Racial Prejudices Research Paper Example | Topics and Well Written Essays - 750 words

Racial Prejudices - Research Paper Example According to Allport (1954), definition of prejudice is a negative bias directed to a particular group of people. On the hand, racism is has a foundation on beliefs and shown in behaviors that believes race to be a biological entity and claims other racial groups apart from their own are psychologically, intellectually and physically inferior (Allport, 1954). Pascoe (1985) describes racism that it results from race prejudice transformation and ethnocentrism through power exercise against another racial group regarded as inferior by institutions and individuals with unintentional and intentional support of the whole culture. Therefore, the racism core includes prejudiced mentality of superiority in a in group with a power exercise to subjugate a group considered out. Therefore, as prejudice is attitudinal in nature mainly, racism extends the attitude into a discriminating behavior against another group. Many theorists have tended to explain why racial prejudice is easy to develop. Som e claim that racial prejudice is one of the by-products of evolution for adaptive strategies for survival that make humans beings to distinguish between a foe and a friend (Oskamp, 2000). Furthermore, the process of natural selection programmed the human brain to depend on physical markers in assessment of a potential threat among competing different racial groupings. This perspective is echoed in prehistoric societies where interpersonal interactions among different tribes were noted to be dangerous in transmission of deadly diseases (Allport, 1954). Adaptive reactions to these threats were to attribute a potential threat to people of an out group who were identified by different physical features. From this perspective, racism and prejudice can be and has been embedded in the cultural, biological and social collective human consciousness. Pascoe (1985) points out that many scholars have conceptualized the psychodynamic of psychological processes thought to explain racial prejudice development and maintenance among the whites. The conceptual perspective views racial prejudice as an unconscious ego mechanism for defense designed for reduction of anxiety among most experience of white people due to conflicted super ego and id based racial feelings and thoughts (Oskamp, 2000). There are different sources of racial prejudice; key among them are various forms of fear. The expectation that another person will do harm , perception that the other’s difference in viewing the world will create to one’s own challenges, presumption that by interacting it will lead to rejection, embarrassment or ridicule and the fear generation of negative consequences due to negative stereotypes. According to Allport (1954), the theoretical support that suggests forcing of people to change their behaviors will results to a long term in change of attitude relates to the theory of cognitive dissonance that stipulates that people cannot think in a particular way and contrarily behave in a manner without interfering with the belief structure. Therefore, according to Pascoe (1985), two strategies can work to this problem: First, attention should be paid to the normative exertion to change behavior as contrary to legal pressure. Second, steps to be taken to make sure that the moral pressure conveyor is someone respected, similar to the target. Oskamp (2000) adds that strategies that try to change the

M5A2 - Leadership and Ethics Essay Example | Topics and Well Written Essays - 750 words

M5A2 - Leadership and Ethics - Essay Example Additionally, Clarke’s roles throughout his career reflect that he had a strong tendency for management rather than as a technical person. Clarke shifted from commercial and marketing positions to the head of stores which had little relevance to his previous positions. Similarly, he later moved from Supply Chain Director to IT Director. Both positions have little in common so it could be surmised that Clarke is more of a manager than a technical person who would be restricted to one field of expertise in TESCO. Moreover, it must also be related that Clarke has been moved around the world when TESCO required solutions to grave problems so Clarke can be seen as an adept manager, especially under pressure. Clarke’s role as a leader is confirmed most after talking to his subordinates. All of the people interviewed, at TESCO, viewed Clarke as an able leader such that they looked up to his example. Moreover, Clarke can be seen as a direction setter for TESCO given that TESCO has switched gears after Clarke took over as Group Chief Executive. 2. Describe the ethical model or framework used by the person to make ethical decisions—include the positives and negatives of your chosen leader's ethical model. Clarke can be seen as using a managerial grid leadership model for taking ethical decisions. The use of the managerial grid leadership model is augmented by the situational theory of leadership where the leader evaluates a situation in order to provide the decision (McKee & Carlson, 1999). The managerial grid model provides for two major constraints that the leader must consider – labour satisfaction and productivity. In addition to these major constraints, the leader may also be considering other smaller constraints such as public image, accountability, legal implications etc. The leader utilising the managerial grid model for ethical decision making tends to evaluate the provided situation in terms of the constraints in the situation (Griff in & Ebert, 2010). The primary aim of the leader is to optimise all available constraints in respect to each other such that no singular constraint overrides any other constraint. It must be kept in mind that labour satisfaction and productivity will operate as primary constraints while other constraints play secondary and tertiary roles only. This particular model of ethical decision making is restricted to Philip Clarke, Group Chief Executive for TESCO only since other managerial grid leadership models would have personalised primary, secondary and tertiary constraints being considered. The managerial grid leadership model for ethical decision making has the distinct advantage of optimising organisational aims and objectives achievement. This takes place as the ethical decision making process optimises inputs for Theory Y under which labour satisfaction is maximised in order to maximise productivity (Griffin & Ebert, 2010). Essentially, as labour satisfaction increases, the achiev ement of organisational aims and objectives becomes easier and simpler but it remains to be seen what direction organisational aims and objectives lie in. Given the nature of economic enterprises, it is common to find productivity at the top of the organisational aims and objectives list but other secondary and tertiary factors may also be available such as safety, ethical practices, corporate social responsibility etc. (Ray,

The Independent Review Essay Example for Free

The Independent Review Essay E. M. Forster (1879-1790) was the author of many well-known novels, and also several volumes of short-stories, essays and criticism. He is best-known for his 1924 novel A Passage to India, which has enjoyed a world-wide audience ever since its publication. Today he is considered as one of the prominent figures of British literature of the first half of the twentieth century. Forster once wrote, â€Å"Life is easy to chronicle, but bewildering to practice. † Edward Morgan Forster himself began his ‘bewildering practice’ on 1 January 1879, in London. When he was eight-years old, he inherited an amount ? 8000 from his great-aunt, Marianne Thornton, of whom he would later write a biography. This inheritance was sufficient to let Forster pursue his education and literary career in relative freedom from financial constraints and worries. Upon his graduation from Tonbridge School, Forster secured admission into Kings College, Cambridge where he studied classics and history, and was partly under the tutelage of Goldsworthy Lowes Dickinson, of whom he would later write a biography. At Cambridge, he was exposed to the values of liberal humanism and cultivated a respect for the freedom of individuality of human beings. Under the influence of the philosopher G. E. Moore, Forster developed an aesthetic belief that contemplating beauty of art constituted a nobler purpose in life. He also became a strong believer in the value of friendships, and struck lasting friendships which meant a great deal to him throughout his life. He would later travel to India with a group of university friends. â€Å"If I had to choose between betraying my country and betraying my friend, I hope I should have the guts to betray my country,† he would later say. During these years of higher education, Forster was a member of an intellectual clique at Cambridge called the Apostles, and through them came into contact with the members of the Bloomsbury Group, with which he would associate more closely in the subsequent years (Childs 6). Completing his education at Cambridge, he left England on a long trip to Italy and Austria, which would last for one year. Forster would spend a significant period of his life traveling. It was around this time, in 1901, that he began exercising his writing skills. He then started working at Working Mens College and subsequently taught at the extra-mural department of the Cambridge Local Lectures Board. Forsters literary career began in 1903, when he began writing for The Independent Review, a liberal publication that he co-founded with Lowes Dickinson and used as a platform for advocating anti-imperialism. Soon, Forster became a published author with the appearance of his first novel Where Angels Fear to Tread (1905). Forster used his knowledge of Italy to create a story that juxtaposed and contrasted the passionate world of Italy with the constricting values of suburban England. The result is a social comedy, which rather interestingly ends up as a tragedy dealing with rather unsavory aspects of death and frustrated love. It is the story of a young English widow, Lilia, who falls in love with an Italian, but the members of her family cannot accept this and try to wrest her back. This work was not well received by the public. By 1910, Forster would have written three more novels. The Longest Journey (1907) and A Room with a View (1908) exhibit a growing maturity in literary skills and artistic scope, and Howards End (1910) saw his rise to fame. Forster wrote most of his short stories and four novels before 1910. In the sixty years he lived after that, he would write only two novels, Maurice, in 1914, and A Passage to India, in 1924 (Tambling 2). After publishing his first novel, Forster left for Germany and worked for several months as tutor to the Countess von Arnim, in a place called Nassenheide. This experience would serve him in the characterization of Schlegel sisters in Howards End. Back in England, in 1907, he took on the role of a private tutor for an Indian Muslim, with whom he developed a close relationship that could be seen as homosexual love. Forsters famous work A Passage to India would be dedicated to this person. Forster was a covert homosexual all through his life. The posthumous publishing of his homosexual novel Maurice (1971) offers strong testimony to his sexual orientation, although it is difficult to ascertain how far his homosexual orientation may have influenced his work in general. However, he certainly felt frustrated for not being able to write about homosexual themes openly and it is possible that he stopped writing novels half-way through his life out of such frustration. In 1907, Forster wrote and published a novel about his Cambridge days, The Longest Journey. It tells the story of an undergraduate and a struggling writer, Rickie Elliot, who abandons friendship for the sake marriage, but is enlightened by his pagan half-brother. The Longest Journey was also Forsters favorite novel, despite the poor response it got from the critics and the public. Around this time, Forster was closely associated with the Bloomsbury Group, and was interacting with people such as Lytton Strachey and Rogery Fry. In his third novel, A Room with a View, which is also his second Anglo-Italian novel partly set in Florence and partly in English suburbia, Forster displays his contempt for English snobbery. It is a light and optimistic tale, a story of misunderstandings which however ends on a happy note as Lucy Honeychurch, the protagonist, acknowledges her love for the impulsive George Emerson over her feelings for the intellectual Cecil Vyse. Forster’s novels have already begun to display a common theme of sensitive characters struggling with the inflexibility of social codes that they are encumbered with as well the relative insensitivity of those around them. It can be conjectured that Forster’s frustration at the opposition of the conservative values of his time to his homosexuality may have taken a general form portraying the oppression of social rigidness in his novels. In 1910 came Howards End which is a social novel about sections of the middle classes, focusing on the question of who will inherit â€Å"Howards End,† which is Forsters metonym for England. The story centers on the relationship between the intellectual German Schelgel sisters and the practical, male-dominated, business-oriented Wilcox family. In the novel, Forster attempted to find a way for Wilcox money to become the support for Schlegel culture, and also for the future of rural England to be taken away from the influence of urban, commercial interests and placed once more in the hands of the farmers. The novel presents an ambitious social message, though not wholly practical or convincing. Howards End finally secured Forsters reputation and established him as a novelist. However, he would only publish one novel in the rest of his long life, besides sporadic publication of short stories, essays and so on. In 1911, Forster brought out a collection of short stories entitled The Celestial Omnibus. In 1912-13 he made his first visit to India, with R. C. Trevelyan, Dickinson and G. H. Luce. Here, he had the chance to observe the British colonial administration first-hand. After this trip, he wrote most of the first section of A Passage to India, but it was not until after a second visit, in 1921, when he spent six months as private secretary to a Hindu Maharajah, that he completed it. His masterpiece was published in 1924 and was unanimously praised by literary critics. Around this time he also worked on the homosexual novel Maurice: A Romance. Though it would not be published until after his death, it was circulated privately at the time, and is a story of cross-class homosexual love the kind of which Forster himself yearned for. During World War I, he worked with the International Red Cross and was stationed in Alexandria, Egypt. He also became a strong supporter of the Alexandrian poet C. P. Cavfy. During his stay in Alexandria, he struck an acquaintance with a teenaged tram conductor, Mohammed el-Adl, with whom he fell in deep love. Mohammed would die of tuberculosis in Alexandria in spring of 1922, and this loss weighed heavily on Forster for the rest of his life. Forster returned to England in 1919, after the war, but set off traveling again in 1921. On this trip to India he worked as the private secretary to the Maharajah of Dewas Senior, and his letters home from the two Indian trips were later published as The Hill of Devi (1953). In 1922 he published Alexandria: A History and a Guide, but could get it into circulation only in 1938. Pharos and Pharillon, which is a collection of Forsters essays on Alexandria together with some translations of Cavafys poems, was published in 1923. All through this time, Forster had been reworking on A Passage to India, which was published in 1924, almost a decade and a half after his previous novel Howards End. It is a novel about the clash between Eastern and Western cultures during British rule in India, and is generally considered among major literary works of the twentieth century. It is the story of Adela Quested and Mrs. Moores journey to India to visit Adelas fiance, and Mrs Moores son, Ronny Heaslop. There they meet a college teacher, Cyril Fielding, who is an avatar of Forster himself, the Hindu Brahmin Dr Godbole and the Muslim Dr Aziz. The novel revolves around Dr Azizs alleged assault Adela. Ms. Quested reports of an attempted assault by the Dr. Aziz and subsequently retracts her complaint. Once again, misunderstanding features prominently in Forster’s narrative. A Passage to India was widely acclaimed. For example, a critic at New York Times wrote: â€Å"The crystal-clear portraiture, the delicate conveying of nuances of thought and life, and the astonishing command of his medium show Mr. Forster at the height of his powers† (Forster, front flap). But mysteriously, at the height of his powers, Forster would choose to renounce novel writing. Some have speculated this could be because he felt he could not write openly and honestly about homosexual relations which he longed to write about. In 1927 he gave the Clark lectures at Cambridge University, which were published as Aspects of the Novel the same year. He was also offered a fellowship at Kings College, Cambridge. In 1928, his second collection of short stories, The Eternal Moment, was published. It is a collection of six stories predominated by fantasy and romance. For a while during the 30’s and 40’s, Forster became popular as a broadcaster on BBC radio. In 1934, he published his first biography Goldsworthy Lowes Dickinson. By this time he had been an active member of PEN, which was an association of writers founded in 1921 to promote the interests of literature. His opposition against the suppression of Radclyffe Halls lesbian novel The Well of Romance in 1928 helped him to become the first president of the National Council for Civil Liberties, in 1934. He was also seen as a noteworthy personage associated with the British Humanist Association. Around this time, Forster enjoyed a fulfilling personal life. He was involved in a happy relationship with a constable in the London Metropolitan Police, and was on friendly terms with his wife. He was part of social circle, which included the writer and editor of The Listener J. R. Ackerley, the psychologist W. J. H. Sprott, the composer Benjamin Britten, and such noted figures of the society. Forster also associated with many writers such as the poet Siegfried Sassoon and the Belfast-based novelist Forrest Reid. In 1936, Forster published his first collection of essays and occasional pieces, Abinger Harvest. At this point, he was elected Honorary Fellow of Kings, which entitled him to live at the college, as he did for the rest of his life. In 1947, he set out on lecture tours in the United States, and two years later he was offered and refused knighthood from the King. The same year he wrote the libretto for Benjamin Brittens opera Billy Budd, based on Herman Melvilles novella. The year 1951 saw the publication of Forsters second collection of essays and articles, Two Cheers for Democracy. In the immediately following years there was the publication of The Hill of Devi and two short-story volumes, under the generic name Collected Short Stories. The last published work of his life was Marianne Thornton, the biography of his great-aunt whose gift allowed him to go to Cambridge. In 1969 Forster was awarded the Order of Merit. He died shortly thereafter. E. M. Forster has never lacked for readers, is widely studied, has had his novels turned into highly marketable films, and has encouraged criticism usually of a strongly liberal-humanist kind, notes Tambling in his introduction to a book of critical essays on E. M. Forster. Forster explored the shortcomings of the English middle class and their emotional deficiencies, employing irony and wit. Today he is remembered for the impeccable style of writing that is evident in all of his novels and short stories. References: Childs, Peter. 2002. â€Å"A Routledge Literary Sourcebook on E. M. Forsters A Passage to India† (Routledge Literary Sourcebooks). London : Routledge. Forster, E. M. â€Å"A Passage to India. † 1989. Orlando, FL : Harcourt Brace Tambling, Jeremy. â€Å"E. M. Forster: Contemporary Critical Essays† (New Casebooks). 1995. New York : St. Martins Press.

Cantaloupe Description Essay Example for Free

Cantaloupe Description Essay The Cantaloupe At first glance, the cantaloupe looks round and light grayish-tan, with a hint of green. From afar it looks round and plain, about the size of a peewee soccer ball. On approach, the circular shape is less perfect with subtle dents and bumps all around. Surrounding the sphere shaped fruit are light tan lines like a dense city map with all the streets intertwining and curving around without any significant pattern, not geometric like gridlines. On the surface, there are small matchbook sized patches color the skin, some more yellow and other patches that are darker green. A particular indention looks like the fruit might have laid on a rock on the ground while it was growing. One end, where the flower might have once been, is the palest of yellow circles. On the opposite edge, the stubby vestige of a stem remains. This dried up nub is the brown and shriveled, slightly indented from the rest of the globe. Surrounding the stem is a dark circle of hunter green. Picking it up from the counter, the weight of this globular object seems significantly heavier than it looks, like a mini bowling ball. Despite the volume, it feels that the weight is not solid which is proven by the hollow sound the fruit makes when tapped, like patting a child on the head. The delineated lines feel like webbing and give the fruit a rough feel, but it’s not an uncomfortable roughness. The experience is somewhere in between a prickly cactus and a furry peach. At this point my mind starts to wander. Should I cut it open now or wait? Should I take a break? I look outside at the fat flakes of snow coming down outside and remind myself to get back to the task at hand. There is no resentment or anger. I look again at this object I have assigned myself to detail. When I am at a loss as to how to describe something in particular my mind wandering happens more frequently. I continue to focus my attention back to the cantaloupe as soon as I realize I’ve been distracted. I hold the cantaloupe to my eye. There is a faint line of brownish green that runs through the net-like lines covering the fruit. Some of the spaces between the lines look like parks because they’re darker green, while others ook grey like the concrete of a parking lot. My mind wanders again and I start to look to see if there are any recognizable maps in squiggles. I see a roundabout that reminds me of an intersection in England and another resembles the neighborhood where I grew up. The intertwining layers of the lines remind me of overgrown vines on a wall covering another layer of skin. The underneath layer has the vague look of green splotches, almost veins, like the streaks that run through blue cheese. I thump the cantaloupe again. It substitutes as a drum to make a tune. Apparently it has different thicknesses inside because the sound it makes when you knock it on the end is a higher pitch than when you rap it in the middle. One spot must be particularly thick because the sound is more substantial. Rubbing the skin makes the same sound as rubbing your hands together on a dry winter day. I try to make other noises using the produce, but intuition tells me that the only way to get another sound is to drop it on the floor. I’m not willing to do that. Before cutting into the orb, I notice a whiff of eau-de grocery store produce aisle a bit past its sell-by date. The smell isn’t strong and it’s only when I touch the fruit to my nose that I smell this. I then sniff each different area of the outer layer and notice that where the flower once might have been the smell is much stronger and sweeter. I scratch my finger nails on the rough skin, but it doesn’t affect the scent the way it would with an orange or lemon. It’s time to cut into the orb. Even as the knife makes the first gouge, clear pale orange juice escapes. I lick my fingers and find the sweet taste refreshing and different. Although the juice is the color of a Satsuma mandarin or a commercial worthy carrot, it tastes nothing like either. Slicing the melon in half, the cantaloupe now resembles a geode, with a plain outside and a brightly colored exotic inside. It’s filled with seeds and goo in the center. The slimy innards resemble the finest angel hair pasta, but instead of being the color of regular noodles, they are varying shades of orange, some even translucent. I carve out this gooey inside and the sweet smell now fills the air with its cloying tropical fermented flower mell. Friends who have been watching a movie in the other room come to see if they can have some, the smell having tempted them away from what they are doing. Ironic, because I’m no longer interested in the cantaloupe and ready to toss it into the composting bin. I send everyone away so that I can continue on. The meaty flesh isn’t too tough, nor is it too soft. I take a bite and let the flavor rush across my to ngue. The taste reminds me of summers on the farm eating the freshest fruits and vegetables straight out of the garden still warm from the sun. There’s a touch of salt in the taste, but the sweetness overpowers it. In spite the firm texture, the fruit feels soft and chewy and the volume of nectar is astounding. The tissue is softer and moister than the similar essence of a pumpkin and more compact than the inside of a fig. Squishing the orange flesh with my fingers, it all but dissolves into juice. What little remains is the finest of strings as soft as silk. I find a seed still attached, that I missed. The kernel is a flat oval with semi-pointed ends. Like a flat football with the air taken away, but miniscule in comparison. It’s almost as though the surrounding fibrous slime is dissolving in the air as I watch. I break open a seed using my fingernail. It’s soft and waxy, not much there. I take a wedge of the sliced cantaloupe and look at the difference between the skin and the edible meat. Like a rainbow, the color changes from thick rind on the outside to the orange moist, fleshy core on the inside. Like the color spectrum, the differences in shades are subtle, but quick. A yellow stratum is the most predominant, but considering the layer in question is less than an eighth of an inch thick, this golden subcutaneous layer isn’t very big. I make sure there isn’t anything I’ve overlooked and to check my notes for missing descriptive words. I’m shocked to look at the clock and see that more time has passed than I would have expected. I went several hours without checking my watch; something I can only do when I’m not bored. Learning to look beyond the obvious is something I already knew how to do. I enjoy observing people and watching facial expressions for meaning. What I’m not good at it is sitting still and holding my attention for long periods of time. Exercises like this help to train my brain to â€Å"settle own, focus, and catch up† as local monologuist Josh Kornbluth says. While I had to make a few self directed corrections along the way, I was fairly pleased that I was able to block out a significant amount of what was going on with family and friends in the other rooms and outdoors. Yes, there were a few times that my attention wandered, but I was back on track in seco nds rather than hours or days. The reward at the end was to finish a paper I was happy with and to share the small remainder of the cantaloupe with my friends while on a weekend away. Mission accomplished!

Sickle Cell Anemia And Hemophilia Biology Essay

Sickle Cell Anemia And Hemophilia Biology Essay Abstract In the following paper, sickle cell anemia and hemophilia disorders were studied extensively. Sickle cell anemia was found to be the disorder where the red blood cells develop into sickle shaped cells due to a mutation of the hemoglobin protein. When the cell becomes sickle shaped, they also become sticky and will clump with other cells in the blood vessel. This can lead to decrease blood flow in that blood vessel which will lead to various effects. Sickle cell anemia is a hereditary disease in that it is passed down generations genetically. The main effect of sickle cell anemia is the decrease in number of red blood cells in the blood and lack of oxygen transport to certain areas of the body. Though are many drugs to help with the pain caused by sickle cell anemia, there is no definitive cure to the disorder. However, the main type of treatment is bone marrow transplant. However this procedure is very risky and not advised unless the symptoms of sickle cell anemia are severe. There is much research being done on sickle cell anemia, but no definitive cure has been found. The life expectancy of patients with sickle cell anemia is from 40 -60 years old and majority of the patients are African descent. Hemophilia is the disorder that prevents the body to stop bleeding. If a person is cut, the body will not form clots to stop the bleeding because people with hemophilia lack a clotting factor. This is also a genetic disorder and is found only on the X chromosome. Hemophilia can be divided into two categories: hemophilia A (lacks clotting factor 8) and hemophilia B (lacks clotting factor 9). About 9 out of 10 people who have hemophilia have type A. Rarely, hemophilia can be acquired. This means that you can develop it during your lifetime. About 18,000 people in the United States have hemophilia. Each year, about 400 babies are born with the disorder. Hemophilia usually occurs only in males (with very rare exceptions). The major signs and symptoms of hemophilia are excessive bleeding and easy bruising. The main treatment for hemophilia is called replacement therapy. Concentrates of clotting factor 8 or clotting factor 9 are slowly dripped in or injected into a vein. These infusions he lp replace the clotting factor thats missing or low. Hemophilia treatment centers are located in many areas of the United States. These centers can provide treatment, education, and support to hemophilia patients, their families, and their health care providers. Sickle Cell Anemia What is Sickle Cell Anemia? Sickle Cell Anemia or sickle cell disease is a blood disorder that is genetic. This disorder affects the red blood cells of the human body and can cause much damage to the body. It causes the red blood cells of the body to become an abnormal shape, usually in the shape of a sickle or crescent. Red blood cells are cells that carry nutrients and oxygen to different organs in the body and carry carbon dioxide back to the lungs. However, Sickle Cell Anemia basically does not allow for the red blood cells to act normally. The way a red blood cell is able to carry the oxygen molecules to the organs is by a protein molecule located on the cell called hemoglobin. This molecule is able to carry oxygen from the lungs to the bodys tissues and return carbon dioxide to the lungs. A defect of this molecule can affect every part of the body that is supplied oxygen by red blood cells which is everything. In Sickle Cell Anemia, the regular hemoglobin is mutated and changes from the normal hemoglobin A to hemoglobin S. the ability for a protein to be mutated that is located on the red blood cells means that this mutation can will be passed down to the persons child, making this disease hereditary. The mutated hemoglobin causes the entire normal red blood cell to become sickle shaped and stickier. The abnormal cells begin to clump together and have a difficult time being transported throughout the body through the blood vessels. When the blood vessels become obstructed by the sickle cells, blood flow decreases in that part of the body. This will cause a lack of oxygen in those areas which, ultimately, leads to those cells death. Another characteristic of Sickle Cell Anemia is that the abnormal red blood cells have a shorter life expectancy. Normal red blood cells usually live up to 120 days and through a process called phagocytosis they are removed from circulation. However, the red blood cells infected with the sickle cell disease live only about 10 to 20 days. This means that the body needs to produce ten times as many red blood cells if the person has Sickle Cell Anemia than a normal person. However, the body cannot produce that many red blood cells that fast. Red blood cells are produced in bone marrow, located in the inner hollow interior portion of bones, by a process called erythropoiesis. The bone marrow cannot produce red blood cells fast enough to replace the dying ones. This will lead to decreased number of red blood cells which can lead to many side effects. Causes of Sickle Cell Anemia Sickle Cell Anemia is a type of disease that someone cannot get unless if they were born with it. This disease is an inherited blood disorder that one is born with. A person is born with genes that give him/her distinctive appearance and personality. They get these genes from their parents, half from each. In Sickle Cell Anemia, there is a specific gene that can be passed down generation which will cause the disorder. This gene, sickle cell gene (HbAS), is a recessive type of gene which means that unless there is another one of it, it will not be expressed. However, that gene will be part of them forever and there will be a 50% chance that their child will have that gene. However, if two people with the sickle cell gene have a child, then there will be a 25 % chance that there child will have the disorder, 50% chance that their child will have only sickle cell gene, and 25% their child will have zero copies of the sickle cell gene. This gene which represents a specific trait will cause the Sickle Cell Anemia. Once the person has the trait, then it will begin to cause the body to make abnormal proteins on the red blood cells called hemoglobin. As discussed earlier, the mutated form of hemoglobin causes the cell to become sickle shaped and cause all sorts of havoc in the body. In addition, a distinctive trait about Sickle Cell Anemia is that once someone gets it, there is no way to get rid of it. Also since this is a genetic disease, there can be different variations of the disease. If a person inherits one sickle cell trait and if the person has the abnormal hemoglobin C (not hemoglobin S which is present in Sickle Cell Anemia), then the person will develop a milder form of the Sickle Cell Anemia disease called HbSC. If a person inherits one sickle cell gene and one gene for beta thalassemia (another type of anemia) which can be 0 or + then the person will either severe case of Sickle Cell Anemia (if HbS Beta 0- thalassemia) or a milder case of it (if HbS beta +-thalassemia). Symptoms of Sickle Cell Anemia Even though that people are born with Sickle Cell Anemia, the symptoms do not appear until after 4 months of age. The symptoms of Sickle Cell Anemia can be divided into three categories: symptoms related to anemia, symptoms related to pain, and symptoms that arise due to disorder. The first category deals with how the lack of red blood cells can affect the body. The most common symptom is fatigue because in order for the body to function and stay alert, it needs oxygen which is what anemia decreases. In addition, anemia causes dizziness, headaches, pale skin, chest pain, coldness in the hands and feet, and shortness of breath. These are all caused by the lack of oxygen reaching certain areas of the body. The second category deals with symptoms that are related to pain. A person with Sickle Cell Anemia is likely to express pain throughout their body which is called sickle cell crisis. This occurs when there is a mass of sickle cells in the blood vessels. With decreased blood flow to organs and limbs, there is usually sharp pain and organ damage. This crisis also has a range on how painful the pain is. If it is an acute pain, then the pain will be mild to severe and may last from hours to days. On the other hand, chronic pain will last for a lot longer period of time and will be hard to bear and mentally draining. This pain may severely limit your daily activities. The final category deals with the complications of Sickle Cell Anemia. This category examines certain complications that arise in certain areas of the body due to the Sickle Cell Anemia. The first complication is called Hand-Foot Syndrome. This occurs when the mass of sickle cells block a blood vessel in the limbs of the body. This will cause there to be pain, swelling, and/or fever. This is syndrome is one of the first signs an infant may have Sickle Cell Anemia. The next complication arises in the spleen. The spleen filters out abnormal red blood cells and helps fight infections. If a person has Sickle Cell Anemia, the spleen may become enlarged due to all of the sickle cells getting stuck in the spleen. If the spleen becomes enlarged, then the person will feel weak, have pale lips, higher respiration rate, extreme thirst, and abdominal pain. To treat the enlarged spleen, the patient should get a blood transfusion. Another complication that can occur is infections. Since Sickle Cell Anemia affects the immune fighting organ, the spleen, both young and old patients will have a hard time fighting infections. Young children who have a damaged spleen will most likely die in a few days due to the infections. Some common infections a child may get are pneumonia, meningitis, influenza, and hepatitis. Another life threatening complication due to Sickle Cell Anemia is acute chest syndrome. This occurs when there is sickle cells trapped in the lungs which may lead to the patient developing pulmonary arterial hypertension. This is when the lungs are damaged which make it hard for the heart to pump blood through the lungs. This will lead to elevated heart rate and pressure. A complication that is common with children is their delayed growth and puberty. This is caused by the shortage of red blood cells in the body. Young children will grow slower and reach puberty later than normal children. Adults will be thinner and smaller than normal adults. A more serious complication that can arise in adults however, is a stroke. Sickle Cell Anemia can cause both types of strokes in adults: a blood vessel in the brain is blocked or a blood vessel bursts. Both types of strokes lead to learning disabilities, brain damage, paralysis, or even death. Sickle Cell Anemia can also lead to priapism. This is when a male Sickle Cell Anemia patient will have painful unwelcomed erections. This will occur because the sickle cells block the blood flow out of an erect penis. Since sickle cells have a shorted life span, they break down too fast for the body to remove them from the body. When a red blood cell dies, it will release the hemoglobin protein in the form of bilirubin. The bilirubin will form stones in the gallbladder called gallstones. This will cause the patient to feel pain, nausea, vomiting, fever, sweating, chills, clay-colored stools, or jaundice. Jaundice is when the skin color of a patient turns to a yellowish color because of elevated bilirubin level in the blood. A more severe symptom of Sickle Cell Anemia are ulcers or sores that begin as small, raised, crusted sores on the lower third of the leg. Leg sores occur more often in males than in females. These sores usually appear between the ages of 10 and 50. The cause of sickle cell ulcers isnt clear. The number of ulcers can vary from one to many. Some heal quickly, but others persist for years or come back after healing. The last major complication of Sickle Cell Anemia is multiple organ failures. This may be one of the more rare complications but is one of the most dangerous. If too many of your organs fail, then there is a high probability that you will die. Though only a few of the symptoms of Sickle Cell Anemia have been presented, there are many more which can lead to serious damage to the body if gone unattended. Demographics Though Sickle Cell Anemia is a worldwide disease, it is most common in people who come from Africa, South America, Central America, specifically panama, the Caribbean islands, Turkey, Greece, Italy, other Mediterranean countries, India, and Saudi Arabia. Statistically, 1 in every 500 African American births has the sickle cell disease and about 1 in every 1,000 Hispanic Americans have the disease. About 2 million people carry the sickle cell trait in America and about 1 in 12 African Americans carry the trait in America. There have been close to 72,000 cases of Sickle Cell Anemia in America and the prevalence rate in America is 0.10% or 272,000 people. The deaths from Sickle Cell Anemia are close to 500 deaths per year. Diagnosis One way someone can find out if they have Sickle Cell Anemia is by a simple blood test. When a baby is born, he/she will go through a series of newborn screening exams which test for diseases or disorders the baby may have. A blood test will show if the baby has the disease or if he/she has only the trait. Once the tests are conformed by a second test, the baby will be sent to a hematologist who is a specialist in blood diseases and disorders for further guidance. There is also a way for a parent to know if their child will have sickle cell anemia before he/she is born. Doctors do this by taking a sample of amniotic fluid or tissue from the placenta and testing it for sickle cell anemia gene instead of the hemoglobin the gene makes. Treatment Treatment for sickle cell anemia can be divided in to the three categories that were created for the different types of symptoms. The first category was the pain category. To treat the pain caused by sickle cell anemia, pain killers and fluids are used. To treat the pain, fluids and pain killers are used because the fluids will prevent dehydration which is caused by the disease. The pain killers that doctors prescribe can include acetaminophen, nonsteroidal anti-inflammatory drugs, and narcotics which include meperidine, morphine, oxycodone and others. Another drug that doctors use for sickle cell anemia is hydroxyurea. This drug will reduce the number of pain crises the patient experiences. This drug does not treat the pain crises when they occur but prevents them from occurring at all. Also research has found that this drug will reduce organ damage and improve growth of children. The treatment discussed in the next category, symptoms that deal with Anemia, can help treat anemia. The treatment is called blood transfusion and is used to treat severe cases of anemia. Blood transfusion is a procedure where blood is given to the patient by an intravenous line. This is done to replace the dead red blood cells that were a result of the disease. The last category dealt with complications that arise due to sickle cell anemia. One complication that can be treated is an infection. Due to the reduced number of red blood cells, the human immune system is weakened and children will be at risk for harmful infections. One infection that usually kills children is pneumonia. To treat pneumonia, children should take vaccines regularly. Also to treat other infections, antibiotic medicines and blood transfusion may be used. To treat the acute chest syndrome that arises from sickle cell anemia, the patient must get treated with oxygen, blood transfusions, and antibiotics. The main medication for this complication is the same one that reduces the number of pain crises, hydroxyurea. To prevent and treat patients with sickle cell anemia that experience strokes, the patient should get ultrasound scans of their heads. This will allow the doctor measure the blood flow to the brain see if there are any complications due to the sickle cell disease. The ulcers in the leg can be treated with pain killers, cleansing solutions, creams or ointments, and skin grafts (for severe ulcers). And lastly, to treat the gallstones, surgery may be needed to remove them from the gallbladder. Surgery can also be used to help patients that have priapism. Since the discovery of sickle cell anemia, doctors have been working hard to find new treatments for the disease. In recent years, there have been new and experimental treatments that help patients with the disease. One of these treatments is bone marrow transplant. Since the sickle cell anemia affects the red blood cell production, it was thought that replacing the material the produces the cells may help people with the disease. After numerous trials, it has been shown that bone marrow transplant is somewhat of a cure. However, the procedure is very dangerous and lead to serious side effects or even death. Due to this risk, only young patients and people with significant symptoms or problems get the treatment. The procedure is still being researched. Another experimental treatment is gene therapy. Gene therapy is when researchers insert the normal gene for hemoglobin creation into the bone marrow of infected patients. Researchers hope that the normal genes will begin to produce the correct hemoglobin or if they can cancel the sickle cell gene by turning it off in babies. In addition, researchers are producing new drugs that may help patients. On drug has butyric acid in it which can increase the amount of normal hemoglobin in the blood. Another drug has nitric oxide in it which makes the actual sickle cells less sticky which will lead to less blocked blood vessels. The final drug contains decitadine. This will increase the amount of certain hemoglobin protein that carries more oxygen. Though there are many drugs that seem that they will work, there still more research to be done. Research Due to the severity of sickle cell anemia, there are many doctors working hard to find a definitive cure. One research that may help with finding a cure dealt with the prevalence of pulmonary hypertension in adults with sickle cell disease. The research group studied the mechanism of its development, and its prospective prognostic significances. They performed Doppler echocardiographic assessments of pulmonary-artery systolic pressure in 195 consecutive patients (82 men and 113 women with the average age of 36). The pulmonary hypertension was prospectively defined as a tricuspid regurgitant jet velocity of at least 2.5 m per second. Patients were followed for a mean of 18 months, and data were censored at the time of death or loss to follow-up. The group reached the following results. They determined that the Doppler-defined pulmonary hypertension occurred in 32 percent of patients. Multiple logistic-regression analysis, with the use of the dichotomous variable of a tricuspid regurgitant jet velocity of less than 2.5 m per second or 2.5 m per second or more, identified a self-reported history of cardiovascular or renal complications, increased systolic blood pressure, high lactate dehydrogenase levels (a marker of hemolysis), high levels of alkaline phosphatase, and low transferrin levels as significant independent correlates of pulmonary hypertension. The fetal hemoglobin level, white-cell count, and platelet count and the use of hydroxyurea therapy were unrelated to pulmonary hypertension. A tricuspid regurgitant jet velocity of at least 2.5 m per second, as compared with a velocity of less than 2.5 m per second, was strongly associated with an increased risk of death and remained so after adjustment for other possible ri sk factors in a proportional-hazards regression model. They came to the following conclusions. They believed that the pulmonary hypertension, diagnosed by Doppler echocardiography, is common in adults with sickle cell disease. It appears to be a complication of chronic hemolysis, is resistant to hydroxyurea therapy, and confers a high risk of death. Social Impact Though many believe that living with sickle cell anemia is impossible, that is not true. The infected people can live like any other person with just a few deviations. The only negative thing about living with sickle cell anemia is that the life expectancy is between 40 and 60 years old. However a person can live longer if they maintain a healthy lifestyle, control the complications that arise from the disease, and if they learn the correct ways to cope with the pain. A healthy life style means you eat healthy foods or foods that contain certain vitamins that may help your body cope with the disease. An example of a vitamin would be folic acid. Also doctors advise patients to drink plenty of water so he/she wont become dehydrated. To help prevent and control the complications of sickle cell anemia, the patient needs to follow certain instructions and warnings. Some of these instructions and warnings include avoiding decongestants and drugs that tighten blood vessels. Also the patient should avoid living in extreme hot and cold areas or in low oxygen level areas (well above sea level cities). Also doctors recommend that the patient avoid or reduce stress in their life and to avoid jobs that require a lot of physical labor. In addition, the patient should get all of the vaccines and flu shots that are available. Though following doctors recommendations will help a patient, learning and studying different treatments and lifestyle choices on their own can help them a lot. If a patient reads about sickle cell anemia, they will be better equipped to deal with symptoms and complications that may arise. If you or someone in your family has sickle cell anemia, you may want help with the stresses of this lifelong disease. Sickle cell centers and clinics can provide information and counseling. Ask your doctor or the staff at a sickle cell center if there are support groups for families in your area. Talking with others who are facing the same challenges you are can be helpful. Its especially important to find ways to control and cope with pain. Different techniques work for different people, but it might be worth trying heating pads, hot baths, massages or physical therapy. Prayer, family and friends also can be sources of support. If you have a child with sickle cell anemia, learn as much as you c an about the disease and make sure your child gets the best health care possible. A child with sickle cell disease has special needs and requires regular medical care. Your doctor can explain how often to bring your child for medical care and what you can do if he or she becomes ill. Conclusion Sickle cell anemia is a significant disease that must be addressed immediately. The number of people that know about sickle cell anemia is alarmingly low and that must change. People must become aware of the dangers of this disease and must do everything in their power to help prevent it from spreading. This disease can lead to death in infants, children, teens, and adults. It is also a worldwide disorder that needs more attention. This disease, which is genetically passed down to people, needs more people researching it and trying to find cures to. Though there are many doctors hard at work to find a cure, there can be so much more that can be done. Though there is a group of people unaware of this disease, it does not mean the work already done should be neglect. Through the hard work of doctors, we have been able to find almost every symptom of sickle cell anemia and how to treat most of the symptoms. To find a cure for sickle cell anemia, everyone must do their part and help in some way. Hemophilia What is Hemophilia? Hemophilia is a blood disorder that prevents your blood to clot normally. When the body experiences an injury where the person begins to bleed, the body reacts in a very unique manner. Blood is a liquid membrane that is composed red blood cells, white blood cells, and platelets. The purpose of the blood is to transport nutrients and oxygen from the lungs to different areas of the body and to transport carbon dioxide and waste from those areas back to the lungs. Blood also serves as a transport system for white blood cells which are part of the immune system and fighters of the immune system. However, blood also serves as a clotting mechanism. In order for the body to clot an injury, platelets must be able to stick together at the injury site. This stickiness is called the blood clotting factor. Hemophilia is a disorder that causes people to have little to none clotting factor. Hemophilia is usually an inherited disease which does not allow your blood to clot externally or internally. People with hemophilia will have a gene that will cause the clotting factor, a protein, to not work properly which will cause the patient to keep bleeding. The clotting factor is needed to form clots with platelets. Hemophilia can be divided into two major types: hemophilia A or hemophilia B. about 9 out of 10 people who have hemophilia will have type A hemophilia which means the body is missing or has low levels of clotting factor 8. If the person has type B, then they are missing or have low levels of clotting factor 9. In addition, hemophilia is usually genetically acquired but some can develop hemophilia during their lifetime. This can happen if your body forms antibodies (proteins) to the clotting factors in your bloodstream. The antibodies can prevent the clotting factors from working. Causes of Hemophilia A person usually inherits hemophilia but as discussed earlier, they can develop hemophilia during their lifetime. If a disease is inherited, then that means the parents of the patient will also have the gene for the disease. In the case of hemophilia, the gene for hemophilia is located on the X chromosome. Females have two X chromosomes, while males have one X and one Y chromosome. Only the X chromosome carries the genes related to clotting factors. A male who has the abnormal gene on his X chromosome will have hemophilia. A female must have the abnormal gene on both of her X chromosomes to have hemophilia; this is very rare. A female is a carrier of hemophilia if she has the abnormal gene on one of her X chromosomes. Even though she doesnt have the condition, she can pass the gene on to her children. If a father does not have the hemophilia trait but the mother does have only one copy of the gene and they have 2 daughters and 2 sons, then each daughter has a 50 percent chance of inheriting the abnormal gene from her mother and being a carrier. Each son has a 50 percent chance of inheriting the abnormal gene from his mother and having hemophilia. However if the father has hemophilia and the mother has neither hemophilia or the hemophilia trait and they have 2 daughters and 2 sons, then each daughter will inherit the abnormal gene from her father and be a carrier. None of the sons will inherit the abnormal gene from their father, and, therefore, none will have hemophilia. Very rarely, a girl is born with hemophilia. This can happen if her father has hemophilia and her mother is a carrier. In addition to the genes that cause hemophilia, there are other factors that may cause it. One factor is the type of clotting factor that the person is missing. If the person has hemophilia A, then the person lacks clotting factor 8. If the person has hemophilia B, then the person lacks the clotting factor 9. Finally, if the person has Hemophilia C which is rare in the United States, then person has a different inheritance pattern and lacks clotting factor 9. Symptoms of Hemophilia The main symptom of hemophilia is excessive bleeding externally and internally. The extent of bleeding depends on the type and severity of the hemophilia. Children who have mild hemophilia may not have symptoms unless they have excessive bleeding from a dental procedure, an accident, or surgery. In addition, the symptoms of hemophilia vary depending on how deficient your clotting factors are. If levels of your deficient clotting factor are very low, you may experience spontaneous bleeding. If levels of your deficient clotting factor are slightly to moderately low, you may bleed only after surgery or trauma. If you bleed spontaneously then you have the following symptoms: many large or deep bruises, joint pain and swelling caused by internal bleeding, unexplained bleeding or bruising, blood in your urine or stool, and prolonged bleeding from cuts or injuries, or after surgery or tooth extraction. Bleeding in the knees, elbows, or other joints is another common form of internal bleeding in people who have hemophilia. This bleeding can occur without obvious injury. At first, the bleeding causes tightness in the joint with no real pain or any visible signs of bleeding. The joint then becomes swollen, hot to touch, and painful to bend. Swelling continues as bleeding continues. Eventually, movement in the joint is temporarily lost. Pain can be severe. Joint bleeding that isnt quickly treated can permanently damage the joint. Internal bleeding in the brain is a very serious complication of hemophilia that can happen after a simple bump on the head or a more serious injury. The signs and symptoms of bleeding in the brain include long-lasting, painful headaches or neck pain or stiffness or convulsions or seizures. Demographics Hemophilia affects 1 in 5,000 male births. About 400 babies are born with hemophilia each year. The exact number of people living with hemophilia in the United States is not known. Currently, the number of people with hemophilia in the United States is estimated to be about 20,000. In the United States, most people with hemophilia are diagnosed at a very young age. Based on CDC data, the median age at diagnosis is 36 months for people with mild hemophilia, 8 months for those with moderate hemophilia, and 1 month for those with severe hemophilia. In about two thirds of cases, there is a family history of hemophilia. The diagnosis of hemophilia is made using a special blood test and most babies can be tested soon after birth. Sometimes prenatal genetic testing is done to diagnose hemophilia before birth. Treatment Though, like sickle cell anemia, there is no definitive cure for hemophilia, there are many treatments that help people cope with the disease. However, the treatments people get is based on the severity of the disease. However there is main treatment for hemophilia; it is called replacement therapy. In this therapy, the missing clotting factor is injected into the body intravenously to replace the clotting factor. Though this treatment sounds good, there is a drawback, the patient has to continuously take injections of the therapy to prevent bleeding. Antifibrinolytic medicines (including tranexamic acid and aminocaproic acid) may be used with replacement therapy. Theyre usually given as a pill, and they help keep blood clots from breaking down. Another complication to this treatment is that the body may develop antibodies that act against the new clotting factor or there might be damage to joints, muscles, or other parts of the body resulting from delays in treatment. Antibodies can destroy the clotting factor before it has a chance to work. This is a very serious problem. It prevents the main treatment for hemophilia (replacement therapy) from working. Antibodies to clotting factor, also called inhibitors, develop in about 20 percent of people who have severe hemophilia A and 1 percent of people who have hemophilia B. When antibodies develop, doctors may use larger doses of clotting factor or try different clotting factor sources. Sometimes, the antibodies go away. Desmopressin (DDAVP) is a man-made hormone used to treat people who have mild to moderate hemophilia A. DDAVP isn

math lesson Essay -- essays research papers

Lesson Plan Title: Alexander, Who Used to Be Rich Last Sunday: Understanding Opportunity Costs Grade Level:2, 3, or 6th Duration: three 50-minute class periods Student Goal: To understand that there is an opportunity cost to every economic decision and that these costs come as a result of limited resources. Student Objectives Students will: †¢ Identify "opportunity costs" in the story and in their own lives. †¢ Create an opportunity costs bar graph as a whole class. †¢ Complete a table of personal spending and savings information. †¢ Write an original story about how they spent and saved their allowance and what they gave up or their "opportunity costs" in order to reach their goals. Materials: †¢ a copy of Alexander, Who Used to Be Rich Last Sunday, by Judith Viorst †¢ chart paper †¢ markers †¢ overhead projector †¢ transparency †¢ student handout: How I Spent & Saved My Allowance (included). This was provided by the teacher in which I was doing my participant observations with. Set Up and Prepare: 1. Use the book Alexander, Who Used to Be Rich Last Sunday, by Judith Viorst. 2. Write the definition of the term "opportunity cost" on a sheet of chart paper and display for the class: Opportunity Cost: what you give up when you decide to do or buy something 3. Draw a bar graph on a transparency. Write the title "Opportunity Costs for a College Education" across the top. Label the horizontal axis "Opportunity Costs." Label the vertical axis "Number of Students." 4. Print out copies of the student handout "How I Spent & Saved My Money" for each student to take home. Directions: PART I: Step 1: Share with students a story about a time when you did not buy something you really wanted so that you could use or save the money for something more important. For example, maybe you didn't go on a vacation so you could save the money for a car you need to buy. Explain that what you gave up is called an "opportunity cost." Direct students' attention to the definition of "opportunity cost" displayed on the chart paper. Step 2: Ask students to share stories from their own lives in which they gave up something to get something else, or to save for something else that they want more. Have them identify their opportunity costs. Ask studen... ... †¢ How much does Alexander have after he buys the gum? ($0.85); after he loses a bet to his mother? ($0.70); after he rents Eddie's snake? ($0.58); after his father fines him for saying naughty words ($0.48); after flushing pennies down the toilet and dropping a nickel through a crack? ($0.40); after paying for Anthony's chocolate bar? ($0.29); after pennies disappear in Nick's trick ($0.25); after paying his father for kicking his brother? ($0.20); after buying things at a garage sale ($0.00). Set Up Shop/ Learning Center: Students set up a shop and role play the parts of customer and shopkeeper, making economic decisions along the way. Have them draw pictures or use manipulatives for the items they are selling in the store. Allow them to determine prices and tag each item. Then give all students the opportunity to be a customer and the shopkeeper. Provide customers with a limited amount of play money to spend in the store. They will need to budget their money so that they can afford all they need to buy. Using play money too, the shopkeepers sharpen their math skills as they make change for the customers. Assignments: Student Handout: How I Spent & Saved My Money

Alan Bennetts Talking Heads Essay -- Alan Bennett Talking Heads Essay

Alan Bennett's "Talking Heads" "Talking heads" by Alan Bennett is a collection of monologues in which the audience are showed into the life of a character and given an insight into the character's personality and situation.peoples lives are portrayed in comic ways leaving the audience feeling sympathy and guilt for the character in laughing at their misfortune. Monologues are a long speech made by one person. This style of script is really effective and has a powerful effect on the audience. These monologues were written for television broadcasting, programmes presented in this way are put under the genre of tragi-comedy. This style of script has a dramatic effect upon the audience because from one statement , several emotions arise, for example Irene writing to someone informing them that their wife is a prostitute it is comic that she would care to write a letter about something that does not concern her of this sort of information but in another way it displays pathos because she is has enough time to spare to have such an interest in finding out information such as this. The talking heads monologues often give an exaggerated story largely influenced by the environment and era in which the characters live in. For example Doris' jaded views of nursing homes which are perhaps stereotypically nursing homes from the era in which she brought up in. This cynical view also emphasises the lack of respect in the ironic way that an elderly person has been influenced by negative views of the older generation. Within this essay I am going to analyse the talking heads scripts and bring about my point of views as well as also using my background knowledge on the era and several other topics which seem to o... ...eotype people which displays irony as they fit into 3 groups of people which are well known to be stereotyped: porn stars, o.a.p's and interfering busy-bodies. "When I saw his vest it had electrician written all over it." Lesley says on meeting a man with a tattoo. I think these stereotypical associations are made due to their ignorance towards different cultures, classes and race. As a conclusion to this essay I feel that Alan Bennett has created these monologues effectively through the use of pathos which is present through all the monologues. He enforces feeling brought about by the pathos with metaphors as well as clichà © phrases.The television episodes are simple but effective in setting an atmosphere appropriate to the monologue. He brings the characters to a level which we can all relate to in some way which makes the impact of tragedy far deeper.