Three Steps to Help You Get Your Essay Writing

Three Steps to Help You Get Your Essay WritingAfter trying to choose the right sample disaster essay, I know that many people are afraid of the rigors of the assignment and the fear of never finishing it. But you can overcome this fear.A successful essay is something that has a big impact on the writer and his or her peers. So how do you get started? Here are three steps to help you get your essay written.One of the first things you need to do when choosing a sample disaster essay is to determine the goal. In other words, what are you trying to accomplish with the essay? What do you want your essay to accomplish?Document your goals. If you are trying to write about disasters and natural disasters and the effects they have on our society and the world, the best choice for you would be to select an essay about natural disasters.Documenting your goals is important because it will give you an idea about how your essay will be structured. The structure of your essay can be very important because it will determine if you finish it within the deadline and whether or not it is worthy of publication.The second step in choosing a sample disaster essay is to make sure you have the right background knowledge. You can't expect to write an essay about disasters and natural disasters and the effects they have on our society and the world if you don't have the background knowledge you need. You will need to find an essay writer who specializes in the subject matter of your choice.The third step is to set a date when you will finish the essay. Many people skip this step and never finish their assignment. You will find this to be very difficult to do if you are really committed to your essay writing.

A Short History of the Chinese in Cuba

A Short History of the Chinese in Cuba The Chinese first arrived in Cuba in significant numbers in the late 1850s to toil in Cuba’s sugarcane fields. At that time, Cuba was arguably the largest producer of sugar in the world. Due to the diminishing African slave trade after England’s abolition of slavery in 1833 and the decline of slavery in the United States, a labor shortage in Cuba led plantation owners to search for workers elsewhere. China emerged as the labor source following deep social upheaval after the First and Second Opium Wars. Changes in the farming system, a surge in population growth, political discontentment, natural disasters, banditry, and ethnic strife- especially in southern China- led many farmers and peasants to leave China and look for work overseas. While some willingly left China for contract work in Cuba, others were coerced into semi-indentured servitude. The First Ship On June 3, 1857, the first ship arrived in Cuba carrying about 200 Chinese laborers on eight-year contracts. In many cases, these Chinese â€Å"coolies† were treated just as the African slaves were. The situation was so severe that the imperial Chinese government even sent investigators to Cuba in 1873 to look into a large number of suicides by Chinese laborers in Cuba, as well as allegations of abuse and breach of contract by plantation owners. Shortly after, the Chinese labor trade was prohibited and the last ship carrying Chinese laborers reached Cuba in 1874. Establishing a Community Many of these laborers intermarried with the local population of Cubans, Africans, and mixed-race women. Miscegenation laws forbade them to marry Spaniards. These Cuban-Chinese began to develop a distinct community. At its height, in the late 1870s, there were more than 40,000 Chinese in Cuba. In Havana, they established â€Å"El Barrio Chino† or Chinatown, which grew to 44 square blocks and was once the largest such community in Latin America. In addition to working in the fields, they opened shops, restaurants, and laundries and worked in factories. A unique fusion Chinese-Cuban cuisine melding Caribbean and Chinese flavors also emerged. Residents developed community organizations and social clubs, such as the Casino Chung Wah, founded in 1893. This community association continues to assist the Chinese in Cuba today with education and cultural programs. The Chinese-language weekly, Kwong Wah Po also still publishes in Havana. At the turn of the century, Cuba saw another wave of Chinese migrants – many coming from California. The 1959 Cuban Revolution Many Chinese Cubans participated in the anti-colonial movement against Spain. There were even three Chinese-Cuban Generals who served pivotal roles in the Cuban Revolution. There still stands a monument in Havana dedicated to the Chinese that fought in the revolution. By the 1950s however, the Chinese community in Cuba was already diminishing, and following the revolution, many also left the island. The Cuban revolution did create an increase in relations with China for a short time. Cuban leader Fidel Castro severed diplomatic ties with Taiwan in 1960, recognizing and establishing formal ties with the People’s Republic of China and Mao Zedong. But the relationship did not last long. Cuba’s friendship with the Soviet Union and Castro’s public criticism of China’s 1979 invasion of Vietnam became a sticking point for China. Relations warmed again in the 1980s during China’s economic reforms. Trade and diplomatic tours increased. By the 1990s, China was Cuba’s second largest trade partner. Chinese leaders visited the island several times in the 1990s and 2000s and further increased economic and technological agreements between the two countries. In its prominent role on the United Nations Security Council, China has long opposed U.S. sanctions on Cuba. The Cuban Chinese Today It’s estimated that Chinese Cubans (those who were born in China) only number about 400 today. Many are elderly residents who live near the run-down Barrio Chino. Some of their children and grandchildren still work in the shops and restaurants near Chinatown. Community groups are currently working to economically revitalize Havana’s Chinatown into a tourist destination. Many Cuban Chinese also migrated overseas. Well-known Chinese-Cuban restaurants have been established in New York City and Miami.

ACT Tutoring

How To Save Money on SAT/ACT Tutoring SAT / ACT Prep Online Guides and Tips As you may have seen in some of my other articles on tutoring, if there's one thing you need to know about tutoring, it's this: tutoring is expensive, particularly high quality tutoring. In fact, I've even written an entire article devoted to the topic of how much you should pay for SAT/ACT tutoring. So how can you save money on SAT/ACT tutoring? Let me give you a few tips, tailored around the case studies of 3 hypothetical students. feature image credit: Money – Savings by 401(K) 2012, used under CC BY-SA 2.0/Cropped from original. Case 1: Anthony - Comprehensive Tutoring Anthony and his parents have decided he needs a tutor to help him with his ACT test prep and bring his composite score up. He took a timed practice test and scored 23 on Reading, 30 on English, 30 on Math, and 20 on Science, giving him a composite score of 26. His scores seem all over the place, and he isn’t exactly sure where to start with his studying. Anthony's family can’t afford a lot of tutoring. Originally, they thought they could save money by hiring a cheap tutor – maybe some high school student who aced the ACT and is charging $30/hour. After all, a $30/hr tutor could make Anthony's budget stretch to many more hours of tutoring than a more expensive tutor, and more hours are always better, right? Probably not. Getting a low quality tutor, even if she's only charging $30/hr, is a waste of time and money for many students. Why? A high school student who's only charging you $30/hr may be able to help with explaining the answers to practice tests, but it is unlikely that she will have the skills and experience necessary to help with comprehensive test prep.For someone like Anthony, who doesn't know what he needs to study, or how he should plan his studying, or where his weaknesses lie, someone who just helps with practice test answers would not be helpful. Cost-Saving Recommendation for Comprehensive Tutoring: Instead, we'd recommend Anthony hire a higher quality tutor, but for fewer hours. How come? Higher quality tutors are able to help you set the stage for your studying outside of tutoring sessions. This means that you are able to stretch what you can get - if you end up spending 9 hours using what the tutor taught you in one $60/hour test prep session, you're effectively paying $6/hour for tutoring. Not too shabby! Anthony goes with a $60/hr tutor for two sessions over the course of 4 weeks, and learns how to better plan his studying and what he needs to focus on. His tutor finds that Anthony is overwhelmed by the large amount of information presented in the Reading and Science questions, and so focuses Anthony's study around becoming more comfortable with the Reading and Science sections and drilling these questions. Anthony creates a study plan with his tutor for 6 hours of study a week, scheduling in practice tests and time to review his mistakes. Even after Anthony's 2 sessions with the tutor are over, he's able to use the study schedule his tutor devised to guide his test prep, right up until testing day. When he takes the ACT for real, he gets a 32 on Reading, 31 on English, 30 on Math, and 30 on Science – huge leaps in achievement for a minor investment in tutoring time. Case 2: Carmela -Partial Tutoring Carmela took the SAT in December and got a 740 on CR, 640 on Writing, and 660 on Math. She’s applying to college as a humanities major, so she really needs to get her score up on the Writing section. What are Carmela's issues with SAT Writing? Well, she keeps messing up the hardest writing questions, and she doesn't really know how to improve her SAT essay. After all, she's good at writing essays in school - shouldn't that just carry over? Why should she bother studying something she's good at in school? Carmela doesn't know how to plan her essay prep and in any case is unmotivated to do so. Cost-Saving Recommendation for PartialTutoring: How does Carmela overcome these obstacles? She gets tutoring only for the hardest problems and for high-level study planning and motivation. Carmela hires a tutor for $50/hr for 4 sessions over 8 weeks. The tutor figures out that Carmela is getting the hardest Writing questions wrong when the answer choices are technically correct but worded in a way they would never appear in real life. She also discovers that Carmela is using mostly abstract reasoning in her practice essays, rather than concrete examples. Carmela's tutor sets out a study schedule for Carmela: half an hour of practice on the hardest writing questions every other day. On the off days, the tutor tells Carmela to start coming up with some historical, literary, or pop culture events that she can mine for examples on the SAT essay, like World War II or The Hunger Games; if she knows a few historical events or pieces of literature really well, she will be able to take examples from them for nearly any SAT essay topic. In addition to giving Carmela specific tutoring tips, the tutor helps Carmela figure out that her target Writing score is a 720, and so she needs to improve by 80 points. With concrete information on how much she needs to improve and how to do so, Carmela is motivated to study for the SAT outside of tutoring as well as during tutoring sessions. After 2 months of tutoring, Carmela takes the SAT again and gets 730 on CR, 730 on Writing, and 690 on Math – a much better score report for a prospective humanities student. Another alternative: If Carmela had only had issues with hardest Writing problems, she could have tried tutoring combined with another test prep strategy, like tutoring and a self-guided online prep program, or tutoring and focused self-study. In this particular case, since Carmela was struggling with motivation to improve her essay as well as with the hardest Writing problems, it made more sense for her to get tutoring that would help her with both. Case 3: Marie -A Limited Budget for Tutoring Marie took the SAT in October of her junior year and got a 660 on CR, 600 on Writing, and 570 on Math. After focused math self-studying, she retook the SAT in March and got a 640 on CR, 620 on Writing, and 740 on Math, which brings her composite superscore up from 1830 to 2020. Marie has a very limited budget ($120), but really wants to solidify her chances of getting into Smith College. The middle 50% of first years who enter Smith have composite SAT scores ranging from 1870-2190, so to increase her chances of getting in, Marie really needs to get her total SAT score to at or above 2190...which is a 170 point increase. How does Marie decide if she should get tutoring? Marie considers her overall budget and her current test prep progress. Can she achieve her results within her current system, or does she need a tutor? Cost-Saving Recommendation for Limited Tutoring Budget: Marie concludes that because she was able to improve her Math score with self-study, she can probably apply the same methods to studying for the Critical Reading and Writing sections. What were these methods? She took timed practice tests, marking every question she wasn't sure about, and thoroughly reviewed the questions she got wrong and the questions she guessed on but got right. During her prep for the SAT Math section, Marie discovered that she had a tendency to rush through reading the question because she was so nervous that she would run out of time, which led to her often answering the wrong question. She spent hours drilling herself on actual SAT Math questions in her weakest areas, elementary algebra and plane geometry, slowly but surely increasing the speed at which she could answer the questions, which in turn helped her slow down when reading the questions. Marie decides that since Smith superscores the SAT (combines the highest scores for each section across all testing dates), and she clearly has an effective test-prep method, she will take the SAT 2 more times (a cost of $105), once after having focused on Writing and once after having focused on Critical Reading. She does and scores 750 on Writing and 790 on Critical Reading, bringing her overall score up to 2280 - well above the composite she needs to get into Smith. So how does this apply to you? Let’s take a look at the tips I mention above, distilled down into a series of hypotheticals. How Can I Save Money on SAT/ACT Tutoring? Do you want the best test prep, bar none? Then get high quality, expensive tutoring. Want good prep but have a limited budget, like Anthony? Spend your money on a higher quality tutor for a shorter amount of time. Only need focused prep, like Carmela? Get a high quality tutor who can focus on that section so you don't buy hours for the other sections. Have a strict budget that limits tutoring? Then use another prep program, and add tutoring sparingly for high level stuff. Is your current method effective? Keep careful watch on how you do on practice and actual tests, note where you need to improve (by section and within a section), and then take more official tests. If your score plateaus, you should consider other options. If you hit your target scores, like Marie did, then you're all set! Use these tips to help you save on tutoring when studying for the SAT/ACT. Dollars by 401(K) 2012, used under CC BY-SA 2.0. What’s Next The best way to save money on tutoring is to make sure you’re getting the best tutor for you. How do you do this? Read more about it here. What should you be looking for in a tutor, anyway? Check out my article on what makes an effective tutor. Want to find out more about PrepScholar Tutoring Program? PrepScholar co-founder Fred Zhang has the article for you. Want to improve your SAT score by 240 points or your ACT score by 4 points?We've written a guide for each test about the top 5 strategies you must be using to have a shot at improving your score. Download it for free now:

Social Class systems Essay Example | Topics and Well Written Essays - 250 words

Social Class systems - Essay Example Studies conducted show that forty two percent of men born in the bottom five social classes stay that way when they become adults. To add to the figures, just eight percent of Americans born at the bottom, rise to the top. From this figures it is safe to argue that contrary to popular belief, America is in fact a caste social system. There are various reasons for this argument, the first being that the country has a thin safety net to cushion children from poverty, therefore less class mobility. We find that in most poor children are raised by single parents, a factor which increases poverty levels. This is compounded, by racial discrimination which leaves most people of color, especially African Americans vulnerable and poor, compared to the other races. The second reason is that in our society, education is enables one to get a higher salary. This leaves people from poor families at a disadvantage because upper income parents invest more in their children’s education to increase their chances of success in life. The children of the high income earners go to the best schools and are prepared to learn. It is safe to argue that most people at the top are there due to their backgrounds, more than merit. Ours is therefore a system of the poor remaining poor and the other way round. The kind of education you get how the police treat you and even who you get married to, is largely influenced by your social

Company law case study analysis Example | Topics and Well Written Essays - 2000 words

Company law analysis - Case Study Example ny is a commercial organization that joins the pass-through taxation of a sole proprietorship or partnership with the limited liability of an organization. However, it is not a corporation, rather, a legal type of a business that offers its owners limited liability at various jurisdictions. Advantages of forming a limited liability company (LLC) include; it involves protection of the company’s assets. It will offer a restricted liability security to them, as the owners, for they are not individually responsible for the company’s liabilities or debts. Therefore, creditors will not chase their personal assets, such as the building, savings accounts, among others, in attempts for them to pay the business debts. In addition, forming an LLC will offer a pass-through taxation, in that; they will not have to pay any taxes at the business level. Any company loss or income will be "passed-through" to them, as the company owners and recounted on their individual income tax returns. Any due tax will, therefore, be paid at the individual level (Martin, 2011, p.28). Another advantage is that there is heightened credibility, whereby, this form of accompany night assist their new company create reliability with its prospective vendors, partners, and customers, since the y will the owners have made an official obligation towards the business (Hollowell, Miller, Clarkson &Cross, 2012, p.58). In addition, if needs limited compliance requests in that, the company will face lesser state-enacted yearly requirements than other forms of corporations. It also has a flexible management structure, such that, they will be free to form any business structure that they will agree on. Therefore, the owners can choose to manage the company or have managers to do so for them, unlike in major corporations that have board of directors and managing officers manage them. Lastly, this kind of a company has less restriction, in that, it they will not be limited on whom an owner can be or the

Hemoglobin Malaria Haemoglobinopathies

Hemoglobin Malaria Haemoglobinopathies Despite major advances in the understanding of the molecular pathophysiology and control and management of the inherited disorders of hemoglobin (haemoglobinopathies), thousands of infants and children with this disease are dying. As a result in heterozygote advantage against malaria the inherited hemoglobin disorders are the commonest monogenic disease. Population migrations have ensured that haemoglobinopathies are now encountered in most countries including the UK. Haemoglobinopathies have spread from areas in the Mediterranean, Africa and Asia and are now endemic throughout Europe, the Americas and Australia. This review examines the available literature to find out more about the prevalence of haemoglobinopathies in the UK. The data on the demographics and prevalence of the gene variants of haemoglobinopathies was extracted from books, journals, reference sources, online databases and published review articles from the WHO. Introduction It has been estimated that approximately 7% of the world population are carriers of such disorders and that 3000 000 4000 000 babies with severe forms of haemoglobinopathies. Haemoglobinopathy disorders occur at their highest frequency in tropical regions and population migrations have ensured that they are now encountered in most countries. Because of this, haemoglobinopathies have become a global endemic, so the World Health Organization published journals and reviews with recommendations on screening programmes and management of haemoglobinopathies. The programmes are tailored to specific socioeconomic and cultural contexts and aimed at reducing the incidence, morbidity and mortality associated with these diseases. www.who.int/en/ The WHO Executive Board wrote a review on haemoglobinopathies. In this article, the WHO Executive Board recognized that the prevalence of haemoglobinopathies varies between communities, and that insufficiency of relevant epidemiological data may hamper effective and equitable management of haemoglobinopathies. On this note England implemented the LIVE programmes. The Executive Board also recognizes that haemoglobinopathies are not yet officially recognized as priorities in Public Health Sector. This raised an issue about awareness of haemoglobinopathies. The WHO Executive Boards advice for prevention and management of haemoglobinopathies was to design, implement and reinforce in a systematic equitable and effective manner, comprehensive national, integrated programs for prevention and management of haemoglobinopathies, including surveillance, dissemination, such programs being tailored to specific socioeconomic and cultural contexts and aimed at reducing the incidence, morbidity and mortality associated with these diseases. www.who.int/en/ With immigration in the UK on its highest, the prevalence of haemoglobinopathies is expected to increase. The NHS has implemented programmes for individuals with haemoglobinopathies by implementation of LIVE program (NHS Plan, 2000). LIVE program is set-up to implement variant screening in the whole of UK by the year 2007. LIVE program started as early as January 2004 in high prevalence. The NHS Trusts involved are to offer variant screening by end of 2004/5 (NHS Plan, 2000). Low prevalence Trust are expected to have implemented the screening program by January 2008 and so far 86 out of 90 Trusts have successfully implemented the program. Antenatal and Newborn Screening programs have compiled a training pack to assist Low Prevalence Trusts with the implementation of haemoglobinopathies screening programmes. The NHS Plan (2000) made a commitment to implement effective and appropriate screening programs for women and children including a new national linked Antenatal and Newborn screen ing programs for haemoglobinopathies. The NHS Plan (2000) recommends that all pregnant women living in high prevalence areas are offered screening for haemoglobinopathies. All pregnant women living in low prevalence areas are offered screening for haemoglobinopathies. If a woman is identified as being at increased risk using the family origin questionnaire, she will then be offered screening for haemoglobinopathies (NHS Plan, 2000). The Low Prevalence Trust is where the fetal prevalence of sickle cell disease is less than 1.5 per 10 000 pregnancies. Low prevalence trusts are to offer screening for variants based on an assessment of risk determine by a question to women about their babys fathers family origin by the end of 2005/6 (NHS Plan, 2000). Background on Haemoglobinopathies Haemoglobin: is the oxygen carrying capacity of the blood and it is also a protein. Haem is iron containing pigment, while globin is made up of chains which are a globular tetrameric protein which accounts for 97.4% of the mass of the haemoglobin molecule (Tortora et.al., 2006) . The globin tetramer consists of four polypeptides which are two alpha (ÃŽ ±) chains and two non-alpha chains. The synthesis of ÃŽ ¶ and ÃŽ µ chains is done during the first 10 to 12 weeks of fetal life. Within the fourth to the fifth week of intrauterine life ÃŽ ± and ÃŽ ² chains are synthesized. The non-alpha is beta (ÃŽ ²), gamma (ÃŽ ³), delta (ÃŽ ´), epsilon (ÃŽ µ) zeta (ÃŽ ¶) chains. Haemoglobin transports oxygen from the lungs to all parts of the body and it gives blood its red colour (Fleming, 1982) Haemoglobin synthesis Haem and globin synthesis occur separately but in a carefully coordinated fashion. Globin synthesis is under the genetic control of eight functional genes arranged in two clusters, the ÃŽ ± globin gene cluster on chromosome 16 and the ÃŽ ² globin gene cluster on chromosome 11. The major haemoglobin in the foetus is HbF (ÃŽ ±ÃŽ ²) 2 and in adults HbA (ÃŽ ±ÃŽ ²) 2 (Fleming, 1982). Haemoglobin Structure The primary structure of haemoglobin is made-up of amino acid sequence of globin. And the secondary structure comprise of nine non-helical sections joined by eight helices; tertiary structure describes globin chain folding to form a sphere and the quaternary structure of haemoglobin describes the tetrahedral arrangements of the four globin subunits ( Fleming, 1982). The external surface of each folded globin is hydrophilic and the inner surface is hydrophobic, this protects the haem from oxidation, which is also why each haem chain sits in a protective hydrophobic pocket. In haemoglobin A, ÃŽ ± ÃŽ ² dimmers are held together strongly at the ÃŽ ±1 ÃŽ ²1 or ÃŽ ±2ÃŽ ²2 junction. The tetramer is held together much less tightly at the ÃŽ ±1 ÃŽ ²2 and ÃŽ ±2 ÃŽ ²1 contact areas (Fleming, 1982). Haemoglobin function Each haemoglobin molecule can carry four oxygen molecules. Oxygenation and deoxygenation are accompanied by molecular expansion and contraction via haem haem interaction (Bienz, 2007). Under physiological conditions, blood in the aorta carries about 19.5ml of oxygen per 100ml of blood. Upon entering the tissues about 4.5ml of oxygen are donated per 100ml of blood. 2,3-DPG is an important modulator of haemoglobin A oxygen affinity in red cells (Fleming, 1982). Haemoglobin disorder (haemoglobinopathies) Haemoglobinopathies is a hematological disorder due to alteration of a genetically defect, that results in abnormal structure of one of the globin chains of the haemoglobin molecule (Bienz, 2007). Haemoglobinopathies are any of a group of diseases characterized by abnormalities, both quantitative and qualitative in the synthesis of haemoglobin (Hb) (Bienz, 2007). Qualitative affecting the quality of haemoglobin e.g. Sickle cell disorder and quantitative affecting the amount of haemoglobin produced e.g. Thalassaemias. Most of them are genetically inherited but occasionally they can be caused by a spontaneous mutation. Haemoglobinopathies are the worlds most common monogenic autonomic and recessive disease in humans (Anionwu et.al., 2001). 2.1Haemoglobinopathies fall into two main types; There are two categories of haemoglobinopathies. The two categories are: qualitative and quantitative; Qualitative affecting the quality of the haemoglobin e.g. Sickle cell disorder. In this disease the globin structure is abnormal. Quantitative the haemoglobin structure is normal but the amount of haemoglobin produced is affected. e.g. alpha and beta thalassaemias (Bienz, 2007). History of haemoglobinopathies In 1910 Herrick wrote an article in it he used the term â€Å"sickle† to describe the shape of the red blood cells of a 20 year old medical student from Grenada. This student had consulted Dr Herrick in 1994 complaining of a cough, fever and Feeling weak and dizzy. He constantly had anaemia episodes, jaundice, chest complications as well as recurring leg ulcers on both ankles. When his blood was examined, his red blood cells showed a large number of thin, elongated, sickle shaped and crescent- shaped forms (Herrick, 1990). The name thalassaemia was coined by the eminent haematologist George Whipple in 1936 as an alternative to the eponymous ‘Cooleys anaemia. He wanted a name that would convey the sense of an anaemia which is prevalent in the region of the Mediterranean Sea, since most of the early cases originated there. Thalassaemia is derived by contraction of thalassic anaemia (from the Greek thalassa -sea, an none and anemia blood) (Fleming,1982). Origins and Geographic distribution of haemoglobinopathies Carriers are found in all parts of the world: people from the North Mediterranean (South Europe) coast are 1-19% carriers. People of Arab origin are over 3% carriers. In Central Asia 4-10% and in South East Asia, the Indian subcontinent and China 1-40% carriers (the very high rates in this part of the world are due to HbE). In the Americas, North Europe, Australia and South Africa the local population has very low carrier rates but thalassaemia is still present because of the significant immigration from high prevalence area (Anionwu et.al.; 2001). Sickle cell and thalassaemia disorder mainly affect individual who are descended from families where one or more members originated from parts of the world where falciparum malaria was, or is still endemic. Population with such ancestry include those from many parts of Africa, the Caribbean the Mediterranean (including southern Italy, Northern Greece and Southern Turkey), Southeast Asia and thalassaemia gene is much wider now due to the hi storical movements of at-risk populations to North and South America, the Caribbean and Western Europe (Livingstone 1985). The geographic distribution of the thalassaemias overlaps with that of sickles cell disease. This is because carriage of these abnormal genes affords some protection against malaria. Thus, being heterozygous for one of these conditions offers a selective survival advantage and increases the opportunity for these genes to be passed on (Campbell et.al.,2004) 4Types and terminology of sickle cell and thalassaemia There are various types of sickle cell and thalassaemia disorders. The thalassaemia syndromes include alpha and beta thalassaemia major as well as beta thalassaemia intermedia. Sickle cell disorders (or Fickle cell disease include sickle cell anaemia (Hb SS), Sickle haemoglobin C disease (Hb SC) ÃŽ ² disease and E beta thalassaemia (www.sickle-thalassaemia.org/sickle.cel.htm) 4.1Sickle Cell Disorder: affects the normal oxygen carrying capacity of the red blood cells. The red blood cell forms a crescent or a sickled shape when it is deoxygenated. The ‘sickled cells are unable to pass freely through capillaries; the sickle cells also get stuck in blood vessels forming clusters which block the blood vessels and the blood flow. They dont last as long as normal, round red blood cells, which leads to anemia. This results in a lack of oxygen to the tissues in the affected area, resulting in hypoxia and pain (sickle cell crisis). Other symptoms include severe anaemia, damage to major organs and infection (NHS Antenatal and Newborn; 2006). There are several types of Sickle cell disease. The most common are: sickle cell anemia (SS), sickle hemoglobin C disease (SC), sickle beta plus thalassaemia and sickle beta zero thalassaemia. Each of these can cause pain episodes and complications. HbSS sickle is due to two sickle cell genes (â€Å"S†), one from each parent. This is commonly called sickle cell anemia. An individual with sickles cell anemia have a variation in the ÃŽ ²-chain gene, which then causes a change in the properties of hemoglobin which results in sickling of red blood cells (www.sickle-thalassaemia.org/sickle.cel.htm) HbSc inherited one sickle cell gene and one gene from an abnormal type of haemoglobin called â€Å"C†. It is due to the variation in the ÃŽ ²-chain gene. An individual with this variant suffers from mild chronic haemolytic anaemia. (NHS Antenatal and Newborn; 2006). HbS beta thalassaeamia: This form of sickle is due to inherited one sickle cell gene and one gene for beta. 4.2Thalassaemias: is a term used for the description of a globin gene disorders that results from a diminished rate of synthesis of one or more globin chains and a consequently reduced rate of synthesis of the haemoglobin or haemoglobins of which that chain constitutes a part ; ÃŽ ± thalassaemia indicates a reduced rate of synthesis of the ÃŽ ± globin chain, similarly, ÃŽ ², ÃŽ ´, ÃŽ ´ ÃŽ ² and ÃŽ µ ÃŽ ³ ÃŽ ´ ÃŽ ² thalassaemia indicate a reduced rate of synthesis of the h, ÃŽ ´, ÃŽ ´, +ÃŽ ² and ÃŽ µ + ÃŽ ³ + ÃŽ ´ + ÃŽ ² chains, respectively (Modell et.al, 2001). Thalassaemia is the most common single gene disorder known. It is autosomal recessive syndromes, which is divided into ÃŽ ±- and ÃŽ ² thalassaemia. Types of thalassaemia There are two types of thalassaemia: (i)Thalassaemia minor (thalassaemia trait) (ii)Thalassaemia major Thalassaemia minor is when a person inherits one thalassaemia gene, while thalassaemia major is a severe form of anaemia if a person inherits two thalassaemia genes, one from each parent (Bienz, 2007). Subtypes of thalassaemia Alpha (ÃŽ ±) thalassaemia results from inadequate production of ÃŽ ± chains, which are normally controlled by two pairs of chromosomes. If one or two are malfunctioning, then there is a healthy carrier state. If three are non- functional then anaemia results, known as HbH Disease, which can be quite severe but usually does not need blood transfusions and is compatible with a normal life span (Anionwu et al, 2001). If all four genes are non functional then the result is severe anaemia of the unborn child, leading to heart failure and death (miscarriage). This condition is known as hydrops felalis (Fleming, 1982). Beta (ÃŽ ²) Thalassaemia is caused by the bodys inability to produce normal haemoglobin, leading to a life threatening anaemia (Bienz, 2007). The severity of illness depends on whether one or both genes are affected and the nature of the abnormality. If both genes are affected, anemia can range from moderate to severe. Beta thalassaemia results from inadequate or lack of production of ÃŽ ² chains (Anionwu et.a.l, 2001). Homozygous, ÃŽ ² thalassaemia has two forms: major, in which the patient can survive only with regular transfusions of blood and intermedia in which the patient can survive with occasional or even with no transfusions at all. The condition requires frequent blood transfusions and treatment to prevent complications from iron overload, such as diabetes and other endocrine disorders (Anionwu et.a.l, 2001). Both of these conditions can restrict a child or adults ability to conduct their normal daily activities and can have profound psychological affects on individuals a nd their families This form of thalassaemia is the most important and constitutes a major public health problem in many parts of the world, because of the high frequency of carriers and the demanding treatment that must be followed (Fleming, 1985). Association of Haemoglobinopathies with Malaria Malariais a vector borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americans, Mediterranean, Asia and Africa. It causes diseases in approximately 515 million people and kills between one and three million people, the majority of whom are young children. Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (Campbell et al, 2004). Sickle cell developed as a by product of human defense mechanisms against malaria. The most severe form of malaria, falciparum malaria, leads to very high death rate in young infants. This is particularly a problem between the time immediately after birth, when they are protected by immunity from the mother, and the time when they are old enough to acquire their own immunity. Malaria is a parasite which lives within the red blood cells and feeds off the protein that is contained within those red cells, haemoglobin (Campbell et al, 2004). When the malarial parasite enters the blood stream through a mosquito bite, it penetrates the red blood cells by attaching to the outside membrane or envelope of the red blood cell and gaining entry (Franklin, 1990). Once in the red blood cell, the malarial parasites use the haemoglobin as a source of energy, so that they multiply within the red cells. The parasites multiple filling-up the red blood cells and once they are filled-up the red cells bur st, thereby releasing the multiple parasites in the blood. Each new young parasite enters a single cell again and multiplies again, thereby causing a disease or infection. Whenever the parasites burst out of the cells they cause illness and fever in patients. Malaria can be severe by causing death; death is believed to be caused by red cells not being able to pass through the narrow gaps in the smallest blood vessels and by blockage of tissues when so many parasites are in the red blood cell (Campbell et al, 2004). Over the years human genes developed ways to prevent malaria becoming serious and potentially lethal, the developments were to prevent malarial parasites from spreading and multiplying (Tortora et.al,2006). The most changes were changes (mutation) in the type of haemoglobin (haemoglobin S) within the red blood cell which would in turn slow down the multiplying of the parasite (Campbell et al, 2004). The individuals with haemoglobin S are known to have a sickle cell trait or being carriers of sickle cell haemoglobin. When sickle-cell haemoglobin has given up its oxygen in the cells, the red cells stick together to form crystalline groupings of haemoglobin known as polymers. The red blood cells become deformed into sickle shapes and the presence of these crystalline polymers within the red cells inhibits the growth of the malarial parasite (Beinz, 2007). Even though individuals with haemoglobin S stills suffer from malaria, they are protected from the most severe effects of malaria (Li vingstone, 1985). Diagnosis Diagnosis for sickle cell disease The most used diagnose test for sickle cell is the haemoglobin electrophoresis. HbS and HbC amino acid substitutions change the electrical charge of the protein, the migration pattern of the haemoglobin with electrophoresis or isoelectric focusing results in diagnostic patterns with each of the different haemoglobin variants. HbSBeta-thal requires careful evaluation of red blood cell count and mean corpuscular red cell volume (MCV) and specifically quantifying HbA, S, A2 and F. In emergency setting, the presence of HbS is detected using a five minute solubility test called sickledex. Sickledex test does not differentiate sickle syndromes from the benign carrier state (HbAS or a sickle trait (NHS Antenatal and Newborn; 2006). Diagnosis for thalassaemias When testing for thalassaemias, a blood test is the simplest and most effective test for diagnosis and also the use of a test called Haemoglobin Electrophoresis. The blood of individuals with thalassaemias tend to be microcytic (smaller in size) and hypochromic (paler in colour) (NHS Antenatal and Newborn; 2006). 7 Pathophysiology 7.1Sickle-cell Sickle-cell anemia is caused by changes (mutation) in the structure of the ÃŽ ² -globin chain of the haemoglobin replacing the amino acid glutamic acid with the less polar amino acid valine at the sixth position of the ÃŽ ² chain. When two wild type ÃŽ ±-globin subunits associate with two mutant ÃŽ ²-globin subunits forms hemoglobin S. Haemoglobin S polymerizes under low oxygen conditions, which causes distortion of red blood cells and also causes red blood cells to lose their elasticity, resulting in red blood cells forming an irreversible sickle shape (Fleming,1982). Very often a cycle occurs, as the cells sickle they cause a region of low oxygen concentration which causes more red blood cells to sickle. Repeated occurrence of sickling causes cells to not return to normal even when oxygen levels are normal. The deformation of cells makes it difficult for the cells to pass through capillaries resulting in vessel occlusion, severe anemia, ischemia and other problems (Beinz, 2007). 7.2Thalassaemias The pathophysiologic effects of the thalassaemias range from mild microcytosis to death in uterus. The anaemia manifestation of thalassaemia is microcytic hypochromic haemolytic anaemia (Belcher, 1993). The haemoglobin abnormality is caused by substitution of a single amino acid for another; or substitution of two amino acids, also amino acid deletion or fusion (point of mutation) and the synthesis of elongated chains. In alpha trait, one of the genes that form the alpha chain is defective (Beinz, 2007). In alpha-thalassaemia minor, two genes are defective and in haemoglobin H disorder, three genes are defective. Alpha-thalassaemia major is most fatal thalassaemia disorder; this is because four of the chains forming genes are defective. Without alpha chains, oxygen cannot be released to the tissues (Belcher, 1993). In beta-thalassaemia haemoglobin abnormality is due to the uncoupling of alpha and beta-chain synthesis. This causes a depression in beta-chain synthesis, resulting in er ythrocytes with a reduced amount of haemoglobin and accumulation of free alpha chains, which are unstable and easily precipitate the in cell (Bienz, 2007). 8.Causes Genetic control of haemoglobin synthesis The synthesis of structurally normal haemoglobin chains is determined by allelic genes situated on the autosomal chromosome (Beniz, 2007). Haemoglobinopathies occur due to an inheritance of one or more faulty copy of gene(s) that contain the information for the cells to make the globin chains. The gene may result in abnormality in the production or structure of the haemoglobin protein causing haemoglobinopathies (Franklin, 1990). Thalassaemia is an inherited autosomal recessive blood disorder. Genetic defects in Thalassaemia results in reduced synthesis of one of the globin chains which make up haemoglobin. Reduced synthesis of one of the globin chains causes the formation of abnormal haemoglobin molecules, which in turn causes anaemia. Anaemia is a symptom of the Thalassaemias. It is caused by under production of globin proteins, often through mutations in regulatory genes (Franklin, 1990). Inheritance of Haemoglobin Disorder Due to haemoglobin mutation, individuals who had haemoglobin trait had a resistance to dying from malaria, therefore passed on their haemoglobin trait gene to their children (Campbell et.al,2004). As time went on more individuals with the trait were born and eventually individuals who had haemoglobin trait had children together (Franklin, 1990). In that satiation (partnership), if both parents carry the trait gene, there is a one in four chance that any one child will receive the haemoglobin trait gene from one parent and also from the other, thereby having a haemoglobin disorder(Franklin, 1990) . Clinical Manifestations 9.1Thalassaemias clinical manifestations Individuals who inherited the alpha trait are usually asymptomatic, with possible mild microctyosis. Alpha- thalassaemia minor has signs and symptoms almost identical to those of beta-thalassaemia; mild microcytic hypochronic anemia, enlargement of the liver and spleen, and bone marrow hyperplasia (Belcher, 1993). Alpha- thalassaemia major cause hydrops fetalis and fulminana intrauterine congestive heart and liver, edema and massive ascites. The disorder usually is diagnosed post mortem (Bienz, 2007). Beta-thalassaemia minor causes mild to moderate microcytic-hypochronic anemia, mild splenomegaly, bronze coloring of the skin, and hyperplasia of the bone marrow. Skeletal changes depend on the degree of reticulocytosis, which in turn depends on the severity of the anaemia (Bienz, 2007). People who have beta-thalassaemia minor usually are asymptomatic, whereas those with beta- thalassaemia major the anemia is severe, resulting in a great cardiovascular burden, with high output congestive heart failure (Belcher, 1993). Blood transfusions can increase the persons life span by a decade or two. Individuals with beta-thalassaemia major have an enlarged liver and spleen, and growth and maturation are retarded (Belcher, 1993). A characteristic deformity develops on the face as the bones expand to accommodate hyperplastic marrow (Belcher, 1993). Both and beta thalassaemias major are life threatening. Children with thalassaemia major usually are week, fail to thrive, how poor development and experience cardiovascular compromise with high-output failure; if the condition goes untreated, these children die by 6 years of age (Modell et.al., 2001) Blood transfusions can return haemoglobin and hematocrit to normal levels, alleviating the anaemia induced cardiac failure. Iron overload and hemochromatosis, which are complications of transfusion therapy, are treated with chelating agents (Bienz, 2007). . 9.2.Sickle-cell clinical manifestations The severity of sickle cell disorder depends on the amount of haemoglobin S and the clinical manifestations, which are signs and symptoms of the individuals with sickle-cell (Belcher, 1993) . Manifestations of the sickling are those of hemolytic anemia; pallor, jaundice, fatigue and irritability. Extensive sickling can precipitate four types of crises: vaso-occlusive or thrombotic crises and a plastic crisis (Belcher, 1993). A vaso-occlusive crises begins with red blood cells sickling in the microcirculation. Vasospasm brings a log-jam effect causing blood flow to stop flowing in the vessels and this will lead to thrombosis (blood clot formation) and infarction of local tissue occur, resulting in ischemia, pain and organ damage (Modell et.al.,2001). Vaso-occlusive crisis is believed to be extremely painful and lasts an average of 4 to 6 days. This crisis may develop spontaneously or may be precipitated by localized hypoxemia (low PO2) exposure to cold, dehydration, acidosis (low pH), or infection. In infancy, sickle-cells first manifestation is the symmetric painful swelling of the hands (see Fig 3) and feet, but in older children and adults, the large joints and surrounding tissues become swollen and painful. Individuals with the sickle-cell disorder suffer from severe abdominal pain caused by infarction in abdominal structures (Belcher, 1993). Any cerebral vascular accidents may cause paralysis or othe r central nervous system deficits, and if penile veins are obstructed priapism may occur. Studies have shown that bone, especially weight- bearing bones, are also a common target of vaso-occlusive damage, this is due to bone ischemia (Bienz, 2007). The spleen of individuals with sickle-cell disorder is frequently affected due to its narrow vessels, functions in clearing defective red blood cells and this results in a sequestration crisis (Belcher,1993). A sequestration crises, is occurrence of large amounts of blood pool in the liver and spleen. It only occurs in young children and death results from cardiovascular collapse (NHS Antenatal and Newborn,2006). An aplastic crisis develops when a compensatory increase in erythropoiesis is compromised; this then results in profound anemia (Belcher,1993). A hyperhemolytic crisis is rare but may occur with certain drugs or infections. G-6-PD deficiency, when also present, contributes to this type of crisis (Belcher,1993). Clinical manifestations of sickle cell disease do not usually appear until an infant is at least 6 months old. The most cause of death in individuals with sickle-cell anemia is infections, but it is major problem at all ages. Infections are due to splenic dysfunction from sickle damage (Belcher,1993). This occurs from a few months of age especially with certain bacteria e.g. pneumococcal sepsis. Infection tends to rapidly overwhelm the immune system (NHS Antenatal and Newborn,2006) . Sickle-cell haemoglobin C is known to be milder, with symptoms related to vaso-occlusive crises resulting from higher hematocrit and blood viscosity. Obstructive crises cause sickle cell retinopathy is most common in older children, and this include renal necrosis, and aseptic necrosis of the femoral head (Belcher, 1993). The mildest of sickle-cell is the sickle-cell thalassaemia the individuals with this form of sickle-cell tend to be microcytic and hypochromic, which makes the cells less likely to clog the microcirculation even when sickling (Belcher, 1993). Severe hypoxia can be seen in individuals with the sickle cell trait and may cause vaso-occlusive episodes. The cells in these people form an ivy shape (Belcher, 1993). Recent studies have shown that stroke is co-exiting with Sickle cell disease. At least 1% of patients with sickle cell disorder suffer from stroke and those individuals result in physical disability, IQ reduction, Learning difficulties, TIAs and seizures (Beinz, 2007). Treatment of haemoglobinopathies. 10.1Treatment in Sickle-cell anemia. Febrile illness: Children with fever are screened (a full blood count, reticulocyte count and blood culture taken) for bacteremia. In young children the fever is treated with intravenous antibiotics, the children would be admitted at the hospital so that they can be monitored (Belcher, 1993).. But older children with reassuring white blood cell counts are managed at home with oral antibiotics, but if the older children have a history of bacteremia episodes, they get a hospital admission. (Modell et al, 2001) Zn administration: is when zinc is given to stabilize the cell membrane (Beinz, 2007). Painful (vaso-occlusive) crises: individuals with sickle cell disorder experiences painful episodes called vaso-occlusive crises. Vaso-occlusive crises is often treated symptomatically with analgesics (Beinz,2007). Pain management requires opioid administration at regular intervals until the crises has gone. The frequency, severity and duration of these crises episodes vary tremendously form episodes to episode or from person to person (Belcher,1993). Individuals who suffer from milder vaso-occlusive crises manage their pain on NSAIDs e.g. diclofenac or naproxen. And if the crises is severe, individuals require inpatient management, where intravenous opioids. Diphenhydramine is used to stop the itchiness associated with the opioids (Modell et al, 2001). Acute chest crises management is similar to vaso-occlusive crises treatment with the addition of antibiotics, oxygen supplementation for hypoxia, and close observation. If the pulmonary infiltrate worsen or the oxygen requirements increase,

English Literature and Background Essay

MA (Previous) Semester I Paper I Paper II Paper III Paper IV Paper V Semester II Paper I Paper II Paper III Paper IV Paper V Semester III Paper I Paper II Paper III Paper IV Paper V History, Structure and Description of English –I English Literature up to the Early Seventeenth Century—I English Literature up to the Early Seventeenth Century—II English Literature of the Seventeenth & Eighteenth Century—I English Literature of the Seventeenth & Eighteenth Century—II History, Structure and Description of English –II English Literature of the Nineteenth Century—I English Literature of the Nineteenth Century—II English Literature of the Twentieth Century—I English Literature of the Twentieth Century—II MA (Final) American Literature—I Indian Writing in English—I Postcolonial Literature English Language Teaching Inter-Disciplinary (ID-I) : Writing for Academic and Professional Purposes Seminar Semester IV Paper I American Literature—II Paper II Indian Writing in English—II Paper III Specializations: 1) Women’s Writing 2) Indian Literatures in Translation 3) Modern Classics in Translation one specialization to be offered in each college Paper IV Project Work Paper V Inter-Disciplinary (ID-II) : Literature and Film Seminar Department of English University College of Arts & Social Sciences Osmania University, Hyderabad MA (Previous) Semester I—(Papers I to V) Semester I—(Papers I to V) Paper I Unit 1 History, Structure and Description of English-I a) Indo-European Family of Languages b) Descent of English: Old English, Middle English and Modern English a) Language as a System of Communication b) Levels of Language Description: Phonology and Morphology a) Phonetic Description of Consonants b) Phonetic Description of Vowels a) Noun Phrase Structure (Determiners, pre and post modifiers, number, and gender) b) The Simple Sentence in English a) Verb Phrase Structure (Verb types, tense, aspect, concord; phrasal verbs) b) Coordination and Subordination (Semantic Implications) Look more:  example of satire in huckleberry finn Unit 2 Unit 3 Unit 4 Unit 5 Paper II Unit 1 English Literature up to the Early Seventeenth Century—I Background Renaissance; Reformation; Development of British Drama; University Wits Poetry Geoffrey Chaucer Edmund Spenser General Prologue to The Canterbury Tales Sonnets 34 (â€Å"Lyke as a Ship†¦Ã¢â‚¬ ) Sonnet 54 (â€Å"Of the World’s Theatre†¦Ã¢â‚¬ ) Sonnet 68 (â€Å"Most Glorious Lord of Life†¦Ã¢â‚¬ ) Everyman in His Humour The Duchess of Malfi The Spanish Tragedie Doctor Faustus Unit 2 Unit 3 Drama Ben Jonson John Webster Drama Thomas Kyd Christopher Marlowe Unit 4 2 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Unit 5 Prose Francis Bacon Sir Philip Sidney Essays (â€Å"Of Truth†, â€Å"Of Death†, â€Å"Of Revenge†) An Apologie for Poetrie Paper III Unit 1 Unit 2 English Literature up to the Early Seventeenth Century—II Background Translation of the Bible; Utopia; Tragedy; Comedy Drama William Shakespeare Drama William Shakespeare Poetry John Donne George Herbert Poetry Andrew Marvell Richard Lovelace King Lear Henry IV: Part I Twelfth Night The Tempest â€Å"A Valediction†, â€Å"The Canonization† â€Å"The Good-Morrow† â€Å"Virtue†, â€Å"Pulley†, â€Å"Collar† â€Å"To His Coy Mistress†, â€Å"Garden† â€Å"To Althea From Prison† To Lucasta, Going Beyond the Seas† Unit 3 Unit 4 Unit 5 Paper IV Unit 1 Unit 2 Unit 3 Unit 4 English Literature of the Seventeenth and Eighteenth Centuries—I Background Allegory; Neo-Classicism; Epic; Rise of the English Novel Poetry John Milton Paradise Lost (Bks I & IX) Poetry John Dryden Absalom and Achitophel â€Å"Mac Flecknoe† Fiction Daniel Defoe Robinson Crusoe Henry Fielding Joseph Andrews Prose John Dryden Essay of Dramatic Poesy (Up to â€Å"Examen of ‘The Silent Woman’†) Preface to Shakespeare (Up to the paragraph Samuel Johnson beginning â€Å"So careless was this great poet†¦Ã¢â‚¬  3 Unit 5 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Paper V Unit 1 Unit 2 Unit 3 English Literature of the Seventeenth and Eighteenth Centuries—II Background Pastoral Poetry; Restoration Comedy; Satire; Sentimental Comedy Poetry Alexander Pope Poetry William Blake â€Å"The Rape of the Lock† (Canto I) â€Å"An Essay on Criticism† (Part I) Songs of Innocence (â€Å"The Lamb†, â€Å"Holy Thursday†, â€Å"The Chimney Sweeper†) Songs of Experience (â€Å"The Tyger†, â€Å"Holy Thursday†, â€Å"The Chimney Sweeper†, â€Å"London†, â€Å"A Poison Tree†) â€Å"Elegy Written in a Country Churchyard† The Way of the World The Rivals â€Å"Sir Roger in Church† â€Å"The Aims of the Spectator† â€Å"Mr. Bickerstaff on Himself† â€Å"The Spectator Club† Unit 4 Unit 5 Thomas Gray Drama William Congreve R B Sheridan Prose Joseph Addison Richard Steele 4 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad MA (Previous) Semester II—(Papers I to V) Paper I Unit 1 History, Structure and Description of English—II a) Word Formation in English b) Change of Meaning a) Levels of Language Description: Syntax b) Varieties of Language: Dialect, Idiolect, Register, and Style a) Word Stress in English b) Properties of Connected Speech: Weak forms/Elision and Intonation a) Behaviourist and Cognitivist Approaches to Language Learning/Teaching; Differences between First Language Acquisition and Second Language Learning b) Role of English in India and the Objectives of Teaching English at the College Level a) Techniques of Teaching Prose, Poetry, Grammar, and Vocabulary b) Language Testing Unit 2 Unit 3 Unit 4 Unit 5 Paper II Unit 1 Unit 2 English Literature of the Nineteenth Century—I Background Romanticism; Fancy and Imagination; Gothic; Historical Novel Poetry William Wordsworth S T Coleridge Poetry P B Shelley John Keats â€Å"Intimations Ode†, â€Å"Tintern Abbey† â€Å"Rime of the Ancient Mariner† â€Å"Ode to the West Wind†, â€Å"To a Skylark† Odes: â€Å"On a Grecian Urn,† To Autumn,† â€Å"To a Nightingale† Emma Wuthering Heights Unit 3 Unit 4 Fiction Jane Austen Emily Brontà © 5 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Unit 5 Prose Charles Lamb William Hazlitt â€Å"Dream Children†, â€Å"Old China† â€Å"The Indian Juggler†, â€Å"The Fight† Paper III Unit 1 English Literature of the Nineteenth Century—II Background Science and Religion; Pre-Raphaelites; Dramatic Monologue; Realism and Naturalism Poetry Alfred Lord Tennyson Robert Browning Poetry Elizabeth Barrett Browning â€Å"Ulysses†, â€Å"Lotos Eaters† â€Å"My Last Duchess†, â€Å"Andrea Del Sarto† Unit 2 Unit 3 G M Hopkins Matthew Arnold Unit 4 Fiction Charles Dickens Thomas Hardy Prose Matthew Arnold John Ruskin Sonnets from the Portuguese 21 (â€Å"Say over Again †¦Ã¢â‚¬ ) 32 (â€Å"The first time that †¦Ã¢â‚¬ ) 43 (â€Å"How do I love thee †¦Ã¢â‚¬ ) â€Å"Pied Beauty†, â€Å"God’s Grandeur†, â€Å"Windhover† â€Å"Dover Beach† Hard Times Tess of the d’Urbervilles â€Å"The Study of Poetry† Unto This Last (Section I) Unit 5 Paper IV Unit 1 Unit 2 English Literature of the Twentieth Century—I Background Modernism; Dada and Surrealism; Symbolism; Stream of Consciousness Poetry W B Yeats T S Eliot â€Å"Easter 1916†, â€Å"Second Coming†, â€Å"Byzantium† The Waste Land 6 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Unit 3 Fiction D H Lawrence Joseph Conrad Prose Virginia Woolf E M Forster Drama G B Shaw J M Synge Sons and Lovers Heart of Darkness A Room of One’s Own â€Å"Art for Art’s Sake† (from Two Cheers for Democracy) Saint Joan Riders to the Sea Unit 4 Unit 5 Paper V Unit 1 Unit 2 English Literature of the Twentieth Century—II Background Postmodernism; Impressionism; Existentialism; Movement Poetry Poetry Ted Hughes Phillip Larkin Seamus Heaney Fiction William Golding Graham Greene Drama Samuel Beckett Tom Stoppard Short Story Roald Dahl A S Byatt â€Å"Thought Fox†, â€Å"Hawk Roosting† â€Å"Churchgoing,† â€Å"Toads† â€Å"Digging†, â€Å"Punishment† Lord of the Flies The Power and the Glory Waiting for Godot Indian Ink â€Å"Lamb to the Slaughter† â€Å"The Umbrella Man† â€Å"Sugar† (from Sugar and Other Stories) Unit 3 Unit 4 Unit 5 7 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Syllabus of M A (English) (With effect from 2009-10) MA (Final) Semester III—(Papers I-V) Paper I Unit 1 American Literature—I Background American Frontier; American Renaissance; American Transcendentalism; American Puritanism Poetry Phyllis Wheatley Walt Whitman â€Å"On Being Brought from Africa to America† â€Å"When Lilacs Last in the Door-yard Bloom’d†, â€Å"Out of the Cradle Endlessly Rocking†, â€Å"Crossing the Brooklyn Ferry† â€Å"I taste a liquor never brewed†, â€Å"She sweeps with many-colored brooms†, â€Å"After great pain a formal feeling comes† The Scarlet Letter The Adventures of Huckleberry Finn The Hairy Ape Death of a Salesman â€Å"The American Scholar† â€Å"Civil Disobedience† Unit 2 Emily Dickinson Unit 3 Fiction Nathaniel Hawthorne Mark Twain Drama Eugene O’Neill Arthur Miller Prose Ralph Waldo Emerson Henry David Thoreau Unit 4 Unit 5 8 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Paper II Unit 1 Indian Writing in English—I Background Indian Nationalist Movement; Use of English for political awakening; Reform Movements; Rise of the Indian Novel Poetry (Selections from Indian Poetry in English. Ed Makarand Paranjape. Macmillan, 1993) Sri Aurobindo â€Å"I have a hundred lives† â€Å"The Golden Light† â€Å"Thought the Paraclete† Toru Dutt â€Å"Sita†, â€Å"Our Casuarina Tree† Sarojini Naidu â€Å"The Pardah Nashin†, Ghanashyam† Fiction Krupabai Satthianandhan Mulk Raj Anand Fiction Raja Rao R K Narayan Prose Rabindranath Tagore B R Ambedkar Kamala: a Story of Hindu life Untouchable Kanthapura The Man-Eater of Malgudi â€Å"Nationalism in India† (from Nationalism) â€Å"The Annihilation of Caste† (Collected Works of B R Ambedkar, Vol III) Unit 2 Unit 3 Unit 4 Unit 5 Paper III Unit 1 Unit 2 Postcolonial Literatures Background Colonialism-Imperialism; Postcolonialism; Nationalism; Diaspora Poetry Christopher Okigbo Edward Brathwaite Judith Wright â€Å"Heaven’s Gate†, â€Å"Death lay in Ambush† â€Å"Didn’t He Ramble†, â€Å"Calypso† â€Å"Eve to Her Daughters†, â€Å"Bullocky† Things Fall Apart The Edible Woman Unit 3 Fiction Chinua Achebe Margaret Atwood 9 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Unit 4 Drama Wole Soyinka Derek Walcott Prose V S Naipaul Ngugi wa Thiong’o Kongi’s Harvest Dream on Monkey Mountain Unit 5 â€Å"Indian Autobiographies† (from Literary Occasions: Essays) â€Å"The Language of African Literature† (from Decolonizing the Mind) Paper IV: ENGLISH LANGUAGE TEACHING Unit I History of English Language Teaching in India: Some important landmarks: a) Critique of Macaulay’s Minute; b) Landmarks of English Education in India after Independence: Kunzru Committee, the three language formula and Kothari commission. c) Ramamurthy Commission Report d) Curriculum and its components; Syllabus/ Paper Design; materials development Major Approaches, Methods and Syllabi: a. Traditional methods – Use of the Grammar Translation method, Direct method, Reading method; b. Structural Approach: Audio-Lingual Method, Types of syllabi: structuraloral-situational, notional-functional; linguistic competence and communicative competence; Error analysis and Remedial teaching c. Communicative approach, Krashen’s Monitor Model (Natural method); task based syllabus d. Humanistic Approaches: Community Language Learning, Suggestopaedia Classroom Techniques: a. Lecture mode; classroom discussion; Peer and pair work; b. Role play; Team teaching; Teaching large classes. c. Teaching Aids: Use of the Blackboard, flip charts, , OHP, audio visual tools, Television, d. Traditional and digital Language Lab; the Computer and the Internet. Teaching of Language skills: a. The teaching of listening, speaking, reading, writing and related study skills b. Teaching of literature c. Stylistic approach to the teaching of literature (norm, deviation, and foregrounding); d. Teaching of language through literature. 10 Unit II Unit III: Unit IV: Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Unit V: Testing and Evaluation: a. Importance of Testing, traditional testing methods; Different types of tests b. Group Discussion (GD) c. Interview d. Course Evaluation Paper V : Inter –Disciplinary ID-I : Writing for Academic and Professional Purposes Unit 1: Language CompetenceA. Communicative Grammar: Nouns, articles, prepositional phrases, tenses subject verb agreement, modal verbs, difference between spoken & written language B. Sentence structure, kinds of sentences-statements, interrogatives, question tags passive constructions, reported speech; use of conditionals, compound & complex sentences C. Academic Reading : read to write- focus on the gist, idiom, rhetoric, style and genre specific features in different texts ; intensive & critical reading, note making Unit 2: Organization of writing A. Guided writing, expansion, use of connectives, sequencing, writing a paragraph free writing, mind mapping. Paraphrasing, summarizing, writing an abstract Writing letters, resume and email ( e-mail etiquette) B. C. Unit 3: Academic Writing A. B. C. proposals, SOPs ( statement of purpose) structure of a report, report writing Writing an essay; (descriptive, argumentative and scientific) Unit 4: Professional Writing A. Inter office memos, professional reports( business, survey, minutes of a meeting) B. Editing, writing a review, creative writing (Ad writing, slogan writing and writing headlines). C. Technical writing; product and process writing, writing a user manual SEMINAR PRESENTATION 11 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad MA (Final) Semester IV—(Papers I-V) Paper I Unit 1 Unit 2 American Literature—II Background American Dream; Multiculturalism; Lost Generation; American Comedy Poetry Robert Frost Wallace Stevens Robert Lowell Unit 3 Fiction Ernest Hemingway Saul Bellow Drama Lorraine Hansberry Neil Simon Short Fiction Henry James William Faulkner Issac Asimov â€Å"West Running Brook†, â€Å"Home Burial† â€Å"Sunday Morning† â€Å"The Emperor of Ice-Cream â€Å"For the Union Dead† â€Å"At a Bible House† The Old Man and the Sea Seize the Day Raisin in the Sun Sunshine Boys â€Å"The Middle Years† â€Å"Go Down Moses† â€Å"The Bicentennial Man† Unit 4 Unit 5 12 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Paper II Unit 1 Indian Writing in English—II Background Decolonization; Counter DisPapers; Partition Literature; Myth and Literature Poetry (Selections from Indian Poetry in English. Ed Makarand Paranjape. Macmillan, 1993) Nissim Ezekiel Kamala Das A K Ramanujan Unit 3 Fiction Salman Rushdie Shashi Deshpande Drama Girish Karnad Mahesh Dattani Short Fiction Bharati Mukherjee â€Å"Enterprise† â€Å"Poet, Lover, Birdwatcher† â€Å"An Introduction† â€Å"The Old Playhouse† â€Å"A River†, â€Å"Love Poem for a Wife-I† Unit 2 Midnight’s Children The Binding Vine Hayavadana Final Solutions â€Å"A Wife’s Story†, â€Å"Management of Grief† (both from The Middleman and Other Stories, 1989) â€Å"The Accompanist† â€Å"A Devoted Son† (both from Games at Twilight, 1978) Unit 4 Unit 5 Anita Desai 13 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Paper: III: (Specializations) A) Women’s Writing B) Indian Literatures in Translation C) Modern Classics in Translation Paper III A) Women’s Writing Unit 1: Background The Woman Question: New Woman; Women’s Liberation Movement; Feminism; Re-reading the Canon Prose Mary Wollstonecraft Unit 2: Vindication of the Rights of Women (Introduction and Chapter 2) The Second Sex (Essay on Biology) Simon de Beauvour Unit 3: Poetry Elizabeth Barret Browing Sylvia Plath Margaret Atwood Grace Nichols Anne Stevenson Fiction Virginia Woolf Nadine Gordimer Drama Carly Churchill Alima Ata Aidoo â€Å"A Curse for a Nation† â€Å"Lady Lazarus† â€Å"Circle† – Mud Poems â€Å"Making Poetry†, The Spirit is too Blunt an Instrument Unit 4: Mrs Dalloway July People Unit 5: Top Girls Anowa Paper III (B): INDIAN LITERATURES IN TRANSLATION Unit 1: i) ii) Background Types of Natya (Nataka, Prakarana, and Prahasana) and Theory of Rasa and Kavya Indian Concept of Translation (from Translation as Discovery by Sujit Mukherjee, Chapter 2 & 3) Scope of Comparative Literature (â€Å"Comparative Literature in India: A Perspective† by Bijay Kumar Das from Comparative Indian Literature ed. Rao & Dhawan) 14 iii) Department of English University College of Arts & Social Sciences Osmania University, Hyderabad iv) Dalit Aesthetics (â€Å"Dalit Literature and Aesthetics† from Towards an Aesthetics of Dalit Literature by Sharavan Kumar Limbale) Poetry Sangam Poety – from Poems of Love and War Trans by AK. Ramanujan, Akam Poems – â€Å"Kurinci† (page 15), â€Å"Neytal† (page 41),†Palai† (page 53), â€Å"Mullai† (page 81), â€Å"Marutam† (page 97), Puram Poems – â€Å"King Killi in Combat† (page 123) Gurram Joshua – I was one of them†, The Bat Messenger† (From Twentieth Century Telugu Poetry. An Anthology ed. By Velcheru Narayan Rao, OUP 2002) Jibananda Das – â€Å"Banalata Sen†, The Naked Solitary Hand† (From Signatures ed by Satchidanandan, Sahitya Academi, New Delhi) Drama Kalidas Unit 2: i) ii) iii) Unit 3 i) Abhgnana Shakuntalam from The Plays of Kalidasa by Barbara Stoller Miller, Ed Columbia University Press, 1984 Silence! the Court is in Session (OUP) ii) Unit 4: i) Vijay Tendulkar Fiction Premchand Godan; a novel of peasant India Tans by Jai Ratan and P. Lal Bombay: Jaico, 1979 ii) U.R Anantha Murthy Smakara: A Rite of Dead Man Trans by A.K. Ramanujan (OUP) Short Fiction Unit 5: i) Folktales – â€Å"Bopoluchi† (A Punjabi Folk Tale), â€Å"Why the Fish Laughed† (A Kashmiri Folk Tale), Folktales from India selected and ed. By A.K. Ramanujan, Penguin Books India, 1994. Ismat Chugtai – â€Å"Chauti Ka Jowra† from Inner Courtyard. Ed Lakshmi Holmstrom, Rupa, 2002. Mahasweta Devi – â€Å"Shishu† from Women’s Writing, Vol II Ed by Tharu & Lalitha, OUP, 1991. ii) iii) 15 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Paper III (C) : Modern Classics in Translation Unit 1: Background Enlightenment; Bourgeois Experience; Epic Theatre ; Magic Realism. Poetry Charles Baudelaire : The Sick muse, Even She was called Bautrice By Many Who knew Not Wherefore, The Remorse of the Dead Pablo Neruda: What Spain was Like, The Heavenly Poets, Opium in the East Joseph Brodsky: Odysseus to Telemachus, Nune Dimmittis, Nature Morte Unit 3: Fiction Gustav Flaubert: Milan Kundera: Drama Anton Chekhov Betrolt Brecht Unite 2: Madame Bovary Book of Laughter Forgetting Unit 4 The Cherry Orchard Mother Courage Unit 5: Short Fiction Franz Kafka Gabriel Garcia Marquez PROJECT WORK Metamorphosis No one Writes to the Colonel PAPER IV Paper V: Inter-Disciplinary (ID-II) Literature and Film Unit1: Background: a) Elements of a narrative: Theme, Plot, Structure, Setting, Character, Point of View b) Narrative devices : genres, montage, film noir, flashback, special effects Unit 2: Drama and Film a) George Bernard Shaw – Pygmalion (1913) b) George Cukor (Director) – My Fair Lady (1964) Unit 3 : Novel and Film a) EM Forster – A Passage to India (1924) b) David Lean (Director) – A Passage to India (1984). Unit 4: Short Fiction and Film a) Ruskin Bond – â€Å"The Blue Umbrella† b) Vishal Bhardwaj (Director) – â€Å"The Blue Umbrella† (2007) 16 Department of English University College of Arts & Social Sciences Osmania University, Hyderabad Suggested Reading Beja, Morris. Film & Literature, an introduction, Longman, 1979. Bluestone, George. Novels into film, Johns Hopkins Press, 1957. Boyum, Joy Gould. Double Exposure : Fiction into Film, Seagull Books, 1989. Corrigan, Timothy, ed Film and Literature: An Introduction and Reader. Prentice Hall, 1999. Das Gupta, Chidananda. Talking about films. Orient Longman, 1981 Deborah Cartmell and Imelda Whelehan, eds. Adaptations: from text to screen, screen to text. Routledge, 1999. Elliott, Kamilla. Rethinking the novel/film debate. CUP, 2003. Literature –Film Quarterly. McFarlane, Brian. Novel to film: an introduction to the theory of adaptation. OUP, 1996. Ray, Satyajit. Our Films, Their Films. Orient Longman, 1976. Reberge, Gaston. The Subject of Cinema, Seagull Books, 1987. Stam, Robert and Alessandra Raengo, eds. A Companion to literature and film. Blackwell Pub., 2004. SEMINAR PRESENTATION