of millions of people across the world. (7) Depression is commonly seen in frail older people as they may face widowhood or loss of function or independence or bereavement. Depression, if left untreated, complicates other chronic conditions such as heart disease, diabetes, stroke, etc. It may also incur health care costs and often accompanies functional impairment and disability. (6) Various systematic reviews and journal articles has demonstrated association between depression and frailty. In this review, focus has made to highlight the role of stressors that leads pathways linking depression and frailty. Prevalence of frailty, depression and their co-occurrence in older individuals Several studies have been carried out to measure the prevalence of frailty in community-dwelling older people as well as those in hospital settings. Majority of the studies have used similar criteria to measure frailty among older adults. Systematic review of frailty prevalence worldwide concluded that 10.7% of community-dwelling adults aged à ¢Ã¢â‚¬ °Ã‚ ¥65 years were frail and 41.6% pre-frail. (8) It was noted that prevalence figures varied substantially between studies (ranging from 4% to 59%) using different criteria to measure frailty. (6) Data from Survey of Health, Aging and Retirement in Europe (SHARE) in 2004 covering more than 10 European countries, showed prevalence of frailty and pre-frailty in 65+ age group as 17.0% (15.3 18.7) were frail and 42.3% (40.5 44.1) were pre-frail. (9) The prevalence of frailty in community dwelling older people ranged from 17%-31% in Brazil, 15% in Mexico, 5%-31% in China, and 21%-44% in Russia. However, prevalence of frailty was again fou nd much higher in institutionalized older patients as 32% in India and 49% in Brazil. Findings of study in outpatient clinics reported prevalence of frailty was 55-71% in Brazil and 28% in Peru. (10) Above finding suggests that older people of low- and middle-income countries were found frail in significant proportions which imply policy and health care provisions for this ageing population. Depression varies in its prevalence in different studies and settings. Prevalence of depressive symptoms was found 14% in Brazilian adults (11), 9% in United States general population (12) and 23.6% (95% CI: 20.3-27.2%) in Chinese older adults. (13) Depressive symptoms were most commonly associated with women (11) (12) (13) and single adults (i.e. divorced, unmarried or widowed) than in married older adults. (13) Prevalence of depressive illness rises further in the event of associated co-morbid condition such as cancer, diabetes, and hypertension[N1]. Median prevalence of minor depression was 14.4% and 10.4%, in medical settings and community-based setting, respectively[N2]. (14) The median global prevalence of serious depression in the elderly population is around 1% 5%. (15) (16) (17) Depressed elders show many phenotypical expressions of frailty and vice versa. Coexistence of both depression and frailty among older people has been investigated in several studies. (18) (19) (20) (21) (22) (23) A recent systematic review examined the relationship between depression and frailty found serious depression in 4 16% of frail individuals who are aged 60 and over. (6) However, this percentage rises to 35% in older population with age 75 years or more. (6) (24) A study conducted within framework of prospective cohort study, the Netherlands Study of Depression in Older Persons (NESDO) found that the prevalence of physical frailty was significantly higher in the depressed group in comparison with non-depressed (27.2% vs 9.1%, p4) was present in as high as 46.5% of the frail subjects. Depressed patients often exhibit symptoms that interfere with their ability to function normally for longer duration which facilitates progression of frailty syndrome. (6) Therefore, in order to improve health and preventing frailty depression in elderly, it is essential for researchers and practitioners to understand the linking phenomena for further research and developing treatment options. Main pathways linking frailty and depression Several studies have identified the possible physiological pathways that link between frailty and depression in older adults. Of which, the main hypothetical pathways identified were vascular depression, chronic inflammation, Hypothalamus-Pituitary-Adrenal (HPA) axis dysregulation and accelerated cellular ageing. Vascular depression hypothesis Alexopoulos et al. (26) proposed that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. This statement was supported by another study of vascular depression based on magnetic resonance imaging (MRI) conducted by Krishnan KR et al. (27). Bivariate analyses and a fully adjusted logistic regression model in MRI study revealed that older age, late age at onset, and nonpsychotic subtype occurred more often in patients with vascular depression than in those with nonvascular depression. He also observed that anhedonia and functional disability were seen somewhat more often in patients with vascular depression. There are several clinical studies that examined vascular disease in depression. Some studies (28) found a highly significant increase in physical illness and vascular risk factors in the late onset group, after adjusting for age when they compared early and late onset late-life depression. (29) On the other hand, several others found no association of depression with cerebrovascular score (30) and vascular disease (31). Depression may occur as a result of vascular disease in a significant subpopulation of elderly persons. (32) Depression has a bidirectional association with vascular diseases and plausible mechanisms exist which explain how depression might increase these vascular diseases and vice versa. Thomas AJ et al summarized that coronary artery disease (CAD) and stroke are all associated with high rates of depression and depression is an independent risk factor for the subsequent development of CAD and stroke. (29) Mechanism of vascular depression can be hypothesized as reduced cerebral blood flow (CBF) in response to given stressors. Normal CBF in adult humans is about 60ml/100 grams/min and regionally, about 70ml/100g/min in gray matter and 20ml/100g/min in white matter. Between the ages of 20 to 65, normal CBF generally declines about 15-20%. It is generally accepted that when CBF reaches 30ml/100g/min, neurologic symptoms can appear and when CBF falls to 15-20ml/100g/min, electrical failure or irreversible neuronal damage can occur even within minutes. (33) Blood flow to the brain is influenced by systemic hemodynamics and cerebro-vascular auto-regulation, with cerebral arteries contracting or dilating as arterial pressure changes. These processes interact to maintain stable perfusion. (33) However, these processes are impaired in the context of vascular disease: hypertension, diabetes, and atherosclerosis lead to vascular wall hypertrophy, reduced arterial lumen diameter, reduced arterial distensibility, and endothelial cell dysfunction. This affects cerebral blood flow. Mild CBF reduction may impair cognitive and affective processes, while greater CBF reduction may cause ischemic injury. The subcortical white matter is particularly sensitive to these changes because it is supplied by terminal arterioles with limited collateral flow and so susceptible to infarction due to impaired autoregulation. Greater white matter hyperintensities (WMH) severity may be a marker of broader deficits in perfusion and autoregulation. Thus, risk factors for vascular disease can lead to subclinical cerebrovascular disease throughout the brain. Katz (2004) theorizes that cerebrovascular disease that causes prefrontal white-matter hyperintensities and vascular depression may also lead to posterior white matter hyperintensities, resulting in characteristics of frailty such as falls, slowness, and weakness. (34) He further stated that if the effects are anterior, the manifestations may include depression. However, if the effects are more posterior, the manifestations may be in the form of disturbances of gait and balance. Several other studies had compared depressed elderly with control group and demonstrated an increase in deep white matter hyperintensities (DWMH) in depression (35) (36) (37), but no or not significant association with peripheral vascular lesion (PVH) (36) (37). The cerebral WM contains fiber pathways that convey axons linking cerebral cortical areas with each other and with subcortical structures, facilitating the distributed neural circuits that subserve sensorimotor function, intellect, and emotion. The va scular depression hypothesis postulates that altered mood regulation and cognitive dysfunction in the elderly are due to subclinical cerebrovascular ischemia that disrupts frontostriatal neural circuits. (38) (39) This disruption of fronto-striatal neural circuits leads to disconnection syndrome that corresponds to the clinical and neuropsychological profile of LLD. (40) Prefrontal WMH also leads to executive dysfunction which affects planning, self-monitoring, attention, response inhibition, co-ordination of complex cognition (as in Trail making Test) and motor control. This leads to frailty. Chronic Inflammation hypothesis Aging- and disease-related processes promote proinflammatory states in older individuals. Administration of cytokines or induction of peripheral inflammation results in an inflammatory response, which in turn is correlated with fatigue, slowed reaction time, and mood reduction. Even without medical illness, depressed individuals exhibit increased levels of proinflammatory cytokines and reduced anti-inflammatory cytokine levels. Proinflammatory cytokines affect monoamine neurotransmitter pathways, including indoleamine 2,3-dioxygenase upregulation and kynurenine pathway activation. This results in decreased tryptophan and serotonin and increased synthesis of detrimental tryptophan catabolites that promote hippocampal damage and apoptosis. Cytokines, including IL-1ÃŽÂ ², also reduce extracellular serotonin levels by activating the serotonin transporter. Effects of the CNS inflammatory cascade on neural plasticity Microglias are primary recipients of peripheral inflammatory signals that reach the brain. Activated microglia, in turn, initiate an inflammatory cascade whereby release of relevant cytokines, chemokines, inflammatory mediators, and reactive nitrogen and oxygen species (RNS and ROS, respectively) induces mutual activation of astroglia, thereby amplifying inflammatory signals within the CNS. Cytokines, including IL-1, IL-6, and TNF-alpha, as well as IFN-alpha and IFN-gamma (from T cells), induce the enzyme, IDO, which breaks down TRP, the primary precursor of 5-HT (serotonin), into QUIN (quinolinic acid), a potent NMDA (N-methyl-D-aspartate) agonist and stimulator of GLU (glutamate) release. Astrocytic functions are compromised due to excessive exposure to cytokines, QUIN, and RNS/ROS, ultimately leading to impaired glutamate reuptake, and increased glutamate release, as well as decreased production of neurotrophic factors. Of note, oligodendroglia are especially sensitive to the CNS inflammatory cascade and suffer damage due to overexposure to cytokines such as TNF-alpha, which has a direct toxic effect on these cells, potentially contributing to apoptosis and demyelination. The confluence of excessive astrocytic glutamate release, its inadequate reuptake by astrocytes and oligodendroglia, activation of NMDA receptors by QUIN, increased glutamate binding and activation of extrasynaptic NMDA receptors (accessible to glutamate released from glial elements and associated with inhibition of BDNF (brain-derived neurotrophic factor) expression), decline in neurotrophic support, and oxidative stress ultimately disrupt neural plasticity through excitotoxicity and apoptosis. 5-HT, serotonin; BDNF, brain-derived neurotrophic factor; CNS, central nervous system; GLU, glutamate; IDO, indolamine 2,3 dioxygenase; IFN, interferon; IL, interleukin; NMDA, N-methyl-D-aspartate; QUIN, quinolinic acid; RNS, reactive nitrogen species; ROS, reactive oxygen species; TNF, tumor necrosis factor; TRP, tryptophan. Regarding LLD, the aging process disrupts immune function, increasing peripheral immune activity and shifting the CNS into a proinflammatory state. Elevated peripheral cytokine levels are associated with depressive symptoms in older adults, with the most consistent finding being for IL-6, but also implicating IL-1ÃŽÂ ², IL-8 and TNFÃŽÂ ±. Proinflammatory states in older adults are associated with cognitive deficits, including poorer executive function, poorer memory performance, worse global cognition, and steeper decline in cognition. Finally, greater IL-6 and C-reactive protein levels are associated with greater WMH burden. In LLD, ischemic lesions are also more likely to occur in the dorsolateral prefrontal cortex (DLPFC), Similarly, depressed elders exhibit increased expression of cellular adhesion molecules (CAMs) in the DLPFC. CAMs are inflammatory markers whose expression is increased by ischemia, supporting a role for ischemia in LLD and highlighting the relationship between vascular and inflammatory processes. HPA dysregulation When the HPA axis is activated by stressors, such as an immune response, high levels of glucocorticoids are released into the body and suppress immune response by inhibiting the expression of proinflammatory cytokines (e.g. IL-1, TNF alpha, and IFN gamma) and increasing the levels of anti-inflammatory cytokines (e.g. IL-4, IL-10, and IL-13) in immune cells, such as monocytes and neutrophils. Excess stress also appears to play a role in the development of depression and can cause dysregulation of the HPA axis. Patients with major depression have been found to have elevated plasma and urinary cortisol levels as well as elevated corticotropin-releasing hormone and decreased levels of BDNF. Prolonged severe stress is thought to damage hippocampal neurons and to reduce the inhibitory control exerted by the HPA axis in regulating glucocorticoid levels. During an immune response, proinflammatory cytokines (e.g. IL-1) are released into peripheral circulatory system and can pass through the blood brain barrier where they can interact with the brain and activate HPA axis. Interactions between the proinflammatory cytokines and the brain can alter the metabolic activity of neurotransmitters and cause symptoms such as fatigue, depression, and mood changes. Increased levels of aldosterone in the circulation stimulate excessive production of collagen, which leads to fibrosis of tissue or organ whereas low levels of adrenal androgen dehydroepiandrosterone sulfate and insulin-like growth factor 1 are associated with frailty. Further, cortisol may mimic the effects of aldosterone. Elevated serum levels of cortisol and aldosterone are independent predictors of mortality in patients with heart failure. Accelerated Cellular Aging hypothesis Accelerated cellular aging, as measured by telomere length (TL) shortening, might also be linked to depression and frailty. At both ends of every DNA strand in a human cell is a telomere.Telomeres prevent chromosomes from becoming frayed, fusing into rings, or binding with other DNA. Telomeres are specialized nucleoprotein structures located at the end of eukaryotic chromosomes. They play a critical role in controlling cell proliferation and maintenance of chromosomal stability. As part of bodys normal aging process, each time a cell divides the telomeres in your DNA get shorter. Add oxidative stress to the mix and telomeres shorten even more rapidly. Oxidative stress is the effect of destructive reactions in your bodys cells caused by too many free radicals or atoms/molecules that have unpaired electrons. In their search for an electron to make them whole, they destroy other cells. Free radicals come from environmental toxins, such as pollution, chemicals, drugs and radiation, and even naturally occur in your own body when you exercise. Antioxidants fight free radicals and stem the causes of oxidative stress. Eventually, bodys cells are unable to divide (or reproduce) and simply die. Eventually, this instability leads to tissue breakdown potentially leading to premature aging. Any stressful condition or anxiety leads to feeling of depression which in turn initiates physiologic body response that includes, increase in stress-induced glucocorticoid release and oxidative stress. Unhealthy behaviour will also stimulate inflammatory response which lead to release of cytokine and can affect telomere length.

The Alluring Amontillado Essays -- Literature

The Alluring Amontillado Revenge is the act of retaliation for an offense or injury caused to a person by another. The act of revenge can become an overpowering and consuming emotion that involves every part of someone’s existence. In â€Å"The Cask of Amontillado,† revenge is the theme that runs throughout the story and drives the motive for murder. The character, Montresor, uses revenge as his motive for killing Fortunato. Fortunato is reminiscent of a fatherly character, which elicits painful memories for Montresor. In eliminating Fortunato, Montresor assumes the role that places him closest to the affections of a motherly figure. Edgar Allan Poe’s life is reflective of the motivations of Montresor’s actions and how the Oedipus complex is featured in this short story. Edgar Allan Poe was born in Boston, Massachusetts in 1809 to parents who were actors at the local theatre. He never knew his father, David Poe, who died in 1810 after abandoning Poe’s mother shortly after Poe was born. His mother, who suffered from consumption, died in Richmond, Virginia in late 1811, orphaning Edgar, his older brother William Henry, and half-sister Rosalie. Soon after their mother’s death, the children were separated and sent to relatives or other families to be raised. Edgar had very little contact with his siblings after their mother’s death. A planter and his wife, who lived in Richmond Virginia, accepted Poe into their family, but never formally adopted him. From the childless wife of Mr. John Allan, Edgar received extensive affection, but it was improbable that she was ever able to give all the affection that he craved from his deceased birth mother. Mr. Allan regarded Edgar with mute affection and mostly offered money in place of any physi... ... who was forever searching for that one elusive person who could give him the validation he so wanted. He appears to have placed so much value on the affections of a mother who would forever be absent. Montresor, in Poe’s fictional story, was successful in committing the revengeful deed he sought. Fortunato, from his grave, forever haunted the lonesome soul of Montresor. Works Cited May, Charles E. Edgar Allan Poe: A Study of the Short Fiction. Boston: Twayne, 1991. Print. Poe, Edgar. â€Å"The Cask of Amontillado.† The Compact Bedford Introduction to Literature: Reading, Thinking, Writing. Ed. Michael Meyer. Boston: Bedford/St. Martins, 2012. 533-537. Print. Pruette, Lorine. "A Psycho-Analytical Study of Edgar Allan Poe." The American Journal of Psychology 31.4 (1920): 370-402. JSTOR. Web. 31 Mar. 2012. .

Harvey Norman Holdings Limited Essay

Introduction: Terms of Reference:This Report is designed to demonstrate the students understanding of IMC. The report was prepared for Mr. Paul Morrissey, Lecturer of Integrated Marketing Communications. Background:The purpose of this report is to help the student get a understanding of hold different marketing techniques are used in everyday situations through different forms of advertising campaigns. The purpose of this is to reinforce the knowledge the student has acquired in class. The company that will be subject of this report is Harvey Norman Holdings Limited. Objectives:To provide and overall situation analysis of the company. To research the company’s advertising campaign and determine who the target  market are. Analyse the key form of marketing communication used and the company’s Unique Selling Point (USP). To analyse the media planning used for the campaign.To provide a detailed overall evaluation of the marketing campaign.Methodology:The information used in this report was found through the use of secondary research in the form of internet based searching. Findings:Overview of Harvey Norman Holdings Limited:Harvey Norman is an Australian company and is a worldwide retailer of furniture, bedding, electrical, and computer. It has been in operation since 1961 when founders Gerry Harvey and Ian Norman set up the business. Harvey Norman has almost 300 stores worldwide. CITATION Har12 l 6153 (harveynorman.ie, 2012)Situational Analysis:Porter’s Five Forces:This model helps illustrate the strengths and weaknesses of an industry through five factors that are as follows: Competition in the market Potential new Entrants Power of suppliers Power of customers Threat of substitute products CITATION Inv12 l 6153 (Investopedia.com, 2012)Competition in the Market: There is large competition in this industry as it is an industry that has been around for a relatively long time. Therefore more companys such as Currys, Ikea, and D.I.D electrical, also compete in this market. Potential New Entrants There is a low threat from potential new competition as there are substantial barriers to entry in this industry. These barriers include: 1. High Capital Requirements: for this industry a new company would be required to stock a large volume of a large range of relatively expensive products as well as a large store to hold it all and large amount of staff and distribution costs. 2. Brand Loyalty because Harvey Norman has worldwide recognition and a strong brand awareness customers would be more inclined to stick with what they know already ie Harvey Norman products. Bargaining Power of Suppliers: For Harvey Norman there is a large range of suppliers for all the types of  products the company sells. Because there is such a large volume of suppliers in this industry ,the suppliers Harvey Norman uses have little to no bargaining power against Harvey Norman as they could just switch to another supplier and so the supplier would lose out on the high volume bulk buying that Harvey Norman would be using. Bargaining Power of Customers: Because Harvey Norman deals in such a large variety of products, from Furniture to computers, it attracts a large volume of customers for each of these product categories. This gives them a large base of customers to start with. Also the fact that Harvey Norman sells alot of recognised brands customers are inclined to purchase what they know. But due to the high competition from other similar businesses, such as Ikea, the customers have a decent amount of bargaining power as they may chose to take their business elsewhere. Threat of Substitute Products: There is very little threat from substitute products to Harvey Norman as a whole due to the large variety of products stocked and the types of products stocked. CITATION wik12 l 6153 (wikiwealth.com, 2012)

“A Question of Torture” by Alfred McCoy

â€Å"In April 2004, the American public was stunned when CBS Television broadcast photographs from Abu Ghraib prison, showing Iraqis naked, hooded, and contorted in humiliating positions while U.S. soldiers stood over them, smiling†. (p.5)Here Alfred McCoy starts his narration. His book â€Å"A Question of Torture† is labeled as a penetration study of fifty years American participation in torture propagation, research and practice. The book reveals degrading and inhumane treatment, cruelty and injustice in US history intensified by tragic personal case studies and experiences.The author deepens in why the tortures were sued, where they were implemented and what the consequences were. It is known that CIA had spent millions of dollars on torture research and the author writes that it combined self-inflicted pain with sensory deprivation with the eternal purpose of creating revolutionary psychological approach. The goal was to develop the first innovation in torture: â⠂¬Å"Still, if genius is the discovery of the obvious, then the CIA's perfection of psychological torture was a major scientific turning point, albeit unnoticed and unheralded in the world beyond its secret safe houses†.   (p.7)The primary techniques in torturing were hooding, isolation, extremes of hot and cold, hours of standing without opportunities to move or to change body position, manipulation of time. In such a way CIA had managed to destroy victim’s senses and his personal identity. All these techniques are claimed to have been used in Vietnam, Iraq, Iran and Central America. For example, Washington is argued to refer to torture in CIA’s prisons and torture-friendly countries.Nevertheless, information obtained through torturing is really worthless as victims were ready to acknowledge their fault even if they were not guilty. McCoy says that the agency used electric shocks and recruited peopled like, for example, Kurt Plotner. The author concludes that t he simplest and cheapest methods work the best and, what is more awful, public accepted them more than physical violence.Book DiscussionI think that the book â€Å"A Question of Torture† is really shocking and impressive study as the author reveals the most contradictive and painful pages of American history.Nevertheless, the book contributes historical filed as McCoy tends to provide neutral and realistic examples how tortures were used by CIA and where they were used. The author frames historical development of tortures stressing they are sanctioned. He seems to be very concerned with the diminished standards of American nation.However, I agree with McCoy that tortures are rarely affective and it is simply a like looking for a needle in haystack. The book teaches us that once torture is implemented, it results in mass tortures as, for example, tortures in Argentina and Chile during their ‘dirty wars’. Moreover, mass tortures are linked to increased rates of jud icial killings.