National Curriculum in Schools in England Essay

National Curriculum in Schools in England - Essay Example From this study it is clear that a curriculum should not burden the leaners by ensuring that the developers constitute the most appropriate concepts for every stage of the learning process thereby guaranteeing optimum learning. This requires the consideration of such pertinent features of the learner as their age and the knowledge gap. Additionally, an effective curriculum introduces concepts progressively thereby ensuring that the learner understands each concept at the most appropriate age. Besides the development of the concepts for the learner, curriculums manage the teachers. According to the paper a curriculum must consider and set feature requirements for the teacher thereby ensuring that only the most effective teachers impart the knowledge in the learners. A curriculum therefore advises the teachers on the best earning aids for every learning stage and the mode of teaching to ensure a productive system. Additionally, curriculums should always reflect the state of the society within which it is applied in a number of ways, the knowledge in the curriculum must have direct relevance with the environment within which it is used. This implies that the curriculum must envision the knowledge growth through time. An effective curriculum therefore has a period lapse within which it is reviewed. In the United Kingdom, the period is four years a time within which the developers remove certain aspects of the curriculum and replacing them with new concepts.  

The Life of Alexander the Great Essay Example for Free

The Life of Alexander the Great Essay At the age of twenty years old, Alexanders reign of the Macedonian throne began in 336 B.C. following the death of his father, Philip II. Olympias, Alexanders mom, was thought to have assassinated her own husband so that the throne would be prepared for her son. When Alexander became King, he wanted to do great things so that everyone would know that he is King. From the beginning of his reign, he always had a passion for fighting and winning wars. He also noticed that he had many enemies and conspirators and to immediately get them out of the way, he had them all executed. In 335 B.C. he destroyed Thebes, located in upper Egypt, for rebelling against him. In the following year, Alexander had the most amazing military campaign by guiding an army consisting of Greeks and Macedonians fighting against the Persian empire with the goal of taking revenge on Greece in order top fulfill his fathers dream. Throughout his lifetime, he accomplished many things, had incredible defeats, and conquered many countries. By this, he earned his title of the great and was most excellently admired for it. His people saw him as an outstanding motivator, leading men into dangerous, unknown regions, earning much respect and inspiring countless soldiers. Alexander didnt much care about his own safety yet placed all of his concern straight on the goal and the ways in which he would complete it. When in battle, he would like to show his equality between him and his soldiers by riding his war horse on the enemys front line, experiencing the same risks and threats as they were. People started urging him to get married and have a child to carry on his great title but he was too busy with his conquests. He had much hope and faith in his troops and thought out his plans well for only the greatest of successes. He was the ideal of male Greek culture. (pg. 130) Seen as a great hero, he helped his troops along to continuous triumphs. When visiting Gordion in Anatolia, he was given the opportunity to be rewarded the lordship of Asia if only he could make loose an unmoving knot binding the yoke of a chariot. Leaving everyone in awe, he sliced the tough knot with a quick slice of his sword. His never failing most high reputation  among the people never failed and the empire continued to grow. He kept a very close eye on the latest technology and techniques in order to keep up with his war successes. Alexanders unique fighting styles made enemies doubt themselves and their abilities to stand strong against him. He always had his plans all laid out and precise and after conquering Egypt and Persia, his strategy showed to be this : establish colonies of Greeks and Macedonians in conquered territory and keep the traditional administrative system in place. (pg. 131) Alexander began his journey of the founding of new cities by naming the first Alexandria after himself, located in Egypt. His maintaining passion for capture and exploration ruled so greatly in his life that his next goal would be to travel to India. Alexandria the Furthest was established on the way and he ended up settling for an alliance sealed by a marriage to the Bactrian princess Roxanne. (pg. 131) Voyaging into India, seventy days of marching through stormy weather led to the disappearance of the soldiers will to win. In 326 B.C., located on the banks of the Hyphasis River, they forced Alexander to turn back. Finally returning back to Persia, he started on the plans of his next attack without delay. His next target would be the Arabian peninsula followed by all of North Africa. Ruling over the Greeks became less important to him and he decided to restore citizenship within the city-states and he made the declaration that he wanted to be honored as if he were a god. Feeling astonished by this peculiar request, the other leaders complied by sending religious gifts showing their respect. Alexander thought so highly of himself because of all of his great and praiseworthy actions , that he started to believe that he was actually the son of Zeus. He felt that he showed to have godlike power therefore he must be as he proclaims he is. On the somber day of June 10, 323 B.C. , the young Alexander passed away due to extreme drinking and high fever. His future plans were ended by his sudden death not too long after the death of his best friend, Hephaistion . Following Alexanders death, a child was born to him and Roxanne. Despite his short reign, he greatly impacted and benefited the future for geography and many other scientific fields. Altogether, Alexander III immensely  extended the influence of Greek civilization and arranged the way for the empire of the Hellenistic period and the annexation of the Roman Empire.

Buddhism Essay -- essays research papers

Buddhism Buddhism, one of the major religions of the world, was founded by Siddhartha Gautama, the Buddha, who lived in northern India from 560 to 480 B.C. The time of the Buddha was one of social and religious change, marked by the further advance of Aryan Civilization into the Ganges Plain, the development of trade and cities, the breakdown of old tribal structures, and the rise of a whole spectrum of new religious movements that responded to the demands of the times (Conze 10). These movements were derived from the Brahmanic tradition of Hinduism but were also reactions against it. Of the new sects, Buddhism was the most successful and eventually spread throughout India and most of Asia. Today it is common to divide Buddhism into two main branches. The Theravada, or "Way of the Elders," is the more conservative of the two; it is dominant in Sri Lanka, Burma, and Thailand (Berry 23). The Mahayana, or "Great Vehicle," is more diverse and liberal; it is found mainly in Taiwan, Korea, and Japan, and among Tibetan peoples, where it is distinguished by its emphasis on the Buddhist Tantras (Berry 24). In recent times both branches, as well as Tibetan Buddhism, have gained followers in the West. It is virtually impossible to tell what the Buddhist population of the world is today; statistics are difficult to obtain because persons might have Buddhist beliefs and engage in Buddhist rites while maintaining folk or other religions such as Shinto, Confucian, Taoist, and Hindu (Corless 41). Such persons might or might not call themselves or be counted as Buddhists. Nevertheless, the number of Buddhists worldwide is frequently estimated at more than 300 million (Berry 32). Just what the original teaching of the Buddha was is a matter of some debate. Nonetheless, it may be said to have centered on certain basic doctrines. The first of the Four Noble Truths, the Buddha held, is suffering, or duhkha. By this, he meant not only that human existence is occasionally painful but that all beings; humans, animals, ghosts, hell- beings, even the gods in the heavens; are caught up in samsara, a cycle of rebirth, a maze of suffering in which their actions, or karma, keep them wandering (Coomaraswamy 53). Samsara ... ...bsp; The heart of Zen monasticism is the practice of meditation; it is this feature that has been most popular in Zen's spread to the West. Zen meditation highlights the experience of enlightenment, or satori, and the possibility of attaining it in this life. The strict training of Zen monks, the daily physical chores, the constant wrestling with koans, the long hours of sitting in meditation, and the special intensive periods of practice, or sesshin, are all directed toward this end. At the same time, enlightenment is generally thought of as being sudden. The meditator needs to be jolted awake, and the only one who can do this is his Zen master (Davids 113). The master-disciple relationship often involves private interviews in which the Zen trait of unconventionality sometimes comes to the fore; the master will allow no refuge in the Buddha or the sutras but demands from his disciple a direct answer to his assigned koan (Davids 114). Conversely, the master may goad the disciple by remaining silent or compassionately help him out, but with the constant aim of trying to cause a breakthrough from conventional to absolute truth (Corless 131).

Punctuality and Time Essay

Advantages: If we be punctual, we can finish up our work at right time. Punctuality checks unnecessary wastage of time. Time is very valuable for us. We can save it only by punctuality. Time and tide wait for none. Seconds, minutes, hours and days pass by in right order. There is a maxim â€Å"We should hold the time by the forelock†. If we be punctual, a single second of us will never go waste. The English men are very punctual. They put on wrist-watches to exercise punctuality. But we, the Indian put on wrist-watches only as ornaments for show. We cannot progress. If we do not be punctual. Punctuality helps us in our progress. It also saves money in other ways. There is a saying. â€Å"A stitch in time saves nine†. So, if we take our food punctually, we will never be sick and so we will never have to spend money on medicines and doctors or to worry our near and dear ones in this connection. And this principle applies well in all other cases. Conclusion: Everybody should be punctual in his everyday life. Every students should make a habit of punctuality. The people who have become great in their lives are very punctual. Punctuality is the first condition for becoming great in life. So, punctuality should be the motto in our life. We should not only be punctual ourselves but also advise others to be punctual. Related Articles.

Monsato Company †A Question in Agricultural Ethics Essay

Monsato Company is a Missouri-based company founded in 1901 by John F. Queeny and his wife Olga Monsato producing saccharine. In the mid-1940s, Monsato Co. began developing agricultural chemicals and throughout the 1960s and 1970s, herbicides were developed and introduced to the farmers. In 1981, a research group was established and the business’s primary focus was molecular biotechnology. In 1982, Monsato Co. bought Jacob Hartz Seed Co., a company known in the Midwest for its soybeen seeds. Also in 1982, scientists working for Monsato Co. produced the first genetically modified plant. In 1996, RoundUp Ready Soybeans were introduced possessing an in-seed herbicide. Several other in-seed herbicides are introduced in 1997 by Monsato Co. such as RoundUp Ready Cotton and RoundUp Ready Canola. Also introduced is an in-seed insect protection called YieldGard Corn Borer. In 1998, Monsato Co. combines the technology of in-seed herbicides with their in-seed insecticides into one product for its corn seed. In 2002, Monsato Co. identifies corn hybrids, which yield more ethanol per bushel than normal corn. Later this same year, they also identify a similar hybrid in their soybeans, which will produce more oil than a normal soybean. In 2004, Monsato Co. creates American Seeds, Inc (ASI) to support regional seed business with capital, genetics, and technology investments. In 2005, Monsato Co. acquires four companies Fontanelle Hybrids, based in Fontanelle, Neb, Stewart Seeds, based in Greensburg, Ind., Trelay Seeds, based in Livingston, Wis., and Stone Seeds, based in Pleasant Plains, Ill. In 2006, they acquire several other local seed companies, some family-owned, including Diener Seeds, Sieben Hybrids, Kruger Seed Company, Trisler Seed Farms, Gold Country Seed, Inc., Heritage Seeds and Campbell Seed. Over the next several years, they also acquire other local and regional companies and continue their research and development of genetically altered seeds. Over the course of a few decades, Monsato Co. has gone from a small company making saccharine to a Midwest agricultural giant manufacturing genetically altered seed. 1 A Possible Solution: Deregulation Although the idea of producing more crops with less cost, such as additional chemicals, pesticides, and herbicides may sound, the fact remains that Monsato Co. is not only toying with nature, they are also putting smaller family-owned companies out of business. In the past several years, organic foods have become more popular. Consumers want to feed their families healthy food, not food filled with chemicals. In 2005, the United States Department of Agriculture (USDA) decided to back Monsato and other biotech companies by supporting the deregulation of genetically engineered (GE) alfalfa. This would mean that the GE companies would have no restrictions on their technology and its use.2 Deregulation has its obvious problems. Organic crop company leaders, such as Stonyfield, Whole Foods, and OrganicValley believe that GE crops use a higher amount of toxins, herbicides, and water. Also the claims of higher crop yield will not be met and the price of this seed will be too costly for the average farmer. There is also the potential of cross-contamination of crops where a farmer using GE seed spreads the toxins to his organic neighbor through groundwater. This could lead to the organic farmer’s crops getting contaminated and his losing his license to sell organic products. Stonyfield and other organic companies opposed this ruling and in 2010 it went to the Supreme Court. The decision was that deregulation could not take place without the USDA making an environmental assessment of the genetically enhanced seeds used, and an injunction was put in place preventing the planting of GE alfalfa seeds. David and Goliath Biotech companies lobbied heavily in Washington. However, the smaller organic supporters caught the ear of the USDA and as a result persuaded them to conduct a meeting of the minds of both sides. The problem was clear – there was an incredible amount of support, political and financial, in favor of GE alfalfa. The result was that the UDSA would allow deregulation. The organic companies and farmers were faced with the fact that GE alfalfa was here to stay. What was left to fight over was whether it would be complete deregulation or one with restrictions. In their opinion, it was better to have some measure of control than no control at all, so the organic community stayed and fought. They brought to the table demands for reassurance that â€Å"(a) organic farmers whose crops become contaminated by GE alfalfa must be compensated by the patent holders for their losses due to losing their organic certification and (b) the USDA must oversee all testing and monitoring of GE crops t o ensure compliance as part of its role in protecting all US agriculture.† 3 The organic community won that portion of the battle. Conclusion The organic community may have won that battle, but they lost the war. Chemical companies and genetically engineered seed are a mainstay in today’s agriculture. Along with that they bring with them the potential for contaminated soil and damaged and lost crops of the small, everyday farmer. These farmers and family-owned businesses are being swallowed up on a regular basis. As the world’s population grows so does the demand for an ever increasing need of better, more enhanced, products. Technology provides us with the knowledge and growth for these, but in its wake leaves behind the things that matter very much to — clean air, clean soil, fresh water and â€Å"pure† food. References 1) Monsato. (2010). Monsato. Retrieved from http://www.monsanto.com 2) Pearson, C. (2010, March). The Most Unethical Company is also Best Corporate Citizen. Cause Integration http://www.causeintegration.com/2010/ the-most-unethical-companyis-a-best-corporate-citizen-what-gives/ 3) Hirshberg, G. (2011, January). Speaking with One Voice to Stop Monsato and Biotech. Huffington Post, http://www.huffingtonpost.com/gary-hirshberg/speaking-with-one-voice-t_b_816447.html

The limitations in Diagnosing Colorectal Cancer Essays

The limitations in Diagnosing Colorectal Cancer Essays The limitations in Diagnosing Colorectal Cancer Essay The limitations in Diagnosing Colorectal Cancer Essay Colon malignant neoplastic disease is the 2nd prima cause of malignant neoplastic disease decease. Most of the instances are sporadic but several familial familial syndromes account for around 5 % of all colorectal malignant neoplastic diseases ( CRC ) . The most common of these syndromes are familial adenomatous polyposis ( FAP ) and familial non-polyposis colon malignant neoplastic disease ( HNPCC ) which is besides known as Lynch syndrome. These make up 3 % of the familial syndromes. Other syndromes include Peutz-Jeghers syndrome and Juvenile polyposis syndrome. This essay will concentrate on the most common familial CRC s. The cistrons that are involved in FAP and HNPCC have been identified. Therefore familial testing can be offered to test for bearer position in these syndromes. Designation of persons who have a sensitivity to CRC is of import to be able to offer them adequate testing to observe tumors at an early phase. FAP FAP is dominantly inherited and is extremely acute demoing a perpendicular transmittal through a household lineage. Its classical phenotype involves the growing of 100s of adenomatous polyps along the colonic mucous membrane. If the polyps are non removed there is near a 100 % opportunity of colon malignant neoplastic disease. The mean age of polyp development and colon malignance is 16 and 39 old ages severally. FAP is found in ~1 per 7-10,000 births in the United States population and histories for less than 1 % of all CRC ( Davidson, 2007 ) . FAP is a monogenetic disease and is caused by the mutant or omission of the adenomatous polyposis coli ( APC ) cistron which is found on chromosome 5. 95 % of APC mutants that lead to FAP is either bunk ( 28 % ) or truncating frameshift ( 67 % ) ( Burt and Neklason, 2005 ) . The staying 5 % is caused by big omissions or rearrangements. The APC cistron is a tumour-suppressor cistron and the APC protein is portion of the Wnt-signalling tract, involved in cell growing control ( Burt and Neklason, 2005 ) . Mutants in the APC cistron hence cause activation of the Wnt-signalling tract and uncontrolled cell growing. There is another discrepancy of FAP known as Attenuated signifier of FAP ( AFAP ) , it has a ulterior age on oncoming ( gt ; 40 ) , less adenomatous polyps ( A ; lt ; 50 ) and a lower hazard of CRC. Some of these patients will hold a mutant in the extreme of the 3 or 5 terminal of the APC cistron compared to those who have extreme polyposis where mutants tend to be in the mid-portion of exon 15. It is of import to be able to separate between the types of FAP to cognize where to test for mutants and how to handle the status. It is besides of import to see a patient s nationality when they present to clinic. This can find their heritage hazard and aid to turn up the mutant. For illustration Ashkanazi Jews have a high prevalence of the I1307K mutant ensuing in a life-time hazard of CRC between 10-20 % . Diagnosis Familial testing is of import in households who are at hazard of FAP due the dominant and high penetrance phenotype. As there is a classical phenotype, FAP is easier to name in clinic. In FAP about all mutants consist of shortnesss of the APC protein. This occurs by point mutants, doing either a frameshift by an interpolation or omission, or a nonsensical codon. Familial Testing for FAP is done by bespeaking the presence of a disease doing mutant by a Protein Truncation Test ( PTT ) . Then the location of the mutant on the APC cistron is found by Conformation-Specific Gel Electrophoresis ( CSGE ) , Single-Strand Conformation Polymorphism ( SSCP ) or Denaturing Gradient Gel Electrophoresis ( DGGE ) . Once the location of the mutant is localised the APC cistron is sequenced to place the disease-causing mutant. For those big omissions and rearrangements, Southern Blotting, Array CGH and MLPA can be used for designation. If all of these methods fail to place the mutant, linkage proving to the APC cistron can be done. As it has become cheaper to sequence the APC cistron late many clinics skip the procedure of turn uping the country of mutant and sequence the whole cistron. Deductions The APC cistron is big and the mutants spread along it. This can do it hard to turn up the mutant. As many households have alone mutants it may be hard to make up ones mind if the mutant found is really infective. In fact in patients showing with phenotypical classical FAP, known infective mutants are merely found in 85 % of them. The remainder, although they may hold alterations in the APC cistron it is unknown what these alterations mean. As this information is uninformative it is non possible to give patients a hazard of acquiring CRC or to test their households to be able to except those who are non at hazard. All of the molecular trials used for FAP have their advantages and disadvantages. PTT fails to observe shortnesss that occur at the very terminal or beginning of a cistron and big mutants. Additionally it can non observe missense mutants. However, if it does happen a mutant it is ever disease doing. CSGE does observe more than 90 % of mutants present. SSCP detect s between 60 % -95 % of mutants and DGGE can observe up to 90 % of sequence alterations. Array CGH will lose little omissions and MLPA can non observe balanced translocations and is sensitive to drosss. Therefore some mutants are being missed. Linkage analysis can be between 90 % -95 % effectual in households that have multiple members affected by the disease. The consequences of linkage give symptomless household members the hazard they have of transporting the mutant. However, if these hazards are non below 5 % or above 95 % they are non really utile in clinic. Furthermore non all households will hold multiple affected members to be able to transport out linkage. Additionally decreased protein look may give rise to disease but causative mutants can be really hard to happen because they may be in regulative countries ( Burt and Neklason, 2005 ) . If a patient presented to clinic with FAP phenotype but when tested no mutant could be found on the APC cistron it is deserving proving the MYH cistron for mutants. The phenotype of MYH-associated polyposis ( MAP ) is similar but less terrible than FAP and it is inherited recessively. It is of import to separate between these different types so that the mutants can be identified so other members of the household can be screened. It is besides of import to handle the patient accurately. 25 % of instances of FAP arise as self-generated APC mutants ( Davidson, 2007 ) . Merely kids of these patients would be at hazard of being a bearer of the mutant. However as these patients will hold no household history an inexperient clinician may non recognize the status as being FAP. HNPCC Persons with HNPCC have an increased hazard of developing CRC. It is the most common signifier of familial CRC accounting for between 3-5 % of all instances ( Davidson, 2007 ) . It is an autosomal dominant status and people who inherit the status have early oncoming of colon malignant neoplastic disease ( A ; lt ; 40years ) . Tumours develop chiefly in proximal colon and a individual affected often has household history of colon malignant neoplastic disease or other associated malignant neoplastic diseases such as endometrial, ovarian, encephalon, little intestinal, pancreatic and urinary piece of land ( Davidson, 2007 ) . However there is no typical signifier of phenotype for HNPCC. It is of import though, due to the higher life-time hazard of developing these malignant neoplastic diseases, to name households affected, so that preventive showing can be offered. Diagnosis The first measure to name HNPCC is when a patient nowadayss in clinic. A standard known as the Amsterdam standards was devised over 15 old ages ago which must be met for an person to be clinically diagnosed. This method has been criticised as being excessively stiff. There are now adopted versions of this standard, such as the Modified Amsterdam and Modified Bethesda. These other standards are more inclusive but less specific for HNPPC. When a household is identified as potentially holding HNPCC, they are eligible for diagnostic showing. HNPCC causes a higher hazard of CRC due to a germline mutant of a mismatch fix ( MMR ) cistron. The cell is so unable to treat DNA fix. Mutation bearers exhibit a characteristic phenotype termed microsatellite instability, characterised by enlargement or contraction of short repetition sequences of Deoxyribonucleic acid at multiple venue ( Syngal et al, 1999 ) . Pathogenic mutants have been found at four mismatch fix cistrons ( MSH2, MHL1, PMS2 and MSH6 ) , but so far most HNPCC instances are caused by mutants in either MLH1 or MSH2 ( Muller et al. , 2004 ) . High microsatellite instability is a signal that the MMR cistron is lacking. A tumor is considered MSI high or unstable if more than 40 % of the venue show instability ( Burt and Neklason, 2005 ) . If an MMR-high reading is found, a farther diagnostic trial, Immunohistochemical staining can be used to place which cistron is most likely to be mutated. This looks for the MMR proteins MSH2, MLH1 and MSH6 in the tumour tissue. In 50 % -70 % of instances, mutants in mismatch fix cistrons can be found by DNA sequencing and the larger omissions and rearrangements which tend to be common in HNPCC can be found by Southern Blotting. Southern Blotting will happen the mutant in a farther 10 % -20 % of people, where sequencing could non. Deductions In clinic a diagnosing is dependent on a patient s household history. If the household history fits the Amsterdam or any of the modified standards so they can be identified as potentially holding HNPPC. However this method of naming has possible defects. A elaborate household history may non be given by the patient as they may non be in contact with other household members or they may go forth out information that they do non believe is critical, such as endometrial malignant neoplastic disease. The sensitiveness of the Amsterdam standards is between 54 % -91 % and the specificity is between 62 % -84 % . This means that a significant figure of HNPCC households could be excluded from proving and testing. The sensitiveness of MSI trials are 62 % . Therefore excess cautiousness should be used when construing consequences, particularly negative consequences. In 15 % of sporadic instances of CRC, MSI can be detected. This occurs due to methylation of the 5CpG island in the boos ter part ( Muller et al. , 2004 ) . The consequence of this trial may take you to believe that the proband has HNPPC and therefore them and their households would be at higher hazard of developing CRC. However this is non caused by a heritable mutant in the germline. In add-on this phenomenon exposes a corresponding restriction in the usage of IHC because MLH1 protein look is lost in tumor every bit good ( Lynch et al. , 2007 ) Additionally, dependable consequences for MSI can merely be obtained if adequate cells are right amplified to look at the microsatellite venue. These trials do non pick up all instances of HNPCC as approximately 10 % of IHC trials will be falsely negative, i.e. protein discoloration is present even though the related cistron is mutationally inactivated ( Burt and Neklason, 2005 ) . This could take to the bar of early sensing. Diagnostic intervention can besides give false positive consequences ; this can take to people having testing that do non necessitat e it and this may take to unneeded psychological emphasis. MSI and IHC trials complement each other and therefore both should ever be taken into history. When the cistron is identified that is likely to be mutated, sequence analysis or Southern Blotting can be performed to place the mutant. However this consequence is non ever informative for households as it can be hard to clearly specify a infective mutant. This means that it is non possible to test other household members for a known mutant. Besides in up to 10 % of people a mutant may non be found. Finally when taking an index instance to look for the mutant, the youngest affected individual should be chose. The older a patient is the more likely their malignant neoplastic disease is sporadic. However in a household the youngest affected individual may non hold to be tested. This leaves it harder to accomplish the consequences wanted. Decision The most hard portion of proving for CRC is cognizing who to prove. In FAP there is a clear phenotype but there are discrepancies such as AFAP and MAP. These besides benefit from proving. HNCPP has no clear phenotype and is much harder to estimate who would profit from proving. There are standards set in topographic point to assist this procedure but as mentioned some people are over looked. For both conditions no individual trial is sufficient to place the mutant. Some mutants may non even be identified and therefore it is of import that a adviser non merely measure the patient on their trial consequences but besides on their clinical diagnosing. Trial consequences are non required for disease direction but are helpful for placing other household members who are at hazard. Mentions Burt, R. A ; Neklason, D. , W. ( 2005 ) . Familial Testing for Inherited Colon Cancer.Gastroenterology128: 1696-1716 Davidson, N. , O. ( 2007 ) . Familial testing in colorectal malignant neoplastic disease: who, when, how and why.Keio Journal of Medicine56 ( 1 ) : 14-20 Lynch, P. , M. ( 2007 ) . New Issues in Genetic Counseling of Hereditary Colon Cancer. Clinical Cancer Research 13: 6857s-6861s Muller, A. , Giuffre, G. , Edmonston, T. , B. , Heinmoller, E. , Brodegger, T. , Tuccari, G. , Mangold, E. , Buettner, R. , A ; Ruschoff, J. ( 2004 ) . Challenges and Pitfalls in HNPCC Screening by Microsatellite Analysis and Immunohistochemistry.Journal of Molecular Nosologies6 ( 4 ) : 308-315 Syngal, S. , Fox, E. , A. , Li, C. , Dovidio, M. , Eng, C. , Kolondner, R. , D. , A ; Garber, J. , E. ( 1999 ) . Interpretation of Familial Test Results for Hereditary Nonpolyposis Colorectal Cancer: Deductions for Clinical Predisposition Testing.Journel of the American Medical Association282 ( 3 ) : 247-253 Bibliography Boultwood, J. A ; Fidler, C. ( 2002 ) .Molecular Analysis of Cancer, Humana Press, New Jersey. Chen, S. , Watson, P. A ; Parmigiani, G. ( 2005 ) . Accuracy of MSI Testing in Predicting Germline mutants of MSH2 and MLH1: a instance survey in Bayesian meta-analysis of diagnostic trials without a god criterion.Biometricss6 ( 3 ) : 450-464 Kerr, D. , J. , Young, A. , M. A ; Hobbs, F. , D. , R. ( 2002 ) .ABC of Colorectal Cancer, BMJ, London. Taylor, I. , Garcia-Aguilar, J. A ; Goldberg, S. , M. ( 2002 ) .Colorectal Cancer 2nd edition, Health Press, London Tomlinson, I. , Ilyas, M. A ; Novelli, M. ( 1997 ) .Molecular Geneticss of Colon Cancer. Cancer and Metastasis Reviews 16: 67-69 Walther, A. , Johnstone, E. , Swanton, C. , Midgley, R. , Tomlison, I. and Kerr, D. ( 2009 ) . Familial Prognostic and Predictive Markers in Colorectal Cancer.Nature Reviews 9: 489-499

Argumentative Writing with Stylistic Devices

Argumentative Writing with Stylistic Devices Argumentative Writing with Stylistic Devices The fact that argumentative papers are actually the most difficult papers to write is very common. However, there are many things involved in writing such. On many occasions when you are putting up an argument, people are not buying what you are writing or saying just because it is the truth. Readers usually tend to look at the beauty of what you are putting into words and how sophisticated and stylish it is. This is why you have to do everything possible to garnish your argumentative paper with numerous stylistic devices. There are many of them, but we will treat only 7 of the most popular ones. Rhetorical question This is actually one of the best stylistic devices you can attract attention to your argument with. It is the concept of asking questions for the simple sake of making an effect, and not because you need an answer. It is used to emphasize a thing that is already known, and it does the job of drawing attention or making the audience reflect over the mentioned issue. For example, who will defend the poor if the government does not involve itself in it?. Metaphor This is another great stylistic device. Here, you try to identify a word or phrase as a similar thing to something it does not have any relationship with. It is still a rhetorical tool used to draw attention to a particular situation. It simply highlights the similarities between the two, which may not be existent after all. An example of a metaphor is orange is the new black. Parallelism This is another great device you must form the habit of using here. You try to draw some parallel between parts of the same sentence. It involves using similar structure/construction in several clauses. This is mainly used to give a good pattern to the passage. An example is what you do in the dark will be revealed, what you do in the open will be revealed. Irony Irony is a good device that entails using an expression to give an opposite meaning. Here, what you say is exactly the opposite of what you mean. This is used to show some emphasis and actually bring some level of humor to your argumentative essay. For example, I hate life because it is very sweet. Repetition Another very important device that is used in the course of argumentative essays. Here, you simply repeat words within the same poetic line or within the same sentence in no particular order. This has a way of making the sentence or even phrases very emphatic and also beautiful to read. Many people do not see this as a stylistic device or figure of speech, but that is actually what it is. For instance what is worth doing is worth doing well. Personification This is described as the concept of attributing the characteristics of human beings to animals and inanimate objects. You make it look as if they have human feelings and behavior. This will always make your narrative more lively and interesting. And that is what your argumentative essay needs to make it less official-like and more reader-friendly. An example is â€Å"The proofs hang over this statement to crash it when the time comes. Hyperbole This is the stylistic device for argumentative writing that is also known as deliberate exaggeration. It is seldom used, and it simply means the use of highly exaggerated terms to draw emphasis and attention to your message. An example is The room was seemingly capable of holding millions of people. So, all in all if you are good at argumentative paper writing without these stylistic devices, it’s certainly more than great. But, in case you are eager to emphasize the message and strengthen your persuasion, these are the tools you must use. Make your academic writing more efficient with the means of stylistics.