The British movie Essay Example for Free

The British movie Essay The implication of escape is shadowed in the present film. One treats Gal as a criminal more eagerly than a fugitive. However, this character is haunted in both direct and figurative meanings. Whereas Don abuses Gal’s stable mode of living by fierce jokes and physical violence, the whole Gal’s background abuses the hero’s soul by ominous signs (e. g. , the rock falling to the pool) and dreams. The conflict between the escapee (Gal) and the persecutor (Don and the criminal world) is revealed in the very title. In the East End vernacular, the phrase sexy beast is used as a compliment and means â€Å"a handsome chap, a reliable mate or a trustworthy accomplice† (Earnshaw 2001, p. 5). The title hints at the positive side of Gal’s London past (material wealth, friends, familiar environment) and, simultaneously, at the darkest sides of the hero’s background made explicit in the dream of a hairy beast pursuing Gal at nights. The same type of the hero as a fugitive is present in Kitano’s Hana-bi. The Japanese title of this film consists of two words, translated to English as ‘fire’ and ‘flowers’ [the English aka ‘Fireworks’]. The main character of the film, Yoshitaka Nishi (Takeshi Kitano), seems to be torn between the ‘flowers’ of his life to the mortally ill wife and the impaired friend, and the ‘fire’ of his hopeless race for peace and stability. Nishi used to be a cop. Nevertheless, hardly can this story be considered a ‘cop’ narrative. The film traces the evolution of the hero from the stage of a law-abider to the one of a fugitive and an outlaw. The narrative implicitly promotes the idea that there are certain moral principles equating a cop, a fugitive and a criminal – the love for the family, the affection for the friend, the acid mourning over acid unbearable existence. Nishi quits his beloved job to take care of his wife. He desperately needs money and borrows a large sum from yakuza. They send over young thugs to play rough with Nishi when he refuses to pay back the interest. The ex-cop assaults the intruders, thus, turning momentarily from a fugitive into a criminal. The movie provides no classification for its heroes. Instead, it shows â€Å"an endless circle† (Cannon, 1997, para. 2, lines 6-8) of the global crime net where plain people such as Nishi, the kin young policemen who replaced Nishi and Horibe, Nishi’s wife and friend try to survive and establish some kind or order and justice. As Cannon (1997, para. 4, lines 2-4) stated, the main character is the embodiment of contradiction: â€Å"[I]n one instant a warm and gentle husband, in the next a sadistic and ruthless bully†. Due to this ambivalence, Hana-bi may be referred to as a critical film which emphasises â€Å"the impossibility of heroism and the inevitability of injustice† (Rafter 2000, p. 12). An avenger The British movie Get Carter and the American film Gangs of New York provide the viewer with remarkable portraits of avengers. Chibnall and Murphy (1999, p. 4) defined revenge films as the ones â€Å"where a wronged man, denied access to the law, pursues his own path of justice†. The movie Get Carter was criticised for its â€Å"perfunctory plot, its mechanical manipulation of characters or a vision of the British underworld that relies totally on cliche† (Andrews 1971 cited Murphy 1999, p. 128). However, the treatment of the main character’s features can hardly be called mechanical. Jack Carter, the hero of the British cult film Get Carter, is â€Å"an implacable avenging angel in a black raincoat† (Billson 1991 cited Murphy 1999, p. 129) revenging on the criminals for killing his brother and seducing his niece. But despite Carter’s motivations for being an almost mythical angel of wrath, he never stopped to be a cruel criminal himself having killed four people and being responsible for even more cases of violence. Jack Carter is neither an upholder of justice nor a saviour of the weak and humble, but he operates by a strict code that he expects his colleagues and enemies to share. [†¦] Carter is confronted by a society afflicted by pornographic malaise. But his righteous anger is less about sleaze itself than about how it has leaked out of its proper underworld milieu to engulf his niece and destroy his brother. Carter is not so self-consciously evil [†¦] or [†¦] morbidly obsessed [†¦] but he does share some of the characteristics of the Jacobean revenge tragedy protagonist. A wrong has been done-less to Carter himself than to his family – which must be righted at whatever cost. (Murphy, 1999, p. 132) Carter is synthetic in his nature. On the one hand, he reaches almost legendary heights in his revengeful crusade. On the other hand, his â€Å"fussy concern with nose drops, vitamin pills and the cleanliness of British Railways cutlery† stands for his â€Å"human frailty† (Murphy 1999, p. 129). The hero of the American film Gangs of New York is neither a pure type of an avenger. On the one hand, Amsterdam Vallon infiltrates the gang of The Butcher Cutting to revenge for the death of Vallon-father. On the other hand, Amsterdam finds the substitute of the father in his once hated target. The character of Amsterdam provides an interesting synthetic type of ‘a man-on-the-run’ (he spent some years in anonymity after his father’s murder till the re-emergence in the rival gang) and ‘a man-in-disguise’.

Health Inequalities And Socioeconomic Status Health And Social Care Essay

Health Inequalities And Socioeconomic Status Health And Social Care Essay For years there has been significant evidence linking socio-economic status and health. Statistics show a graded relationship, meaning the higher your social position the greater your level of health (figure 3). This shocking data not only shows the most deprived dying 7 years earlier than the least; they will also have a disability for a longer period of their shorter lives, which is likely to take affect before the ever increasing pension age, 17 years before that of the most affluent (Marmot 2010). Figure 3: Life expectancy and disability-free life expectancy at birth, persons by neighbourhood income level (ONS 2009). Recession does not uniformly impact the health of the nation, affecting different social-classes in different ways and by variable amounts, further accentuating health inequalities (Marmot and Bell 2009).This essay will examine how the behavioural, psycho-social, materialist and life-course aetiological pathways are involved in the health effects of the economic downturn on different socio-economic groups. Unemployment will be discussed in detail being the major variable during an economic downturn, having both direct and secondary causes, and a significant influence on health. Later, other indirect influences such as job insecurity and public sector cuts will also be discussed. Unemployment has a serious affect on health showing a much higher mortality rate for unemployed men (Figure 4). However some of this difference may be attributed to the theory of selection that ill people are more likely to become or remain unemployed, rather than exposure where unemployment causes health deterioration (Burgard et al. 2007). Although some less healthy individuals may lose their jobs before others, the sheer scale of unemployment during economic downturn will make exposure dominant. Contrasting to others Martikainen et al. (2007) argue that the mortality and therefore health during unemployment is often better during a recession due to better support in the form of unemployed peers. However in terms of the nation as a whole increased unemployment deteriorates health, and when considering the individual, although support from peers is important the financial strain combined with other factors such as increased cost of living and public sector cuts, discussed later, wil l exceed this positive effect. Figure 4: Mortality of men in England and Wales in 1981-92, by social-class and employment status at the 1981 Census (Bethune 1997). Unemployments major impact is on an individuals mental health; Price et al. (1998) associated unemployment with decreased self-esteem and perceived competence, increased depression and anxiety along with an increased risk of suicide attempt, alcohol abuse and violence. However other research has indicated that the lack of income outweighs the stress related consumption of cigarettes and alcohol (Ruhm 2005) or that health damaging behaviours are influenced by feelings of control and expectation of future employment (Catalano 1997). Several studies link these psychological affects such as job stress increasing risk factors such as hypertension and serum cholesterol (Weber et al. 1997). In conjunction with this it seems the most common impacts of unemployment on physical health are on the cardiovascular system with Gallo et al. (2006) estimating a doubling of the risk of stroke and myocardial infarction with involuntary job loss. The financial sector initiated the current recession so was the first to directly feel its effects, for example Northern Rock being taken into state ownership and forced to make 800 compulsory redundancies (Treanor 2008). The secondary impact of the recession involved decreased lending from the financial sector, forcing companies to close altogether or relocate abroad for a cheaper workforce, meaning mass unemployment and unlikely reemployment (Clancy and Jenkins 2009). Next as the government feels the squeeze public sector cuts are causing further unemployment. Generally speaking the lower-classes are the most likely to become unemployed, occurring mainly via secondary impacts since they are the first to be made redundant during public sector cuts and they dominate industries such as retail and manufacturing which are the most suitable for relocation abroad (Clancy and Jenkins 2009). This unemployment causes a loss of income resulting in severe financial strain; with debt continuing to accumulate as they struggle to find a job and suffer with the social stigma associated with unemployment, individuals feel out of control with increasing levels of stress, depression deteriorating their health (Price et al. 2002). As money becomes increasingly tight basic needs such as nutrition and access to healthcare impact their physical health, this lack of finances means decreased opportunity for social activities and coping strategies further worsening their mental health (Price et al. 1998). Some people may lose hope all together and turn to health de structive behaviour such as smoking, alcohol and perhaps even suicide as described earlier. However in areas of high unemployment, the presence of many individuals in the same situation may protect individuals from such psychosocial impacts (Brenner and Mooney 1983). The more affluent are also at risk of unemployment, many directly from the recession as higher socio-economic groups dominate the financial sector, however like the lower-classes the decreased lending and public sector cuts cause widespread unemployment but on a much smaller scale. The contrast with that of the lower-classes is that their higher salary over the years often enables them to have sufficient savings that can act as a buffer, whilst they wait for the economy to recover and apply for new jobs, which they are more likely to get due to their higher qualifications (Elliott et al. 2010). These wealthier individuals suffer more in terms of psychological health; many experience a loss of identity, as their job defines them and without it they feel lost and unaware of their place in society (Price et al. 1998). Their physical health may not be affected with finances available to provide food and other essentials, however it is these same finances that have the capacity to fund sm oking, alcohol and even drug abuse. Unemployment indirectly impacts on the health of their entire family. The  Office of Population, Censuses and Surveys revealed wives of unemployed men experienced 20% excess deaths to those with employed husbands (Moser and Goldblatt 1990). There are also strong links between unemployment and domestic violence, unwanted pregnancy, divorce and impaired infant growth (Mathers and Schofield 1998). Social support from family and friends is crucial to combat unemployments negative psychological effects, but unemployment itself disrupts social support and friendship networks, often resulting in conflict (Price et al. 1998). The financial strain of recession puts significant pressures on parenting and ultimately deteriorates the health and development of their children which will affect them throughout their life-course (Solantus et al. 2004). This is accentuated by the government increasing the cost of university, denying those with potential in lower social-classes, the opportunity of u pward mobility. These family impacts are more prominent in lower socio-economic groups, with greater financial burden meaning lower control and more pressure on relationships. Some of the more indirect impacts of recession on health are not directly linked with unemployment, although some such as job insecurity and unsuitable reemployment may be associated with it. Job insecurity is a feature of modern Britain with our shift from manufacturing to service sector employment still struggling against strong international competition. The economic downturn increasing unemployment worsens the UKs already high job insecurity, with more people worried about their own or their companys longevity. The mechanism by which job insecurity impacts health is similar to that of unemployment; many view job loss anticipation as the first step of unemployment. With Petterson et al.(2005) observing insecure workers exhibiting declining concentration and increased irritation and long term sick leave its no wonder they may soon become unemployed. Dekker and Shaufeli (1995) even argue that it may be more difficult to cope with job uncertainty due to not knowing what to expect. These impacts relate to feelings of low control over their future, but this differs for the individual, the level of insecurity and the prospect of reemployment. Redundancies within an organisat ion can affect the health of all the employees, with those remaining exhibiting a lack in trust of those in power, competition with other workers at risk and resentment for those already redundant (Campbell and Pepper 2006). Unsatisfactory reemployment is an indirect impact due to decreased job opportunities, affecting those who have recently become unemployed and those looking for first time employment. The depression caused by unemployment itself severely reduces the chances of reemployment and the longer they spend unemployed they become deskilled making it even more difficult to escape the spiral of disadvantage (Price et al. 2002). Most would think its beneficial to gain employment and income, but the pressures of financial strain make lower socio-economic groups more likely to accept unsustainable employment, that is temporary, high-demand and low-pay. Whilst it may help financially in the short-term it wont have any long-term improvements and due to the type of work being unrewarding, monotonous and insecure means it has negative health implications such as depression, hence it may be just as bad as unemployment (Grzywacz Dooley 2003). Along with unemployment and pay cuts, a higher cost of living involving increasing VAT and escalating food and petrol prices all create financial strain, especially in the lower-classes, which itself causes negative health effects as discussed with unemployment. However this decreased disposable income reduces public spending, causing the local economy to fail (Brenner and Mooney 1983). Although large areas such as cities contain people of all socio-economic status, they are segregated into smaller communities of a particular social-class. Lower-class communities have the least public spending so are the worst affected; places like the high street which are important hubs for social integration soon become dilapidated, increasing levels of depression, crime and social exclusion, severely impacting the health of the community (Yuill 2009). Increased poverty and ill health puts tremendous pressure on public services such as social welfare, primary health care and the police. Public sector cuts in these areas further worsen the health impacts by reducing their ability to cope and reducing availability of such services to an ever increasing number of people who require them. In conclusion, the economic downturn has several impacts on the health of the UK, both directly and indirectly. These impacts do affect everyone so no groups should be ignored, but its clear that socio-economic status influences the mechanisms and severity by which it impacts peoples health. The majority of research indicates that lower-classes are the worst affected; they are most likely to become unemployed, experience job insecurity and undertake unsuitable employment (Clancy and Jenkins 2009). They also experience greater financial strain from pay cuts and increased cost of living, all of which result in more serious health connotations. Higher socio-economic groups dont experience such a financial loss and are considered to have more control over their futures due to assets such as savings and good qualifications, but they do experience negative mental health impacts, such as loss of identity, different to that of lower-classes (Price et al. 1998). Indirect impacts of the recess ion such as reduced public spending and public sector cuts reduce service availability, particularly in deprived areas where they are needed the most. It is important to understand that its not just about individuals, the recession indirectly affects family and friends and that lower-class families raising a child in times of struggle will severely affect that childs health throughout their life-course (Marmot and Bell 2009). Reference list Bartley, M. 2004. Health inequality an introduction to theories, concepts and methods. Cambridge: Polity Press, pp. 22-32. Brenner, M. and Mooney, A. 1983. Unemployment and health in the context of economic change. Social Science Medicine 17, pp. 1125à ¢Ã¢â€š ¬Ã‚ 1138. Burgard, S. Brand, J. and House, J. 2007. Toward a better estimation of the effect of job loss on health. J Health Soc Behav 48, pp. 369-384. Campbell, R. and Pepper, L. 2006. Downsizing and social cohesion: the case of downsizing survivors. New Solutions 16(4), pp. 373à ¢Ã¢â€š ¬Ã‚ 393. Catalano, R. 1997. An Emerging Theory of the Effect of Economic Contraction on Alcohol Abuse in the United States. Social Justice Research 10(2), pp. 191à ¢Ã¢â€š ¬Ã‚ 201. Clancy, G. and Jenkins, J. 2009. The impact of the recession on the Labour Market. ONS presentation at Cardiff University (14.07.2009). Dekker, S. and Schaufeli, W. 1995. The effects of job insecurity on psychological health and withdrawal: A longitudinal study. Australian Psychologist 30(1), pp. 57à ¢Ã¢â€š ¬Ã‚ 63. Denny, E. and Earle, S. 2005. Sociology for nurses. Cambridge: Polity Press, pp. 140-148. Elliott, E. Harrop, E. Rothwell, H. Shepherd, M. and Williams, G. 2010. Working paper 134: The impact of the economic downturn on health in Wales: A review and case study. Cardiff school of social sciences (November 2010), pp. 29-59. Gallo, W. Teng, H. Falba, T. Kasl, S. Krumholz, H. and Bradley, E. 2006. The impact of late career job loss on myocardial infarction and stroke: A 10 year follow up using the health and retirement survey. Occupational and Environmental Medicine 63(10), pp. 683à ¢Ã¢â€š ¬Ã‚ 687. Graham, H. 2007. Unequal lives: Health and socio-economic inequalities. Buckingham: Open University Press. Grzywacz, J. and Dooley, D. 2003. Good jobs to bad jobs: Replicated evidence of an employment continuum from two large surveys. Social Science and Medicine 56, pp. 1749-1760. Marmot, M. (Chairman). 2010. Fair society healthy lives strategic review of health inequalities in England post 2010. London: The Marmot Review, pp.44-77. Marmot, M. and Bell, R. 2009. How will the financial crisis affect health? BMJ 338(b) 1314. Martikainen, P. Mà ¤ki, N. and Jà ¤ntti, M. 2007. The effects of unemployment on mortality following workplace downsizing and workplace closure: a registerà ¢Ã¢â€š ¬Ã‚ based followà ¢Ã¢â€š ¬Ã‚ up study of Finnish men and women during economic boom and recession. American Journal of Epidemiology 165(9), pp. 1070à ¢Ã¢â€š ¬Ã‚ 1075. Mathers, C. and Schofield, D. 1998. The health consequences of unemployment: the evidence. Medical Journal of Australia 168, pp. 178à ¢Ã¢â€š ¬Ã‚ 182. Moser, K. Goldblatt, P. Fox, J. and Jones, D. 1990. Unemployment and mortality. Longitudinal study: Mortality and Social Organisation. London: OPCS. ONS. 2009. Health expectancy at birth. Office for National Statistics [online]. Available at: http://www.statistics.gov.uk/StatBase/Product.asp?vlnk=12964 [Accessed 9th March 2011]. ONS. 2010. SOC2010 volume 3 NC- SEC user manual [online]. Available at: http://www.ons.gov.uk/about-statistics/classifications/current/soc2010/soc2010-volume-3-ns-secrebased-on-soc2010user-manual/index.html [Accessed 27th February 2011]. Parliament. 2005. Select Committee on Science and Technology  First Report [online]. Available at: http://www.publications.parliament.uk/pa/ld200506/ldselect/ldsctech/20/2004.htm [Accessed 27th February 2011]. Petterson, I. Hertting, A. Hagberg, L. and Theorell, T. 2005. Are trends in work and health conditions interrelated? A study of Swedish hospital employees in the 1990s. Journal of Occupational Health Psychology 10(2), pp. 110à ¢Ã¢â€š ¬Ã‚ 120. Price, R. Choi, J. and Vinokur, A. 2002. Links in the chain of adversity following job loss: How financial strain and loss of personal control lead to depression, impaired functioning, and poor health. Journal of Occupational Health Psychology 7(4), pp. 302-312. Price, R. Friedland, D. and Vinokur, A. 1998. Job loss: Hard times and eroded identity in J.H. Harvey (Ed.) Perspectives on loss: A sourcebook. Philadelphia: Taylor Francis, pp. 303à ¢Ã¢â€š ¬Ã‚ 316. Ruhm, C. 2005. Healthy living in hard times. Journal of Health Economics 24(2), pp. 341à ¢Ã¢â€š ¬Ã‚ 63. Solantaus, T. Leinonen, J. and Punamà ¤ki, R. 2004. Childrens Mental Health in Times of Economic Recession: Replication and Extensions of the Family Economic Stress Model in Finland. Developmental Psychology 40, pp. 412à ¢Ã¢â€š ¬Ã‚ 429. Strully, K. 2006. Job loss and health in the US labour market. Demography 46, pp. 221à ¢Ã¢â€š ¬Ã‚ 226. Treanor, J. 2008.  Northern Rock to make 800 compulsory redundancies.  The Guardian [online] 31.07.2008. Available at: http://www.guardian.co.uk/business/2008/jul/31/northernrock.creditcrunch [Accessed: 06.03.11]. Weber, A. and Lehnert, G. 1997. Unemployment and cardiovascular diseases: a causal relationship? International Archives of Occupational Environmental Health 70(3), pp. 153à ¢Ã¢â€š ¬Ã‚ 160. Yuill, C. 2009. The Credit Crunch and the High Street: Coming Like a Ghost Town. Social Research Online [online] 14(2). Available at: http://www.socresonline.org.uk/14/2/12.html [Accessed: 8th March 2011].

Religion :: essays research papers

MY RELIGION Religion was a small part of my family when I was young. I remember getting dressed in a pretty dress and jelly shoes every Sunday morning. Attending a small Baptist church located in the country on a windy, dirt road was our assumed religion. Sometimes my mother and I would go or my favorite sister would take me. However, when my mother would take me and my sisters, there were instances when my mother would flee from the church to the van, for what reason, then I did not know. Of course, I would run only to find her to be in the van with tears streaming down her cheeks and smoking a cigarette. I never understood the meaning until I grew older and learned of the unrighteous things she had done in the past. The preacher’s sermon would attack her conscience terribly. I believe my mom wanted her kids to know about the Creator and endured the ‘mental pain’ to complete the task. Soon enough when I turned twelve, things changed and we did not attend church that regularl y and eventually leading to not at all. In middle school, I made a friend, Kelly, who attended church every Sunday. My mom did not frown upon me being with her so I would spend some Saturday nights with Kelly and wake up to attend church with her. It was great fun because there was a band and they made it lively. Unfortunately, Kelly moved away and we lost touch completely and I did not attend church again until I met my husband thirteen years later. A long time, yes I know! To be upfront, he is an Atheist and has been through a lot of ordeals in his life and blames God for it so no matter how many times I try to steer him into believing, it fails. His father attends Easter service every year in a Presbyterian church and always asks us to come. I always do and I bring along our son who is now three-years-old. I know he does not understand but I want for him what I had when I was younger.

mardi gras :: essays research papers fc

Mardi Gras, literally â€Å"Fat Tuesday,† has grown in popularity in recent years as a raucous’ sometimes hedonistic event. Buts its roots lie in the Christian calendar, as the â€Å"last hurrah† before Lent begins on Ash Wednesday. That is why the enormous ends abruptly at midnight on Tuesday. There are well-known season-long Carnival celebrations in Europe and Latin America, including Nice, France; Cologne, Germany; and Rio de Janeiro, Brazil. The best known celebration in the United States is in New Orleans and the French-Catholic communities of the Gulf Coast. Another popular site for the celebration of Mardi Gras is Galveston, Texas. Mardi Gras has become a major influence to the people and the economy of Galveston. With its great history and deep economic impact Mardi Gras is beneficial to both the community and visitors to the Island.  Ã‚  Ã‚  Ã‚  Ã‚  The first celebration took place in 1867, when a dramatic entertainment and masked ball took place in t he old Turner Hall. The dramatic entertainment was a scene from â€Å"‘King Henry IV,’ featuring Alvan Reed (a justice of the peace weighing in at 350 pounds!) as Falstaff† (Mardi Gras!). The first time Mardi Gras was celebrated to any great extent was in 1871, when there were two night parades by separate organizations, one known as the Knights of Momus and the other as the Knights of Myth, both of which devised masked ball, exquisite costumes. In the years that followed, the parades and balls grew more elaborate and attracting attention throughout the state. After the hurricane of 1900 the events were discontinued for several years. The celebrations were gradually revived, but not on an extensive scale. It was not until 1914 that a group called the â€Å"Kotton Karnival Kids† staged parades for both Mardi Gras and the Galveston Cotton Carnival. â€Å" The 1917 masked ball took on added glamour with the first official appearance of King Frivolous and his court,...†(Mardi Gras!). The king was given the key to the city. With the outbreak of World War I, Mardi Gras was confined to small single day festivities. Shortly after the war the celebration a new revival. It was not until the threat war once again placed the celebration on hold. â€Å"In 1985, native Galvestonian George P. Mitchell and his wife, Cynthia, launched the revival of a citywide Mardi Gras celebration† (Mardi Gras!). Now under the supervision of the Galveston Park Board of Trustees, Mardi Gras spans two weekends and several days in between with parades, masked balls, and many different theatrical entertainments.

The Realm of Desire and Dream: Brazil and its Self-Constructing Middle Class of the 1980s, 1990s and Today :: Essays Papers

The Realm of Desire and Dream: Brazil and its Self-Constructing Middle Class of the 1980s, 1990s and Today The discourse of self-definition in Brazil is based on perceptions of economic success, material value and social prestige. Throughout the 1980s and early 1990s, there was a general scramble to reconstruct individual identity in social success and achievement. â€Å"Assertions of moral and cultural (class and racial) superiority† make up the discourses of national and regional identity, while simultaneously setting up the social building blocks of discrimination and stratification (25). Through the strange consumption of not only goods, but the commodification of experiences, the Brazilian middle class sought to redefine their lives and social status, and ultimately create a world that thrives on social division and prejudice. In Maureen O’Doughterty’s Consumption Intensified, â€Å"the dual vision† of the â€Å"immediate reality of crisis and the desired reality of the First World† is shown to have shaped middle class consciousness and desire, and further deepen the marks of division within this â€Å"heterogeneous† middle class (O’Doughterty 15, 5). â€Å"Transnational consumption, in the form of travel experiences, especially to Disney World, and consumption of imported goods† is a surprising social construction of value and rank, and expresses the influence of a foreign ideal on Brazilian social identity (23). Sustained comfortable living, and superiority over another class of people, was desperately appealing to many Brazilian families in the throes of the economic crisis, as demonstrated by the commodification of a Disney experience in the United States through bought and displayed goods, and the suggestion of expense that goes with it. The suggestion of expense and wealth throughout the crisis shaped the new concept of a Brazilian middle class â€Å"character,† a quality of living that could not be removed by an instable economy and loss of existing values. The presentation and propagation of this â€Å"character† was an extension of the old lush life prior to the crisis, and a dogged determination to hold to â€Å"traditional values.† Throughout the economic crisis, the middle class wanted to be perceived as continuing to enjoy â€Å"lush private space where elevated social status is proclaimed, cared for, and safeguarded† (O’Doughterty 9). Yet the â€Å"sense of past and hopes were contradicted by the experience of inflation crisis,† and a new social construction of reality emerged that was tangible in all its effects and efforts (O’Doughterty 9). The act of consuming goods itself is political, and â€Å"consumption is central to middle-class self-definition, not only in prosperity, as has more usually been shown but in any and all circumstances, even in recession† (O’Doughterty 11).

The Role of Inflammation in the Advancement of Chronic Obstructive

The Role of inflammation in the advancement of Chronic Obstructive Pulmonary disease. Introduction Chronic obstructive pulmonary disease (COPD) is the collective term used for respiratory disease, including chronic bronchitis and emphysema. The disease develops slowly and is often not diagnosed until it is advanced and irreparable damage is evident (Global Initiative for Chronic Obstructive Lung Disease, 2011). The disease is characterised by airflow obstruction and lung parenchyma.Parenchyma, associated with emphysema, is the permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by airway wall destruction, without obvious fibrosis (Demirjian and Kamangar, 2011; Atsuyasu et al. , 2007). Airflow limitation results from loss of elastic recoil and reduced airway tethering. Chronic bronchitis leads to narrowing of airway calibre, increasing airway resistance. Patients may display signs of one or both of these diseases as they frequently occur in associat ion with each other.Common symptoms are wheezing, coughing, shortness of breath on exertion, production of sputum and recurrent respiratory infections (Global Initiative for Chronic Obstructive Lung Disease, 2011). There are a host of triggers that exacerbates symptoms including smoking and environmental pollutants, resulting in chronic inflammation (Kazuhiro and Barnes, 2009; Manuel et al. , 2002). â€Å"Inflammation is defined as the presence of redness, swelling and pain, caused by the presence of edema fluid and the infiltration of tissues by leukocytes† (Nairn & Helbert, 2002, pp15).Inflammation is a key biological response to eliminate harmful pathogens, but there is increasing evidence to suggest that chronic inflammatory responses are accountable for the advancement of this disease and other chronic diseases including coronary artery disease, cancer, rheumatoid arthritis and multiple sclerosis. This review explores the correlation between COPD and inflammation and the subsequent effects on the systemic systems and the link with coronary heart disease (Mantovini et. al. , 2008; Mohr & Pelletier, 2005; Sattar et. al. , 2003; Powells et. al. , 2001; Danesh et. al. 2000; Murdoch & Finn, 2000). Methods Search engines used were Google Scholar and Pub Med using the keywords COPD, inflammation, disease, apoptosis, interleukin 8, cytokines, coronary heart disease and COPD. Searches were restricted to dates between 1999 and 2012. The majority of the included papers were obtained from the reference lists of other research papers. COPD risk factors: COPD is strongly linked with repeated exposure to noxious particles or gases and cigarette smoke has been acknowledged as a prime risk factor (Fabri et. al. , 2006; Lindberg et al. , 2005; Pauwels and Rabe. 2004, Association for Respiratory Technology & Physiology, 2000). Smokers have an increased prevalence of respiratory and lung function abnormalities, a greater rate of decline in FEV1 and a higher mortality rate than non-smokers (World health organisation, 2012). However, only a third of smokers develop COPD which implies that other factors such as genetics and environment are involved (Agusti, 2003). Exposure to air pollution caused by heating and cooking with bio-mass fuels in poorly ventilated housing are major risk factors for COPD, especially in developing countries (Pauwels & Rabe, 2004).The most documented COPD genetic risk factor is the deficiency of Alpha -1-antitrypsin, a polymorphic glycoprotein which offers anti-protease protection against the serine proteinease, neutrophil elastase (Abboud & Vimalanathan, 2008; Devereux, 2006; Siafakas & Tzortzaki, 2002; Fabbri et al. , 2006). Research studies (in vitro) indicated that Alpha – 1 – antitrypsin also possesses anti-inflammatory capabilities that extend beyond its anti-protease role, including regulation of CD14 expression (Nita, Serapinas & Janciauskiene, 2007), inhibition of TNF-? ene upregulation (Subramaniyam , 2007) and inhibition of lipopolysaccharide activation of monocytes and neutrophil migration (Janciauskiene et al. , 2004). Deficiency of Alpha -1-antitrypsin is associated with COPD progression in both smokers and non-smokers, although far greater in smokers (Bergen et al. , 2010; Fabbri et al. , 2006; Siafakas and Tzortzaki. , 2002; Foos et al. , 2002). Studies have suggested that smoking with this genetic disposition will substantially increase risk of developing COPD (Kohnlein & Welte, 2008; Pauwels & Rabe, 2004; Foos et al. , 2002; Siafakas & Tzortzaki, 2002; Association forRespiratory Technology and Physiology, 2000). Pathogenesis of COPD Exposure to noxious particles â€Å"†¦ triggers cytokine activation to recruit cells, which play a vital role in removing the noxious agents†¦ † (Nairn & Helbert, 2007, pp22). An infiltration of neutrophils, eosinophils and CD8+ T-lymphocytes into the airways and lungs follows (Demedts et al, 2006; Mahler et al. , 2004; Sopo ri, 2002). High concentrations of chemokines, interleukon-8 (IL8) and tumor necrosis factor-a have been found in patients with COPD which are potent activators and chemo-attractants of leukocyte subpopulations (Murdoch and Finn, 2000; Yamamoto et al. 1997). The interaction of chemo-attractants with leukocytes initiates a series of coordinated and cellular events, which includes phagocytosis, release of soluble anti-microbials and formation of reactive oxygen compounds involved in intracellular killing (Murdoch & Finn, 2000). Neutrophils and macrophages release elastase, stimulating the production of mucus to assist in ridding the airways of the irritants and subsequent waste generated by the inflammatory response (Shimizu et al. , 2000).Other processes such as neutrophil necrosis and reactive oxygen species further contribute to mucus hyper secretion (Kim and Nadel, 2004; Mizgerd, 2002). When an inflammatory response is no longer needed protease inhibitor cells dampen the response. Research suggests that the inhibiting response in COPD is not triggered and chronic inflammation presides, representing a crucial mechanism in the pathogenesis of COPD (Demedts et al. , 2006; Hodge et al 2004). Hypersecretion of mucous can inhibit the ciliated epithelium from transporting mucus from the airways.Subsequent delays in bacteria clearance results in bacterial colonisation, which stimulates further granulocytic recruitment to the airways, escalating the inflammatory response. Chronic inflammation is linked with tissue destruction, imbalance of proteolytic and anti-proteolytic activity, hyper secretion of mucus, increased apoptotic activity and oxidative stress which contribute to the progression of COPD. Long term, chronic inflammation can result in widespread airway and parenchymal cell destruction which further contributes to disease progression (Mantovini et al. 2008; Mohr and Pelletier, 2005; Sattar et al. , 2003; Sopori, 2002; Powells et al. , 2001; Danesh et al. , 2 000; Murdoch & Finn, 2000). Research suggests that macrophages express a markedly lower amount of toll like receptors in COPD suffers, resulting in a decreased recognition of microbes, facilitating damaging microbial colonisation, which may explain the increased amount of respiratory infections in COPD sufferers (Schneberger, 2011; Droemann et al. 2005). Infection initiates a biased release of inflammatory mediators which may escalate the pathogenesis of the disease (Gaschler et al. 2009, Ritter et al. , 2005; Sethi, 2000). Oxidative stress Demedts et al, 2005 found that the alveolar macrophages of COPD sufferers produced much higher levers of oxygen radicals and myeloperoxide which are important for the destruction of inter-cellular pathogens. Oxidant/anti-oxidant imbalance can result in the inactivation of anti-proteinases, airspace epithelial injury, increased sequestration of neutrophils in the pulmonary microvasculature, and gene expression of pro-inflammatory mediators, all of which exacerbate the inflammatory response (MacNee, 2000 Drost et al. 2005). Emphysema like changes have been show in the CT scans of malnourished women, suggesting that diet has an effect on lung tissue in the absence of smoking (Coxon et al. , 2004). Dietary supplementation then may be a beneficial therapeutic intervention in this condition, as antioxidants not only protect against the direct injurious effects of oxidants, but fundamentally alter the inflammatory events that play an important part in the pathogenesis of COPD (Coxon et al. , 2004; MacNee, 2000). Apoptosis and COPDResearch suggests that there is increased apoptosis of epithelial cells in smokers and COPD patients. Apoptosis persisted despite smoking cessation which suggests apoptosis may play a part in driving the inflammatory process and progression of the disease (Hodge et al. , 2003). Increased apoptotic alveolar epithelial and endothelial cells in the lungs not counterbalanced by proliferation and sufficient ph agocytic clearance results in destruction of lung tissue and development of emphysema (Demedts et al, 2006; Kazutetsu, Naoko & Atsushi, 2003; Barnes et al. 000) Apoptosis can be induced by various stimuli, including oxidative stress, elastase and infiltrating cytoxix CD8 + T cells which are all associated with inflammation (Kazutetsu, Naoko and Atsushi, 2003). Efferocytosis allows for the removal of apoptotic material with minimal inflammation and prevents the development of secondary necrosis and ongoing inflammation. Failure of this highly conserved process may contribute to disease pathogenesis by impeding both the resolution of inflammation and the maintenance of alveolar integrity (Mukaro and Hodge, 2011; Taylor et al. , 2010; Morimoto et al, 2006; Vandivier et al, 2006).Proteolytic/Anti-proteolytic activity Mukaro and Hodge, (2011) suggests that in COPD there is an imbalance between proteolytic and anti-proteolytic activity, a prominent factor in the pathogenesis of this disea se, which may contribute to lung parenchymal destruction. Research has also found that macrophages demonstrate defective phagocytic ability against common airways pathogens in COPD (Taylor et al. , 2010; Hodge et al. , 2003), The findings of Berenson et al. , (2006), supported a paradigm of defective immune responsiveness of alveolar macrophages, but found no significant differences in the blood macrophages of COPD sufferers.Taylor (2010) believes that persistence of bacteria as a consequence of defective phagocytosis may be a chronic antigenic drive for chronic inflammation. Systemic effects of COPD â€Å"Chronic inflammation is present in all disease processes, mediating all stages of disease from initiation, manifestation and maturation† (Sompayrac 2003, pp12). Compelling epidemioligical data links systemic inflammation to atherosclerosis, ischemic heart disease, strokes, and coronary deaths (Danesh, Whincup and Walker, 2000; Ridker, 1999).These observations have been stro ngly supported by experiments that show the direct effects of certain inflammatory markers, such as C-reactive protein (CRP), on the pathogenesis of plaque formation (Zwaka, Hombach and Torzewski, 2001; Lagrand, Visser & Hermens, 1999). A study by Gan, Man & Sin, 2003) found that patients with COPD were 2. 18 times more likely to have an elevated circulating c-reactive protein levels. Evidence strongly suggests that there is relationship between COPD, systemic inflammation, and cardiovascular diseases.Studies show that patients with mild-to-moderate COPD, cardiovascular disease is the leading cause of morbidity and mortality (Din and Man, 2009; Pope et al, 2003). As these diseases share similar risk factors such as smoking, increased age and inactivity, causation is unclear and is likely to be due to multiple factors, including lifestyle, environmental and genetics (Gan, 2005; Agusti et. al. 2003). Discussion Inflammation, it would appear, is a double edged sword; crucial for cleara nce of pathogens and recovery from injury; but can also contribute to life threatening chronic diseases (Smith, 1994; Sporori, 2003).COPD is a complex condition, influenced by multiple genetic and/or environmental risks. A cycle of low grade inflammation is the consequence, with destructive and damaging effects, resulting in mucus hyper-secretion, airway obstruction, increased elastase production and oxidative stress, which encourage further inflammation and destruction. COPD is associated with exposure to smoke or noxious gases, however inflammation may also be caused by irritation from coughing, wheezing, respiratory infections and mucus production. Most exacerbations of COPD are caused by bacterial or viral infection (Sanjay and Murphy, 2008; Sanjay 2008).Mucosal cells produce mucus, which irritates the airways causing airway obstruction. This subsequently reduces FEV1, and cough effectiveness, which contributes to the build up of bacterial mucus. Imbalance between proteolytic an d anti-proteolytic activity presides, creating an ideal environment for infection. Research suggests that macrophages express a markedly lower amount of toll like receptors in COPD suffers, resulting in a decreased recognition of microbes, facilitating damaging microbial colonisation, which may explain the increased amount of respiratory infections in COPD sufferers (Schneberger,2011; Droemann et al. 005). Infection initiates a biased release of inflammatory mediators which may escalate the pathogenesis of the disease (Gaschler et al. , 2009, Ritter et al. , 2005; Sethi, 2000). Researchers have found high levels of neutrophils, macrophages and CD8+ cells in ex smokers (Lappers et al. , 2006). Thus, suggesting that inflammatory changes in COPD, although initially induced by inhalation of noxious agents, are fundamental to the disease process, rather than to the initial trigger per se (Gamble et al, 2007). Studies have shown that airway epithelial and T-cell apoptosis in COPD continue s despite smoking cessation (Lappers et al. 2006). Excess apoptosis results in inappropriate destruction of host tissue, leading to atrophy and tissue necrosis, which in turn further stimulates the inflammatory response and perpetuates the situation. We have already ascertained an imbalance between the proteolytic and anti-proteolytic activity and this is another factor that contributes, resulting in failure to resolve the inflammatory reaction rapidly (Hodge et al. , 2005). Un-cleared apoptotic cells may undergo secondary necrosis with discharge of injurious cells contents resulting in tissue destruction and further inflammation.Inability to remove apoptotic cells and debris created overwhelms the normal clearance mechanisms, stimulating further inflammatory responses, further contributing to COPD pathogenesis (Sanjay and Murphy, 2008; Sanjay 2008). It has been identified that the immune system may become less responsive, the longer that chronic inflammation presides, which may lea d you to believe that this would initiate an inhibitory effect on the inflammatory process. However this is not the case and the inflammatory process persists, presenting as low level chronic inflammation.In addition a less responsive immune system is more susceptible to infection, exacerbating the inflammatory response (Sanjay and Murphy, 2008; Sanjay 2008). There appears to be strong epidemiological links between cardiovascular disease and COPD. The same inflammatory markets are evident in both suggesting a systemic link. Both diseases share similar risk factors, so it is difficult to determine initiation of the diseases. One could also argue that the debilitating effects of COPD, which include a reduced exercise capacity, dyspnoea and deconditioning increase the risk of cardiovascular disease development.In conclusion, it appears that adaptive immune is active in the disease progression of this complex pathophysiological syndrome. Particularly elaboration and production of cytoki nes, chemical mediators and auto-antibodies, which directly injure respiratory tissues. CD8+ mediates tissue destruction, whereas CD4 orchestrates inflammatory responses, which facilitates humoral immune responses (Gadgill and Duncan 2008). Conclusions made in this review are only valid within the boundaries of the research and papers used. 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The Assassin – Creative Writing

He stood alone in the dilapidated old home. The shadows were gathered and the man in the moon was screaming in agony. His face was expressionless, with eyes as sharp as a spinning needle, His skin was pasty white. The television emitted a soft glow upon his face, highlighting his pupils. In his hand, was as blade, long and sharp, The very point was shimmering as he slid the cloth up and down the side of the machete-like knife, he pulled his slimy, greasy lips back over his yellow stained teeth and smiled. He sat in his armchair in front of the television and slid the knife into the holder around his waist. Then a loud ringing pierced the silence, He picked up the receiver and a shadowed, scratchy voice began to give him details; â€Å"11:45, Elm Street,† He carried on, â€Å"He's a â€Å"6'2†³ft dark haired guy; He will be wearing a suit and will be carrying a gun†. He was waiting for one last detail â€Å"à ¯Ã‚ ¿Ã‚ ½16,000†. Then he dropped the phone and looked at the clock, â€Å"10:55pm† He left for Elm Street. The night was cold; snow fell gently, giving the road a smooth, white blanket. The car engine purred as he sat waiting and watching. The victim was seen, the engine was stopped. He stepped out of the car and began to walk to where the victim's car was parked. Both men were headed to the parked car. The victim was a middle-aged man, shivering in the cold. When they both reached the car, the Assassin walked up to the victim from behind. There was a flash of steel, a blood boiling scream and a final splash of blood. Then there was silence. 6 Weeks later. Punchenello's hotel. It was old and beaten up. Most of the guests were drug addicts, drug dealers or prostitutes. On the top floor were two men; the first was Mr.Punchenello and the other was one of his men, Jack Finito, † He took out Louie, cut a great hole n his back.† â€Å"We gotta get this guy boss† Louie Punchenello was getting frustrated, â€Å"Ok, ok, ok! I know just the guy to pop him, leave it to me† Punchenello sounded confident that his man would take care of business. Back at the Assassins home, he was shining his blade when he received a letter that read. Dear Mr.Payne I know of your recent doings. 6 weeks ago you did a little job for someone, now I need you to do a job for me. Come to Punchenello's hotel tonight at eleven if your not there, we will come find you. We need your skills Max, 11'o clock. Yours Jack Finito The letter sounded fishy so Max would have to have a little more firepower, just in case. Max went to see a man called Alex Gigoni A.K.A â€Å"Ammo† he supplied Max with more than a knife. A colt commando, pump-action shotgun and a few Molotov Cocktails. The clock hit 10'o clock and Max was preparing his weapons, shining his blade. The time flew by and it was soon â€Å"10:35† and Max was on his way. The car engine died and he stepped out, In front of the hotel. He knocked firmly on the door and Jack Finito opened it â€Å"Come in Mr.Payne, your late†. The room was suddenly filled with men, all armed and pointing their guns towards Max. Reacting almost immediately Max dived out of the room while hurling a Molotov Cocktail into the room. The bottle hit the floor with a crack and a burst of flames flooded the room, it was like a bottle of fire had been opened. Max stood at the door of the blazing inferno, pulled out dual Berrettas waiting for men trying to get out of the smoke; there were no survivors. Max had been set a trap, but he hadn't taken the cheese, so he was going after the rat, Punchenello at the top floor of the hotel. The elevator obviously hadn't been used in years and there were at least 6 floors. He would have to climb the stairs without being spotted by more of Punchenello's men. Max flew up the stairs and standing there was Finito, Jack jumped out of skin, â€Å"MAX PAYNE! How the hell did you survive that?!?† â€Å"Lets just say an angel was watching over me† â€Å"Your Finito, Finito† and with that Max pulled the trigger on his handgun and blew Jack away. He carried on flying up the stairs still holding his guns firmly between his sweaty palm and fingers, he came to the penthouse door he could hear heavy breathing on the other side of the door. He smashed the door open and saw Punchinello on the phone. Punchinello jumped out of his seat and reached for his gun. â€Å"I wouldn't do that if I were you† Max said in a cocky voice. Punchinello smiled I think that tables have already turned Max. Max felt a guns barrel stick into the back of his head leading him into a chair in front of Punchenello's desk. Max saw him, he was 7ft tall and built like an Ox still pointing his gun straight as Max's forehead. â€Å"Hello Max† He said, Max hid his guns around his back waiting for his back to be turned. Punchenello began to speak to Max about how not to cross paths with serious men † We are dangerous Max, please don't think about making any more business around these parts. We own this town now and we wouldn't think twice about disposing of you†. The large man in front of him pulled the gun away from Max, and Max sighed a sigh of relief. Punchenello carried on talking, but Max wasn't listening he was figuring out how to kill both of them so quickly that no sound could be heard†¦ then Max remembered his blade†¦ with his knife in one hand and his handgun in the other. Max jumped out of his seat and drove the 8-inch knife deep into the hired Assassins back killing him instantly. Max rolled on the floor and jumped up, pumping Punchenello full of lead he could use his finger as a pencil. Someone must of heard the gunshots because the whaling of sirens could be heard in the distance.. Max jumped down the fire escape and ran into the night†¦ then he pulled his slimy, greasy lips over his stained yellow teeth and smiled. The Assassin – Creative Writing Engulfing his surroundings, as it crept out from the opening of his mouth, the smoke slowly drifted away from his lips. He leant back onto the damp wall, creating a haze of thick opaque smog and slowly tilted his head backwards in ecstasy. He gently exhaled into the cold bitter air of the night. Frequently he would be startled by the wail of police sirens, but they became increasingly fainter as they moved further and further away, the occasional barking of a dog and the rustling of leaves through the alleyway in which he was standing were the only other sounds that could be heard. The adrenaline surged throughout his body and he was left fidgeting in anxiety. The potent smell of marijuana was vivid in the depths of the alley where he gripped a neatly rolled and tightly packed cannabis joint; he inhaled deeply and was breathing with deep satisfaction. As the THC floated through his bloodstream and as the dopamine was released in his brain, he suddenly felt tranquilized and more relaxed. He closed his eyes, trying to calm his nerves and he swayed uneasily for a second, before shaking his head and regaining control. The darkness of the early morning was menacing; few stars glittered in the night sky and the subtle glow of the moon was partly concealed by the passing clouds, where black faded into hues of dark blues and deep, daunting violets. The gloom was still surrounding him and the frosty mist shrouded everything wanting to be seen. His shifty eyes watched in anticipation from the corner of an alley way for any kind of living being, while he clenched the revolver that was held in his right hand. The rubber soles of his sneakers were damp from the dew. From his still position, he could see the door of the apartment from the light of a street lamp. He was trying to remain hidden to maintain his stealth. The rest of the scenery was unfocused in his vision, as he stared at the door in expectancy. There was no one to be seen in the empty street. The only breathing creatures around were a few alleyway rats, shuffling around near the dustbins. The sight of marshy greens and soiled browns merged together to create the outlook of a risky situation. He became slightly excited as a midnight blue BMW M3 coupi was approaching from a distance; roaring from afar, before breaking quickly causing a loud screech leaving visible skid marks on the tarmac, the car slid to stop outside the apartment door where it knocked three dustbins over. He noticed the scratch on the driver's side door and the damaged bumper from the collision. Even though the thought of his mission was driving him; he knew it had to be done with care. He kept calm and composed still with the cannabis joint hanging from the tip of his lips. It began to drizzle with rain; he lifted up his hood and placed it over his head to conceal his face. He pushed away from the wall, concentrating on his assignment. He dropped the joint as all of the contents had burnt away and stamped it out. Desperately trying to make as little noise as possible, he stood up straight and prepared himself with not even a prayer in mind, for the sin he was about to commit. A tall middle-aged man emerged from the vehicle; the man looked well off with pinstriped trousers, a white shirt that became drenched instantly due to the precipitation, a colourful tie and a blazer that he slung over his shoulder. He slammed his car door in a manner which made it obvious he was agitated due to his collision with the dustbins. He sighed loudly with disappointment as he observed the damage to the bumper and the scratch. The rain turned from a light drizzle to a heavy shower, the victim walked a couple of paces through the large puddles towards the building. Little did this man know that he was being closely watched, were these the last breaths of his life? He paused at the door while he searched for his keys. As he established the pocket in which his keys were, before he had the chance to reach them, the loud sound of a gunshot echoed through the neighbourhood. A 9mm bullet penetrated through his head like a key in a lock, knocking him to the ground instantly. Within a second, his mind departed the scene of flesh, blood and bones. Tearing his soul away from him, like pulling cotton through a bush of thick thorns. The victim lay there, the most stupid of people would be able to realise that this man was dead. It was a disturbing sight but the assassin still stood in the same position in which he had fired the weapon, with no mercy or reconciliation. The assassin slowly brought the gun back down to his side. He tucked the weapon into the back of his jeans. The assassin withdrew a cigarette from his a box of twenty Silk Cut. He lit it and took a deep draw and exhaled in a way of relief. He poked his head out of the alleyway to check if anyone was in sight, yet nobody but a stray cat was there. The surroundings were still; the atmosphere was damp, depressing and dead. The corpse was lying frozen by the curb. In a cavalier fashion, he walked out of the back alley with his shoulders shrugged in chilliness; his head low in cautiousness, and took a sharp left into a side street towards his carbon black Mercedes SLR. Unexpectedly, the wailing of a distant police siren grabbed his attention. The sound grew louder and louder and it seemed to be coming closer. A single drop of sweat began to form above his brow. What if he had been seen? What if for the first time, he had blown his cover? At that moment, a white police car rapidly passed by as he stood in panic. He sighed in relief and continued towards his automobile, uncaringly rattling his keys in his hand. His firm, steady footsteps represented his attitude, hard, harsh and heartless. He entered his car; seated himself, wedged the key in the ignition, turned on the engine. He took one last look at the scene through his rear view mirror and drove away never to return.