Galactosemia Disorder: Causes, Forms and Treatments

Galactosemia Disorder: Causes, Forms and Treatments Abstract: Carbohydrates are vital for energy in all living organism and also in the biosynthesis of essential glycoconjugates. One of these carbohydrates is a monosaccharide called galactose which is broken-down in humans by the Leloir pathway of the galactose metabolism.[1] Within this pathway, there are three main enzymes that is responsible for modifying galactose in order to convert it into glycolysis for the production of energy – galactokinase (GALK1), galactose-1-phosohate uridyl transferase (GALT), and galactose-6-phosphate epimerase (GALE). A deficiency in any of these enzymes results in a disorder in the human called galactosemia. The second enzyme of this pathway, GALT which produces uridine diphosphogalactose (UPD-gal) from galactose-1-phosphate (gal-1P), a deficiency in this is the most severe of the three galactosemia disorders. GALK1 is rare and the symptoms are much milder than that of GALT with the rarest of the disorder being GALE. Galactosemia is established shortly a fter an infant starts feeding and even though a strict galactose-free diet is introduced promptly eliminating any acute symptoms, the long-term complications unfortunately has already taken place. While early detection can lead to relatively normal life, this inherited disorder is unable to break down simple sugar called galactose and with excessive buildup causes liver, brain, and eye damages. Introduction: All living organism make use of carbohydrates or sugars for the formation of cellular energy along with the synthesis of essential cellular glycoconjugates. In humans, we not only consume carbohydrates but we’re also able to synthesize altered carbohydrate monomers by means of reversible metabolic pathways. Galactose is typically in many of our dairy products that we consume as a carbohydrate monomer which is part of the disaccharide lactose. The human body is able to break down galactose using the Leloir pathway of galactose metabolism. This pathway consists of three enzymes, each structuring a different metabolic intermediate functioning together to accomplish one objective and that is to modify galactose into glucose in order to release it into glycolysis for the production of energy. The three enzymes are, Galactokinase (GALK1), galactose-1-phosohate uridyl transferase (GALT), and galactose-4-phosphate epimerase (GALE). An absence or mutations in any of these enzymes resul ts in a disorder in the human called galactosemia. The second enzyme of this pathway, GALT which produces uridine diphosphogalactose (UPD-gal) from galactose-1-phosphate (gal-1P), a deficiency in this enzyme is the most severe of the three galactosemia disorders. GALK1 is rare and the symptoms are much milder than that of GALT causing cataracts of the eye with the rarest of the disorder being GALE with acute symptoms as in GALT. UDP-gal in the Leloir’s pathway plays crucial role in synthesizing several essential glycoconjugates along with ultimately being used for energy production. GALT deficiency in humans’ results in a disorder called galactosemia, a potentially fatal disorder if left untreated immediately after birth. Galactose Metabolism (Leloir Pathway): Figure 1. Galactose Metabolism (Leloir Pathway) in the Liver. The galactose metabolic pathway, also known as Leloir pathway named after Luis Federico Leloir who revealed the principal mechanisms of galactose metabolism and defining the cause of galactosemia.[2] This is the only mechanism of galactose metabolism in humans which contains three enzymes, galactokinase (GALK1), galactose-1-phosphate uridyl transferase (GALT), and galactose-4-phosphate epimerase (GALE) which are responsible for their respective role in the Leloir pathway.[3] Upon entrance of the cell, galactose is first phosphorylated by GALK to yield galactose-1-phosphate, which is one of the two substrates of GALT. From here, GALT modifies it further to one uridine diphosphogalactose and one glucose-1-phosphate from one uridine diphosphoglucose and one galactose-1-phosphate. The expected product of GALT, UDP-gal, is the substance of GALE. As GALE epimerizes UDP-gal to produce UDP-glu, which is modified furthermore to enter glycolysis or be used as UDP-glu to synthesize necessary glycoconjugates in the cell.[4] [5] Further modification of UDP-glu consist of the loss of uridine monophosphate in order to produce glucose-1-phosphate. The mutase enzyme then yields glucose-6-phosphate, a glycolytic intermediate that moves into glycolysis to harvest energy in the form of ATP.[6] Since galactose is an essential component of many glycoconjugates, some UDP-gal is used for the synthesis of these sugar moieties which highlights the significance of GALT in the meta bolism and cellular consumption of galactose.[7] Galactosemia: Galactosemia is an autosomal recessive inborn error in the metabolism which affects how the body breakdown the sugar galactose with a rate of about 1 in 62,000 individuals.[8] As a result, those individuals with galactosemia has difficulty digesting this simple sugar that are often found in many foods which is primarily part of a larger sugar called lactose. Lactose produces one molecule each of the simple sugar glucose and galactose which is nearly found in all dairy products and baby formulas.[9] The disorder is typically diagnosed soon after birth, as infants are either breast-fed or formula-fed. However these newborn starts to express characteristic complications that tend to develop after the consumption of milk over a short period of time like nausea, vomiting, jaundice, and lethargy.[10] The accumulation of galactose is toxic to the body if not digested by the appropriate enzyme quickly causes serious health complications to the newborn. Treatments currently involves managemen t of galactose-free diet, although some drug tests in the disorder process have been proposed. Laboratory tests are available to confirm of the disease by measuring the enzyme activity of galactose-1-phosphate uridyl transferase or GALT which is the second step in the pathway of galactose metabolism.[11] There are 3 forms of this disorder: galactose-1-phosphate uridyl transferase (GALT), galactose kinase (GALK1), and galactose-4-phosphate epimerase (GALE) with each form having a relative differences in severity. Those individuals who expresses any of these disorders will have elevated levels of galactose in their blood along with high levels of galactose in the urine. For this reason, hospitals now carry out galactose tolerance tests which are now considered essential for the identification of the disease. Once confirmation of this disorder has been done, the newborn is treated using a dietary galactose restriction by replacing breast or milk base-formula with soy base-formula. Although most of the prominent features of this disease will improve such as nausea, diarrhea, cataracts, or enlarged liver and spleen will gradually regress once placed on the dietary restriction there is one chief symptom which does not show much improvement which is mental retardation due to the damage of the central nervous system.[12] It’s for this reason, that early diagnosis and prompt therapy are crucial. Cause of Disorder: Galactosemia means â€Å"galactose in the blood†, since these individuals are not able to break down galactose to produce energy, this sugar therefore builds up in their blood resulting in high levels of galactose-1-phosphate in the tissues. The pathway for galactose is more complex than most other simple sugars with three enzymes that are essential to convert a molecule of galactose into glucose-6-phosphate. Therefore, any type of genetic mutations in any part of the galactose pathway will cause severe life altering changes effecting organs and intellectual capacity if not treated right away. We can see from Fig. 1 that there are multiple steps in the breakdown of galactose into glucose-1-phosphate and be able to enter into glycolysis where it is broken down into glucose our main energy source. The GALK1 is the first enzyme in the galactose pathway and from this figure we can clearly see how by a mutation in GALK1 could cause so much chaos in the breakdown of galactose. The ability for our bodies to breakdown galactose into glucose plays a crucial for life. As a result, individuals with galactosemia, the GALT enzyme is either missing or not working properly and therefore unable to digest galactose into glucose causing large buildups in the blood. Overtime, this buildup if remain untreated will develop into fatality and although certain damages are able to regress a few of the many will not be irreversible. Forms of Disorder: There are several forms of galactosemia which are caused by mutations of a specific gene affecting different enzymes that are involved in the process of breaking down galactose. The classic galactosemia or galactose-1-phosphate uridyl transferase (GALT) is also known as galactosemia type I, is the most common and severe form of this disorder. Classical galactosemia affects 1 out of 60,000 newborns. In the classic galactosemia, infants are born without the GALT enzyme and are either fed breast-milk or milk-base formulas. In newborns nearly 90% of their carbohydrates comes from lactose, human breast milk comprises of nearly 6% to 8% lactose and most infant formulas comprises of 7% lactose.[13] Therefore all these milk-based products are immediately substituted with lactose free formulas such as soy-based formulas to lessen any further damage to the newborn. Fortunately, most cases of classic galactosemia are detected early enough by newborn screenings and a galactose-free diet is quickly put in place. Within galactosemia type I, there is a rare type of galactosemia called â€Å"Duarte variant†, it is often but not always detected during newborn screening since this is a milder form requiring less treatment or in most cases, no treatment but an erythrocyte GALT enzyme activity test may be performed to confirm this variant form of the disease. Galactokinase deficiency (GALK1) is also known as galactosemia type II which is rare genetic causing cataract damage due to a lack of galactokinase.[14] Galactosemia type II affects fewer than 1 out of 100,000 newborns. GALK1, is responsible for one step in the galactose metabolic pathway that converts galactose to galactose-1-phosphate which is then converted to glucose. A mutation in this gene results in galactose and an associated sugar called galactitol to buildup in the cells that constructs the lens of the eye.[15] With high level of these accumulations in the blood will damage the lens which will cause cataract and lead to blurred vision – a characteristic in galactosemia type II. Galactose-4-phosphate epimerase deficiency (GALE) is also known as galactosemia type III and the rarest of the three forms of galactosemia. Those who have this may have mild to severe symptoms which may include cataracts, delayed growth and development, along with liver disease, and liver problems. There has not been many reported with the GALE mutations as this is the fewest of the galactosemia disorders. GALE, is an enzyme that instructs the production of an enzyme called UPD-galactose-4-epimerase and responsible for converting UDP-galactose to UDP-glucose. Since GALE is the rarest of the disorder, those affected with galactosemia type III may or may not have any of the complications characteristically related to galactosemia and often do not require treatment. In general, those who have this disorder whose had high level of these enzymes in the blood will still lead to complications such as damaged tissues or organs, cataract, to intellectual disabilities and damages to the liver, kidneys and brain.[16] Newborn Screening: With the high rate of associated with untreated individuals, newborn screening for galactosemia and other inherited genetic disorders are available in all of the 50 states and provinces of the United States. To screen for galactosemia, infant blood and urine samples are screened for the presence of GALT and any galactose metabolites.[17] The samples are first tested for the concentration of galactose and GALT activity, and if galactose levels are high and/or GALT activity is low, then the samples are then assayed for galactose-1-phosphate and further tested of the more common DNA mutations associated with galactosemia.[18] . GALT enzyme presence of less than 32  µmol/L (normal 150-500  µmol/L) is usually indicative of GALT-deficient galactosemia.[19] Newborn screening is essential in early detection and treatment of galactosemia patients efficiently. It is vital to their physical and mental health to avoid as much damage to the individual as possible. Studies has shown that approximately 80% of children given newborn screening for galactosemia were diagnosed within 2 weeks of age, compared to approximately 35% of whom were not screened. From those whom were screened 20% were free of GALT deficiency symptoms at the time of diagnosis.[20] Although nutritional therapy is frequently used which gradually improves the symptoms in patients with galactosemia disorders by introducing these individuals to a galactose-free diet.[21] In most cases, as long as the disease has not advanced too much, most of all acute symptoms gradually regress and often times completely disappear with dietary restriction alone. Many newborns will show rapid weight gain along with no more nauseating or vomiting. The organs like the liver and spleen that would be enlarged due to excess galactose in the body also returns to normal size along with cataracts, if present, will start to regress and most of the time will disappear completely.[22] Unfortunately, there is one significant symptom that shows no signs of improvement – mental retardation or intellectual disability like speech defects and other neurological or physiological abnormalities.[23] Since newborn screening is not performed until at least 24 hours after an infant has begun feedi ng, galactosemia infants will consume galactose before being diagnosis. A more efficient and timely screening methods are necessary to decrease the cases of infants who are already exhibiting disease symptoms at the time of diagnosis. Diet: The most common and most effective form of treatment so far for galactosemia is dietary restriction of galactose consumption. By having galactosemia patient avoid lactose or ingesting food containing galactose they are able to minimize any further damage to their body. For infants, it’s particularly imperative as lactose is present in all milk-base products and studies has now shown that there are some free-galactose in some fruits and vegetables. A study by Gross and Acosta in 1991 indicated monomeric galactose contents in approximately 45 different fruits and vegetables. For example, artichoke, mushrooms, olives, and peanuts all contained less than 0.1 mg of free galactose per 100 mg of plant tissue. In persimmon and tomato contained approximately 34.5 mg of free galactose per 100 g of plant tissue. Fruits and vegetables like dates, papaya, bell pepper, and watermelon were found to have upwards of 10 mg of free galactose per 100 g of plant tissues.[24] Conclusion: Although uncommon due to the effective newborn screening, undiagnosed galactosemia can lead to liver cirrhosis, mental retardation, and even death. [25] Girls with galactosemia have been found in later years to have higher rates of ovarian failure even with dietary intake. It’s important to understand that with acute symptoms at birth can managed with diet but the long-term affect involving impaired sexual and mental function are still prevalent among galactosemia individuals. References: Antshel, K. M., Epstein, I. O., Waisbren, S. E. (2004). Cognitive strengths and weaknesses in children and adolescents homozygous for the galactosemia Q188R mutation: a descriptive study. Neuropsychology, 18(4), 658-664. Hardin, J., Bertoni, G., Kleinsmith, L.J., (2012) Becker’s World of the Cell, 8th Ed, International Edition. Pearson Education, Inc. Glenview. pp. 242 Isselbacher, K.J. (1957), Clinical and Biochemical Observations in Galactosemia. The American Journal of Clinical Nutrition. Vol. 5, No. 5, pp. 527-532. Grossiord, B. P., Luesink, E. J., Vaughan, E. E., Arnaud, A., de Vos, W. M. (2003). Characterization, Expression, and Mutation of the Lactococcus lactis galPMKTE Genes, Involved in Galactose Utilization via the Leloir Pathway. Journal of Bacteriology. Vol. 185, No. 3, pp. 870-878. Kalckar, H. M., Kurahashi, K., Jordan, E. (1959). â€Å"Hereditary Defects in Galactose Metabolism in Escherichia Coli Mutants, I. Determination of Enzyme Activities†. Proceedings of the National Academy of Sciences of the United States of America, Vol. 45, No. 12, pp. 1776-1786. Asada, M., Okano, Y., Imamura, T., Suyama, I., Hase, Y., Isshiki, G., (1999). Molecular characterization of galactokinase deficiency in Japanese patients. Journal of Human Genetics. Vol. 44: 377-382. Lai, K., Langley, S. D., Khwaja, F. W., Schmitt, E. W., Elsas, L. J. (2003). GALT Deficiency Causes UDP-Hexose Deficit in Human Galactosemic Cells. Glycobiology. Vol. 13, No. 4, pp. 285-294. Berry, G.T., Classic Galactosemia and Clinical Variant Galactosemia. 2000 Feb 4 [Updated 2014 Apr 3]. GeneReviews ® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2014.http://www.ncbi.nlm.nih.gov/books/NBK1518/ Ai, Y., Zheng, Z., O’Brien-Jenkins, A., Bernard, D.J., Wynshaw-Boris, T., Ning, C., Reynolds, R., Segal, S., Huang, K., and Dwight Stambolian. (2000), A Mouse Model of Galactose-Induced Cataracts. Human Molecular Genetics. Vol. 9, No. 12, pp. 1821-1827. Fridovich-Keil, J.,Bean, L., He, M., andRichard Schroer., Epimerase Deficiency Galactosemia. 2011 Jan 25 [Updated 2013 Oct 24]. GeneReviews ® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2014.http://www.ncbi.nlm.nih.gov/books/NBK51671/ Freer, D. E., Ficicioglu, C., Finegold, D. (2010). Newborn Screening for Galactosemia: A Review of 5 Years of Data and Audit of a Revised Reporting Approach. Clinical Chemistry, Vol. 56, No. 3, pp. 437-444. Waggoner, D. D., Buist, N. R., Donnell, G. N. (1990). Long-term Prognosis in Galactosaemia: Results of a Survey of 350 Cases. Journal of Inherited Metabolism Disorder., Vol. 13, No. 6, pp.802-818. Gross, K. C., Acosta, P. B. (1991). Fruits and Vegetables are a Source of Galactose: Implications in Planning the Diets of Patients with Galactosemia. Journal of Inherited Metabolism Disorder, Vol. 14, No.2 253-258. ~ 1 ~ [1] Kurt J. Isselbacher, â€Å"Clinical and Biochemical Observations in Galactosemia.† The American Journal of Clinical Nutrition 5 (September-October 1957): 527-532. [2] Benoit P. Groissard et al., â€Å"Characterization, Expression, and Mutation of the Lactococcus lactis galPMKTE Genes, Involved in Galactose Utilization via the Lenoir Pathway.† Journal of Bacteriology 185 (February 2003): 870-878. [3] Herman M. Kalckar et al., â€Å"Hereditary Defects in Galactose Metabolism in Escherichia Coli Mutants, I. Determination of Enzyme Activities.† Proceedings of the National Academy of Sciences of the U.S.A. 45 (December 1959): 1776-1786. [4] Groissard, 870-878. [5] Kalckar, 1776-1786. [6] Groissard, 870-878 [7] K. Lai et al., â€Å"GALT Deficiency Causes UDP-hexose Deficit in Human Galactosemic Cells.† Glycobiology 13 (January 2003): 285-294. [8] Boris B.T. Wang et al., â€Å"Molecular and Biochemical Basis of Galactosemia.† Molecular Genetics and Metabolism 63 (1998): 263-269. [9] Jeff Hardin et al., Becker’s World of the Cell (Glenview: Pearson Education Inc., 2012), 242002E [10] Isselbacher, 527. [11] Wang, 263. [12] Isselbacher, 528. [13] Gerard T. Berry, MD., â€Å"Classic Galactosemia and Clinical Variant Galactosemia.† GeneReviews ® [Internet] – NCBI Bookshelf (1993-2014). [14] Minoru Asada et al., â€Å"Molecular Characterization of Galactokinase Deficiency in Japanese Patients.† Journal of Human Genetics 44 (1999): 377-382. [15] Yunjun Ai et al., â€Å"A Mouse Model of Galactose-Induced Cataracts.† Human Molecular Genetics 9 (2000): 1821-1827. [16] Judith Fridovich-Keil, PhD et al., â€Å"Epimerase Deficiency Galactosemia.† GeneReviews ® NCBI Bookshelf (2011-2013). [17] Dennis E. Freer, Can Ficicioglu, and David Finegold., â€Å"Newborn Screening for Galactosemia: A Review of 5 Years of Data and Audit of A Revised Reporting Approach.† Clinical Chemistry 56 (March 2010): 437-444. [18] Freer et al., 437-444. [19] Freer et al., 437-444. [20] D.D. Waggoner, N.R M. Buist, and G.N. Donnell., â€Å"Long-term Prognosis in Galactosemia: Results of A Survey of 350 Cases† Journal of Inherited Metabolic Diseaase 13 (November 1990): 802-818. [21] Isselbacher, 528. [22] Isselbacher, 528. [23] Wang, 263. [24] K.C. Gross and P.B. Acosta., â€Å"Fruits and Vegetables Are A Source of Galactose: Implications in Planning the Diets of Patients with Galactosemia.† Journal of Inherited Metabolic Disease 14 (1991): 253-258. [25] Kevin M. Antshel et al., â€Å"Cognitive Strengths and Weaknesses in Children and Adolescents Homozygous for the Galactosemia Q188R Mutation: A Descriptive Study.† Neuropsychology 18 (October 2004): 658-664.

Marketing Make Up

There are several marketing approaches that can be used to launch a new product in the market. However, there are also some advantages and disadvantages which can be incurred while putting a definite advertising strategy into action. One type of marketing is called the USP or the Unique Selling Proposition. This aims to present the uniqueness of the product which other commodities do not have. The main advantage of such process can be attributed by setting apart the make up brand’s features and effects to one’s visual appeal. An additional or breakthrough substance can be realized for marketing attraction. However, the main disadvantage is that the product’s effect can vary from person to person. It is possible that there will be a group of consumers who will not be able to acquire the brand’s promise and may end up tarnishing the credibility of the brand. Another type of advertising technique is called Comparative Advertising. The process involves the acquisition of another brand name with the same product line up and comparing its quality and features side by side with the brand being advertised. This can be a very good approach in catching the attention of the consumers since the ready made features of the products can be observed in a form of testing. However, there can also be issues wherein consumers may realize that if they are getting the same characteristics of the product, then most likely brand will not be a factor but consequently the market price. Fear appeal is commonly used in relaying the consequential pattern of events if no reliable product is available. Because of such effect, the consumers will be forced to purchase a marketed item because of their anxiety experiences as pictured in the advertisement. The major attribute here is to arouse the consciousness of the viewers to change their attitude in buying and divert their attention to the brand being advertised (Associated Content, 2007). On the negative aspect, the advertiser will not have any clue whether the consumers will alternatively change their buying habits in favor of the brand. Since different perception and individual opinions will be involved, it can be very difficult to identify whether the people who will see the advertisement will get the intended message. Using a celebrity endorsement can also be one of the most effective ways to advertise a make up brand. Apparently, celebrities can easily attract buyers because of their reputation status in the entertainment industry. The more popular the actress is, the higher the probability that the masses will believe her position in using the make up brand. One grave consequence of this however can be on the part of investment cost. Since these individuals will require an enormous talent fee, a huge decision making process should be implemented by the advertiser. A slice of life ad is a technique in which situations with problems are presented to be solved using the product. Usually, these ads are too dramatic that audiences will be able to impart and relate their personal experiences (Answers, 2007). This can help the brand name to completely interact on the personal feelings of the consumers. One possible negative effect can be realized due to the limitation of the scope. Of course, not all people will be able to consider the situations presented in the advertisement to be factually true. The form of advertising in the essence of sex appeal is also used for many cosmetic and personal care brands. Since the make up industry primarily targets the female populace, different strategies of projecting the highest levels of sex appeal are instrumented. One good approach is to present and ad which focuses on the physical characteristic of the model. This will become the standard of the viewing consumers which will help in making them buy the item. However, giving them (consumers) the idea of involving sex appeal considerations can easily lure them to purchase other product lines which may use more appealing models. Lastly, the humor approach in advertising can be used. In some cases, humorous advertising can make it very light for the viewers to accept the main advantages of using the product being advertised. However, it can also project a certain form of apathy since the advertisers or the brand itself may project non-professionalism which may affect their credibility. References Answers Corporation. 2007. Slice of Life. Answers.com. Retrieved November 26, 2007 from http://www.answers.com/topic/slice-of-life-advertisement?cat=biz-fin. Associated Content. 2007. Fear Appeal Messages and their Effectiveness in Advertising-Severin and Tankard. Retrieved November 26, 2007 from http://www.associatedcontent.com/article/27813/fear_appeal_messages_and_their

Remember the Titans Essay - 681 Words

Remember the Titans 2000 Jerry Brucknerimer *STARS* Coach Boon- Denzel Washington Coach Yoast-Will Patton Julius- Wood Harris Gary Berter- Ryan Hurst The movie Remember the Titans takes place in Virginia. The year was 1971 when there were no racial mixings in the schools the previous years. The movie starts practically the day that the announcement of desegregation was going to come into action. The movie is in a small Virginia town where they say that football is as big as life. The high school team is known for being great and when they here that blacks are entering their school now known as TC Williams High they are furious. The school comes in and fires the old head coach and replaces him†¦show more content†¦The people who hired him said that they didnt even think that he would have made it out of camp. The football teams love lived on and they stuck together for their first win. As a victory the quarterback who everyone called Sunshine tried to take a few black teammates to dinner. The owner refused service and that was the beginning of them falling apart all over again. The team calls their own meeting trying to get back together, although they are undefeated they werent playing well and they knew that wouldnt work for long. On a major game referees were bribed to call multiple penalties against the Titans, but Coach Yoast knew what they were doing and said he would go to the papers. Turns out they were trying to get Coach Yoast back at the head job and forget about Boon. After a major victory the team captain is involved in a major car wreck and was paralyzed from the waist down. Even though they lost a lot they went on and won the state title. The movie ends at the paralyzed players funeral a few years later. They all came back for it and were reminded of the Titans. 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What makes this movie classic is how the players and coaches were able to overcome the issue of segregation and build relationships to form a championship team. Building relationships When the school board announced there will no longer be any form of segregation in schools, the black andRead MoreRemember The Titans ( 2000 )914 Words   |  4 PagesRemember the Titans (2000) is based on the true story of the Alexandra, Virginia, football team in 1971. The movie shows the desegregation of the schools in Alexandra and specifically follows the story of their football team. The town was on edge when forced to open their schools up to other races and ethnicities besides Whites. To make matters worse, the football team was forced to replace their white, head football coach, whom was about to be inducted into the Hall of Fame, with an African AmericanRead MoreRemember The Titans ( 2000 )903 Words   |  4 PagesRemember the Titans (2000), is based on the true story of Coach Herman Boone, the football coach of T.C. Williams High School in Alexandria, Virginia. Now Coach Boone becomes the football coach around 1970, and he is promoted to be the Head Coach of the team, and he is an African-American, while the high school is newly desegregated and starting the controversial practice of â€Å"bussing† black students to the high school. Now the film starts with Coach Boone being appointed by the school board as theRead MoreRemember the Titans Leaderhip7514 Words   |  31 PagesÃŽ ¿ÃŽ ¼ÃŽ ¬ÃŽ ´ÃŽ ± πΠ¿ÃŽ ´ÃŽ ¿ÃÆ'φÎ ±ÃŽ ¯Ã ÃŽ ¿Ãâ€¦ τωÎ ½ ÃŽ ­ÃŽ ³Ãâ€¡Ã Ãâ€°ÃŽ ¼Ãâ€°ÃŽ ½ 19 5.3 ΟÎ ¼ÃŽ ¬ÃŽ ´ÃŽ ± τωÎ ½ ÃŽ ¤ÃŽ ¹Ãâ€žÃŽ ¬ÃŽ ½Ãâ€°ÃŽ ½ 20 6 ΕΙÎ £ÃŽâ€"ΓÎâ€"ÃŽ £ÃŽâ€¢ÃŽâ„¢ÃŽ £ ΓΙΑ ΒΕΛÎ ¤ÃŽâ„¢ÃŽ ©ÃŽ £ÃŽâ€" ÃŽ ¤ÃŽâ€"ÃŽ £ ΑÎ  ÃŽÅ¸ÃŽ ¤ÃŽâ€¢ÃŽâ€ºÃŽâ€¢ÃŽ £ÃŽÅ"ΑÎ ¤ÃŽâ„¢ÃŽÅ¡ÃŽÅ¸ÃŽ ¤ÃŽâ€"ÃŽ ¤ÃŽâ€˜ÃŽ £ ÃŽ ¤ÃŽ ©ÃŽ  ΑÎ ¤ÃŽÅ¸ÃŽÅ"ÃŽ ©ÃŽ  ΚΑΙ ΟÎÅ"ΑΔÎ ©ÃŽ  24 7 ΛΕΙÎ ¤ÃŽÅ¸ÃŽ ¥ÃŽ ¡ÃŽâ€œÃŽâ„¢ÃŽâ€˜ ΚΑΙ ΑÎ  ÃŽÅ¸ÃŽ ¤ÃŽâ€¢ÃŽâ€ºÃŽâ€¢ÃŽ £ÃŽÅ"ΑÎ ¤ÃŽâ„¢ÃŽÅ¡ÃŽÅ¸ÃŽ ¤ÃŽâ€"ÃŽ ¤ÃŽâ€˜ ÃŽ ¤ÃŽâ€"ÃŽ £ ΔΙΚÎâ€"ÃŽ £ ÃŽÅ"ΑÎ £ ΟÎÅ"ΑΔΑÎ £ 26 ΕΙÎ £ÃŽâ€˜ÃŽâ€œÃŽ ©ÃŽâ€œÃŽâ€" ÃŽâ€" â€Å"ÃŽ £Ã ÃŽ ³ÃŽ ºÃ ÃŽ ¿Ãâ€¦ÃÆ'ÃŽ · ÃŽ ¤ÃŽ ¹Ãâ€žÃŽ ¬ÃŽ ½Ãâ€°ÃŽ ½Ã¢â‚¬  - â€Å"Remember the Titans† ÃŽ µÃŽ ¯ÃŽ ½ÃŽ ±ÃŽ ¹ ÃŽ ¼ÃŽ ¹ÃŽ ± ÃŽ ±ÃŽ ¼ÃŽ µÃ ÃŽ ¹ÃŽ ºÃŽ ¬ÃŽ ½ÃŽ ¹ÃŽ ºÃŽ · ÃŽ ±ÃŽ ¸ÃŽ »ÃŽ ·Ãâ€žÃŽ ¹ÃŽ ºÃŽ ® Ï„Î ±ÃŽ ¹ÃŽ ½ÃŽ ¯ÃŽ ± πΠ±Ã ÃŽ ±ÃŽ ³Ãâ€°ÃŽ ³ÃŽ ®Ãâ€š Ï„Î ¿Ãâ€¦ Jerry Bruckheimer ÃŽ ºÃŽ ±ÃŽ ¹ ÏÆ'ÃŽ ºÃŽ ·ÃŽ ½ÃŽ ¿ÃŽ ¸ÃŽ µÃÆ'ÃŽ ¯ÃŽ ±Ãâ€š Ï„Î ¿Ãâ€¦ Boaz Yakim, ÃŽ · ÃŽ ¿Ãâ‚¬ÃŽ ¿ÃŽ ¯ÃŽ ± ÃŽ ºÃâ€¦ÃŽ ºÃŽ »ÃŽ ¿Ãâ€ ÃÅ'Ï ÃŽ ·ÃÆ'ÃŽ µ Ï„Î ¿ 2000. ÃŽâ€" Ï„Î ±ÃŽ ¹ÃŽ ½ÃŽ ¯ÃŽ ± ÃŽ ²ÃŽ ±ÃÆ'ÃŽ ¯ÃŽ ¶ÃŽ µÃâ€žÃŽ ±ÃŽ ¹ ÏÆ'ÃŽ µ ÃŽ ±ÃŽ »ÃŽ ·ÃŽ ¸ÃŽ ¹ÃŽ ½ÃŽ ¬ ÃŽ ³ÃŽ µÃŽ ³ÃŽ ¿ÃŽ ½ÃÅ'Ï„Î ±, ÃŽ µÃŽ ¯Ãâ€¡ÃŽ µ ÃŽ ¼ÃŽ µÃŽ ³ÃŽ ¬ÃŽ »ÃŽ · ÃŽ µÃâ‚¬ÃŽ ¹Ãâ€žÃâ€¦Ãâ€¡ÃŽ ¯ÃŽ ±, ÃŽ ±Ãâ‚¬ÃŽ ¿ÃŽ ºÃÅ'ÃŽ ¼ÃŽ ¹ÃÆ'ÃŽ µ ÃŽ ¬Ã ÃŽ ¹ÃÆ'Ï„Î µÃâ€š ÃŽ ºÃ ÃŽ ¹Ãâ€žÃŽ ¹ÃŽ ºÃŽ ­Ãâ€š ÃŽ ºÃŽ ±ÃŽ ¹ πΠ±Ã ÃŽ ¿Ãâ€¦ÃÆ'ÃŽ ¹ÃŽ ¬ÃŽ ¶ÃŽ µÃŽ ¹ Ï„Î ±Read MoreAnalysis Of The Movie Remember The Titans 1113 Words   |  5 PagesMovie p roject â€Å"Remember the titans† was a movie that was released on September 23, 2000. The movie was directed by Boaz Yakin. The movie includes famous stars such as Denzel Washington as Coach Herman Boone, Will Patton as Coach Bill Yoast, and Wood Harris as Julius `Big Ju . The movie takes place in Alexandria, Virginia. The schools in Alexandria were segregated based on race. It was in 1971 when the school board forced the people to combine the white schools and the black schools in to one called

The Catcher in the Rye - Character Analysis of Holden...

The Catcher in the Rye - Character Analysis of Holden Caufield In J.D. Salingers novel The Catcher in the Rye, the main character, Holden Caufield, describes in detail the parts of his life and his environment that bother him the most. He faces these problems with a kind of naivety that prevents him from fully understanding why it is that he is so depressed. His life revolves around his problems, and he seems helpless in evading them. Among others, Holden finds himself facing the issues of acceptance of death, growing up, and his own self-destructiveness. One of the hardships Holden must cope with is his inability to come to terms with death, in particular that of his younger brother, Allie. Holden seems to have experienced a†¦show more content†¦In chapter twenty-five, Holden, while walking along Fifth Avenue, begins to believe that he will not be able to get to the other side of the street each time he reaches the end of a block, as if he will just fall off. He talks aloud to Allie to help him get through the ordeal. Holden also continues to see Allie as one of the few things he likes about life. Yet another demon that Holden avoids is the process of having to grow up. Throughout the book, he seems hesitant to develop any real ambitions or goals. He is a perpetual failure at school. He refuses to associate himself with mature ways of living, and so isolates himself from anyone his own age or older. This is all directly connected to Holdens picture-perfect image of his childhood. He sees this particular period of his life as his own personal paradise. He does not want to finalize the fact that he has to concede its innocence in the end. Towards the end of the book, Holden shows his desire for life to remain as it was by saying, ...certain things should stay the way they are. You ought to be able to stick them in one of those big glass cases and just leave them alone. Holden does not want to join a world of phonies and greed, a world lacking in carelessness and irresponsibility. He wont, whether consciously or not, accept the fact that he has no choice. A final conflict in the life of Holden Caufield is his own self-destructiveness. That he isShow MoreRelatedEssay on Franny and Zooey and Holden Caufield694 Words   |  3 PagesHolden as a Foil ti Zooey Although they are the protagonists from two separate books, Franny Glass, a teenage girl in J.D. Salinger’s Franny and Zooey, and Holden Caufield, a young man in Salinger’s novel Catcher in the Rye, serve as foils to each other. Both suffer unnecessarily due to their interaction with those whom they are close to, due to their relationships with themselves, as well as due to their views on the world. In the end, however Franny and Holden change their values and thereforeRead MoreCatcher in the Rye4413 Words   |  18 PagesThe Catcher in the Rye â€Å"Is The Catcher in the Rye, as a work of literature still relevant for today’s youth?† Name: Sara Sigurdson Course: English A1 Supervisor: Mr. Peter Steadman Word count: 3851 Candidate number: 00136022 Table of Contents Content Page Number Abstract 3 Introduction 4 The Actual Catcher in the Rye 4 The Sexual Matter 5 The Caulfield Family 6 Narrator and Protagonist 8 Role Model 9 Mr. Antolini 10 Targeted Audience 10 Guidance 12 Read MoreThe Traumitized Life of Holden1747 Words   |  7 Pagesdisorders by inspecting the unconscious mind. According to Jacques Lacan, a psychiatrist, â€Å"Human behavior is often something of puzzle, requiring concerted acts of investigation to discover root causes and multiple effects† (105). Holden Caufield in the novel The Catcher in the Rye by J.D. Salinger, is a perplexed adolescent that is living in misery and agony from the past. From a psychoanalytical perspective, readers can understand Holden’s behavior throughout the novel as a troubled teenager trying to