Myostatin Boy Essay Example for Free

Myostatin Boy Essay Many scientists believe the find could eventually lead to drugs for treating eople with muscular dystrophy and other muscle-destroying conditions. And athletes would almost surely want to get their hands on such a drug and use it like steroids to bulk up. The boys mutant DNA segment was found to block production of a protein called myostatin that limits muscle growth. The news comes seven years after researchers at Johns Hopkins University in Baltimore created buff mighty mice by turning off the gene that directs cells to produce myostatin. Now we can say that myostatin acts the same way in humans as in animals, said the boys physician, Dr. Markus Schuelke, a professor in the child neurology department at Charite/ University Medical Center Berlin. We can apply that knowledge to humans, including trial therapies for muscular dystrophy. Given the huge potential market for such drugs, researchers at universities and pharmaceutical companies already are trying to find a way to limit the amount and activity of myostatin in the body. Wyeth has Just begun human tests of a genetically engineered antibody designed to neutralize myostatin. Dr. Lou Kunkel, director of the genomics program at Boston Childrens Hospital and professor of pediatrics and genetics at Harvard Medical School, said success is possible within several years. Just decreasing this protein by 20, 30, 50 percent can have a profound effect on muscle bulk, said Kunkel, who is among the doctors participating in the Wyeth research. Slow wasting process Muscular dystrophy is the worlds most common genetic disease. There is no cure and the most common form, Duchennes, usually kills before adulthood. The few treatments being tried to slow its progression have serious side effects. Muscle asting also is common in the elderly and patients with diseases such as cancer and AIDS. If you could find a way to block myostatin activity, you might slow the wasting process, said Dr. Se-Jin Lee, the Johns Hopkins professor whose team created the mighty mice. Lee said he believes a myostatin blocker also could suppress fat accumulation and thus thwart the development of diabetes. Lee and Johns Hopkins would receive royalties for any myostatin-blocking drug made by Wyeth. Dr. Eric Hoffman, director of Childrens National Medical Centers Research Center for Genetic Medicine, said he believes a muscular dystrophy cure will be found, but he is unsure whether it will be a myostatin-blocking drug, another treatment or a combination, because about a dozen genes have some effect on muscles. He said a mystotatin- blocking drug could help other groups of people, including astronauts and others who lose muscle mass during long stints in zero gravity or when immobilized by illness or a broken limb. Eventual health problems? Researchers would not disclose the German boys identity but said he was born to a nd three other close male relatives all were unusually strong, with one of them a construction worker able to unload heavy curbstones by hand. In the mother, one copy of the gene is mutated and the other is normal; the boy has two mutated copies. One almost definitely came from his father, but no information about him has been disclosed. The mutation is very rare in people. The boy is healthy now, but doctors worry he could eventually suffer heart or other health problems. In the past few years, scientists have seen great potential in myostatin-blocking strategies. Internet marketers have been hawking myostatin-blocking supplements to bodybuilders, though doctors say the products are useless and perhaps dangerous. Some researchers are trying to turn off the myostatin gene in chickens to produce more meat per bird. And several breeds of cattle have natural variations in the gene that, aided by selective breeding, give them far more muscle and less fat than other steer. He could do the iron cross when he was 5 months old, said his adoptive mother, Dana Hoekstra of Roosevelt Park. She was referring to a difficult gymnastics move in hich a male athlete suspends himself by his arms between two hanging rings, forming the shape of a cross. Liam has the kind of physical attributes that bodybuilders and other athletes dream about: 40 percent more muscle mass than normal, Jaw-dropping strength, breathtaking quickness, a speedy metabolism and almost no body fat. Liam can run like the wind, has the agility of a cat, lifts pieces of furniture that most children his age couldnt push across a slick floor and eats like there is no tomorrow without gaining weight. Liam Hoekstra was hanging upside down by his feet when he performed an inverted sit-up, his shirt falling away to expose rippled abdominal muscles. It was a display of raw power one might expect to see from an Olympic gymnast. Liam is 19 months old. The so-called myostatin blockade has generated tremendous interest in the bodybuilding community. Some nutritional supplements claim to block myostatin, but researchers have said the claims are not scientifically valid. If the myostatin protein is knocked out, muscles grow and rejuvenate much more uickly,

Right to Die Legislation Cases

Right to Die Legislation Cases Fermin Flores The Declaration of Independence gave us the freedom of life, liberty, and the pursuit of happiness. Now there are some times when these freedoms are placed into the hands of another for example a judge. A policy that brought the attention of Americans in the late 1900’s. Various court cases have been brought about to the public of several people who were in critical conditions and may not make it or could not recover, one of which where a man with locked-in syndrome, which paralyzed one’s muscles and brainstem, wanted to end his life. The right to die is a case where one chooses to die whether they were told that they had a certain amount of time left to live. Also, if they are in critical danger and someone chooses that choice for that person who can’t do it themselves. Choosing when one must die or live goes against the 14th amendment which gave every American the full and equal benefits of the laws. Having the choice of choosing whether someone lives or not ties in with abortion. One mother choosing over if a baby should live or not. The right to die is an issue which some still discuss today through if one has a choice or not. Society today has been leaning more towards helping those who are severely ill and cannot recover to give them the choice of ending it. Back then this was different, Americans and government did not acknowledge the right to die choice. The Supreme Court declared that the constitution did not mentioned â€Å"suicide† and plenty of Americans were uncomfortable. (http://www.economist.com/blogs/democracyinamerica/2014/10/right-die). At least 20% of Americans who attend church believe that one must not suffer from a serious condition with irreversible effects. The reason why we think this way is because some may have experienced this first hand or have thought of the feeling of being in critical condition not being able to do almost anything without the help of a machine or someone else. Oregon voters passed a law in 1994 and went into effect into 1997 that gave anyone the option to end their life through medication. This was called the Death-With-Dignity law which allowed mentally competent, terminally ill adults to hasten their end which later Washington and Vermont adopted. (http://www.deathwithdignity.org/access-acts) In 1983, a woman by the name of Nancy Beth Cruzan was gravely injured from an automobile accident (http://www.oyez.org/cases/1980-1989/1989/1989_88_1503). She was taken to the hospital where she had to be sustained by artificial feedings. Her parents, whom saw no other possible way of recovery for their daughter, wanted to terminate her life-support system. The hospital declined their attempt without the approval of a judge. The Missouri Supreme Court declared that there had to be â€Å"clear and convincing† evidence to which the patient wanted a decision like this to be made. Nancy’s co-workers were brought together by her parents and they all announced that she would not want to be sustained in a disabled condition. The Supreme Court took this as evidence and let Nancy go. Back in 1975, 21 year old Karen Ann Quinlan collapsed and fell into a coma (http://www.ncll.org/liberty-centers/center-for-life-defense/cld-articles/57-how-the-right-to-die-came-to-america) and was placed into the hospital with a ventilator. She was unable to eat nor breathe on her own to the point where her parents wanted to remove her from the artificial life support. As a hospital’s policy, they denied their request and later was taken into court which they ruled in favor of Ann’s parents. Karen was removed from her ventilator in 1976 but miraculously started breathing on her own again. Choosing the right to die for someone else who is in critical condition will be difficult for the hospital and the family. In order for one to make a life or death choice for someone in critical condition, some requirements must be met: The patient must no longer be competent to make the choice themselves, meaning they have no knowledge of what’s happening. Also, the patientâ⠂¬â„¢s conditions must be that he or she cannot recover. Another case of the right to die, 57 year old Paul Lamb was caught in a car accident 23 years ago which paralyzed him from his neck down. With the help of his daughter and the wife of a previous paralyzed man named Tony (who fought to end his life but the court didn’t allow him) Paul, followed Tony’s legacy, and took his battle to the court just to end up losing on July 30th, 2013. The court did allow, however, for a third man to appeal for the right to die, but the law did not make it clear whether the doctor or nurse will be prosecuted by the government if they helped in the procedure. In one of the most recent news, a woman by the name of Brittany Maynard was diagnosed with brain cancer which gave her only six months to live. She thought of ways to give herself and her family the least amount of pain possible. After researching, she found Death-with-Dignity and moved to Oregon, one of five states that allow Death-With-Dignity. (http://www.cnn.com/2014/10/07/opinion/maynard-assisted-suicide-cancer-dignity/) Within the news, she mentioned â€Å"I do not want to die. But I am dying. And I want to die on my own terms,† she wanted the choice to die in peace and surrounded by her loved ones than to die in pain, alone in a hospital. One must consider how painful it would be to stay in the bed for the rest of their life due to a serious accident. Letting the people you love the most go with the consent of the judge is one of the most heartbreaking event a relative can experience. In the year 1947, only 37% of the citizens felt that doctors should be legally permitted to end a patient’s life if there was no way for them to get cured. Fast forwarding 55 years later, the government placed the same poll again hoping for different results. (http://www.gallup.com/poll/6265/right-die-dead-rights.aspx) That year, in 2002, 72% of Americans now felt that doctors should help end a patient’s life. Without a doubt, one should cherish every single moment they spend with a certain person like as if it’s the last time you may see them. Whether you think nothing will happen wrong or that they are safe from any harm, live your life out. You don’t know if one may get diagnosed with a serious life-threate ning or get attacked until it happens. With all said, if all of the states decide to adopt the Death with Dignity law, new opportunity will be open to those who are severely ill. This can have two results, one of which will result in new arguments. It will open the gate for those with suicidal thoughts and may think they have a chance to get a law passed to allow those who feel â€Å"alone† to end their life. On the other hand, it gives those with severe issues to have their easy, unpainful way out.

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.

Oliver Cromwell as a Hero or Villain Essay examples -- History Ireland

The aim of this essay, is to answer the long-awaited question 'Was Oliver Cromwell a hero or a villain? This question, is a hard one to answer. James Heath once said "His name and memory stink." In opposition, Samuel Pepys said "People look back and praise him." True? Or Not? This essay will argue Edmond Ludlow's words," How glorious, but then such betrayal!" Oliver Cromwell was neither a hero nor a villain. The evidence and opinions gathered will state, how he went from good to bad, and from bad to evil. Oliver Cromwell, was a puritan gentleman from Huntingdon. He was born on the 25th of April 1599, and brought up in a very wealthy family, and a high social class. Cromwell, was an MP for Huntingdon, from 1628-1629. He had no fighting experience then, and was very worried about the Roundhead army, at the battle of Edgehill. Cromwell then went home to Huntingdon, and began to train his own army. Cromwell was a magnificent soldier. He created a whole new army from scratch, and he trained his army, in a special and unique way. Cromwell would do anything to win his battles, and beat Prince Rupert and if it meant making a whole new army, than so be it. To do this, he picked his people of their ability, 'men of spirit', and not on their status. He did this believing that this was right, as they were doing Gods will. It also made the people happy, and so he continued doing so. He also paid the men. He paid them 12D a day, so that encouraged more men to stay. He was a strict commander, and his orders had to be obeyed. Also, he always chose the right moment in a battle to attack. Some local Roundheads, thought that Cromwell should have ... ...er, but he just did what he felt he had to do. One thing which I agree on, is that he could have gone about it a different way. Also, I agree in one thing that he said, and also believed in. That was that "The end justifies the Means." What he meant by that, was that no matter what happens, something good always comes out at the end, and it's the end outcome that really matters. The words that I will leave you with, are the words of one Richard Baxter, a parliamentarian. We are not sure whether we can trust these words or not, as being a parliamentarian, he would have been a bit sympathetic to Cromwell, but it's quite reasonable. "No man was better and worse spoken of than he, he meant honestly, and was pious till power corrupted him, he thinketh that the end being good and necessary, the necessary means cannot be bad"

The Creation of the American Democracy Essays -- American America Hist

The Creation of the American Democracy When the Framers of the Constitution met in Philadelphia, they came together with one common purpose in mind. They needed to form a fair and solid system of government that would stand the test of time; one that was both fair for the people and would not involve a monarchy. Each of these men had their own ideas on what would constitute this system, however, so many compromises had to be made. Together, the men gathered in Philadelphia created a federal system of government and drafted a constitution outlining this government. They took care in developing three branches of federal government with a system of checks and balances so that no one branch would gain too much power, thus avoiding any chance of regressing back into the government from which they had just escaped. The Framers even made sure that the most powerful branch had a check system within itself by creating a bicameral legislature, consisting of a Senate and a House of Representatives which could not function one w ithout the other. The federal government that resulted from all of this deliberation was an overall system of democracy, although some undemocratic issues were involved. The American system of government is ultimately a democracy, because it is ultimately a true system of the people. However, not everything done at the Constitutional Convention was democratic. When representatives from the states met in Philadelphia, the majority were rich, educated, upper-class landowners. They claimed to have the best interests of the people in mind, and in most cases they did. That was, after all, the reason they were brought together. However, they still took some measures to ensure that the interests of the comm... ...te, and/or country. For this reason, the Electoral College system of electing our President should be redone and possibly eliminated. A leader must have the support of his country, and this can be assured only through a democratic election. The Bill of Rights is perhaps the best example of the democratic aspects of our government. It gives everyone equal freedoms and liberties, and it is truly in the best interests of everyone. When the Framers of the Constitution met in Philadelphia, they gathered to create a democratic government: a government that worked for everyone and had the common interests of the people as its central purpose. Although some things done at the convention were indeed undemocratic, democracy ultimately prevailed and we were given a strong government with the ability to be amended to fit the common interests of the people throughout time.

Online Examination System Essay

The purpose of on-line test simulator is to take online test in an efficient manner for various branches/semesters/courses at the same time and no time wasting for checking the paper. The main objective of on-line test simulator is to efficiently evaluate the candidate thoroughly through a fully automated system that not only saves lot of time but also gives fast results. It is targeted at removing all the paper work in the examination process. The system is designed by keeping future in mind so that it can be used in any educational institutions as well as in corporate World with little changes. It saves a lot of time as it allows number of students/trainees to give the exam at a time and displays the results as the test gets over, so no need to wait for the result. Administrator has a privilege to add new teachers and students to the test papers. User can register, login and give the test with his specific id, and can see the results as well. This software can be used anywhere any time as it is a web based application (user Location doesn’t matter). No restriction is there that examiner has to be present when the candidate takes the test. The current system is analyzed thoroughly and all the bottlenecks are identified. 2. Users demonstrable needs are captured and freezed. User needs a web-based system, which will remove all the problems in existing system, the user is facing. The user wants a web- based system, which will reduce the bulk of paperwork, provide ease of work, flexibility, fast record finding, modifying, adding, removing and generating the reports. A new system has been proposed on my perception of the system, in accordance with the problems of existing system by making a full layout of the system on paper. 4. The feasibility of the system proposed was analyzed by comparing the following factors with both the existing system and proposed system. The proposed system was found feasible in terms of cost, effort, time and labor. Analysis of the system is complete. 5. Database design is complete. 6. System coding is in progress.

“Brown girl, brownstones” by Paule Marshall Essay

Plot summary The prose fiction Brown girl, brownstones by Paule Marshall, is a bildungsroman with autobiographical elements, tracking the life and experiences of the main protagonist, Selina Boyce and the family and friends in her life. Marshall uses various elements and techniques in the prose, to bring about different themes, characteristics and aspects in her novel. The text is set mainly in the 1930’s Brooklyn, New York, at a community of brownstone houses occupied by the Bajan immigrants. Though there are various perspectives of other personas in the prose, Marshall uses a third person narrative to show the first person perspective of Selina. The story begins with Selina at ten years old and continues until she is no longer a minor. It shows the theme of identity as Selina is trying to find who she is amongst members in her family. â€Å"But they have taken no photographs†¦Ã¢â‚¬  was one of the first time Selina’s loneliness can be seen in the text. She is jealous of the fact her parents took photographs of the family before the death of her infant brother, yet took no keepsakes of hers. Then it goes on to where Marshall is a very descriptive narrator, using a cinematic effect in her story telling. The scenes shift continuously to suggest simultaneous action which produces a dramatic effect that helps to build conflict and suspense. She also uses devices and diction to bring about various themes and symbolic elements in her text. She uses the technique of epigraph to start each chapter, it is a type of foreshadowing, hinting of what will happen throughout the chapter. It also helps to characterize individuals in the story. Contrast is also a reoccurring technique in the text, as characters such as Silla and Deighton, Ina and Selina, have contradictory personalities. There is also contradiction in the symbols and diction in the text. Words such as ‘winter’ and ‘Sun’, ‘darkness’ and ‘light’, are contradictory symbols referring to the characteristics of individuals such as Selina’s parents in the text. The write r involves the use of the Bajan dialect as well as English, as if trying to incorporate the reader in the culture of Barbados and also add credibility and realism to the story. It suggests pride in the Bajan culture. The author uses various figurative devices in the text. There is a heavy focus on the use of personification and architectural imagery. Symbolism is evident in the prose; using colors such as red to represent romance and sexual relationships; and white, and  brownstones to represent upward mobility, status and unattainable goals. Land in the text is also symbolic of independence and opportunity. The use of conflict, such as; mother-daughter, husband-wife, black-white, is brought out by the symbols and conflicting elements in the prose. It shows the destruction in relationships, and accentuates climatic moments, such as when Deighton, used the money Silla stole from him, or when Silena told the whole Bajan association, she’d tricked them. Marshall uses devices such as; imagery, epigraph, motif, foreshadowing, pathetic fallacy and biblical allusion, to show racism, identity, women in society, family, deceit, and various other themes in the prose fiction. The denouement, begins with Silena recognizing who she is and making final decisions for herself. After all her trials and lost relationships, she finally covers her identity, accepting who she has become, the trials she is yet to face and the people in her past who has made her who she is today. Especially her mother, whom she had always fought against. Rational The life of Deighton Boyce, was the subject chosen for the poem between many view Deighton as a problem in the text Brown girl, brownstones, giving him no sympathy. The poem was intended to convey sympathy for Deighton. His life in the poem is specifically intriguing as though he causes many shifts in characteristics of others in the text, his own life is not emphasized. The poem will hopefully give an explanation of the circumstances surrounding the issues of Deighton death, and his life. Mocking Jay I saw a song bird fight a bird of prey, Beautiful-ugly, he was, filled with sorrow, was she. Night and day, He sang a tune of love and wonder, She sang back of vicis and plunder, I tried to save that mocking Jay, But the night stole him away. Where are you my mocking Jay? Trapped in the tomb of brown stones? Your young are calling, where are you? Won’t you fight the snow away? Don’t you hear the light’s moans? Has she trapped him too? No longer perched on your window silla They’ve clipped your wings You’ve destroyed their prison The flock screams their Bajan banter Fly away home my mocking Jay Swim home my song bird But, mocking Jay’s never dive†¦ I’ll send a new light your way†¦ For you to see through winter’s clock†¦ To save your flock†¦ To blind your eyes†¦ And save you from the dark†¦ Shattered tunes of my broken song bird Remember your prayers Eulogy. The sad broken memory. The life you ran away. Dead like marrow staining the asphalt. Staining corals a sea away. Songs long dead, I’ll sing them to you. I’ll pray your tarnished soul away. Deighton, my mocking Jay. Analysis The poem â€Å"mocking Jay†, is a kind of stanzaic elegy, in tribute to a character in the prose text â€Å"Brown girl, Brownstones†. The poet uses the mimicking bird, mocking jay, to represent the character Deighton in the prose text. Not only do mocking jays have a gift in music, which was one of the professional genres Deighton attempted, but they repeat everything sung to them in a mocking manner. Deighton, like these birds, reflects a mocking version of the negatives surround him; from using the money his wife stole from him, to purchase frivolous gifts to spite her; to changing his course of study every time he is confronted with racism or barriers. Deighton also  has the dream like (surreal), and fun loving attributes common to these birds. The poem comprises of four sestets, a couplet a single line and a septet. The stanza formation, is quite symbolic. The first stanza is the first of the four sestets. At the end of each sentence in this sestet is a comma. This represents the fact that this relatively pleasant chapter in his life is not yet complete, it won’t end in a ‘happy ever after’. It is as if to say that the beginning of their relationship was an unfinished dream. The second sestet ends in a question within, as if questioning the relationship, not understanding the change in the relationship and in Silla. The third sestet ends without punctuation is representative to all the times Deighton and the audience were waiting to see Silla’s response to sightings behavior. The final sestet concludes with â€Å"structured-chaotic† punctuation, of when Silla’s revenge unfolds it was chaotic in the circumstances of deportation, but structured in that it was her plan all along. Combining with the lack of punctuation, the couplet of stanza five signifies hi s never ending pain. It symbolizes that, as the lack of punctuation prevents the sentence from truly being complete, his pain and suffering will not end even in the afterlife. The single line consists of one word â€Å"Eulogy†, this refers to the speech given at a funeral or a recollection of the past doings of an individual after he is dead. This word being the shortest stanza, represents the lack of quality and memorabilia Deighton has left behind with his children. The final stanza a sestet can be tied to the biblical representation of the day God rested. The number seven represents the change that occurs after an accomplished cycle. Deighton, accomplices all he could so the last stanza represents his death the final rest he accomplished after his life cycle. The poem has a steady rhythms. Though not all stanzas have a structured rhyme scheme, the poem still flows as if it does. It is like the steady yet unusual flow of life, just as the poem is a depiction of Dighton’s life as was repre sented in the prose fiction. The first stanza contains a set of rhyming couplets, repeating the first rhyme in the last stanza (an â€Å"a, a b, b a, a† format). The last rhyme however is a forced rhyme, this is there to show that leaving the omnipresence was not something the Jay wanted, but was what was forced on him. The second stanza consists of alternate rhymes that emphasize the questioning in this stanza, that he is running alternate scenarios in his mind as to why the wife who used to love him hates him so  much now. The fourth sestet has the last rhyme, â€Å"clock† and â€Å"flock†. This symbolizes that the time he has left with his children is limited as his death is nearing. The rest of the poem is rhyming going parallel to the pores fiction as explanations are revealed in the story, the confusion and rhyming stops. The poem commences with the omnipresent narrator giving a visual imagery of the meeting between two contradicting birds. The â€Å"song bird† represents something happy, passive and peaceful, while â€Å"bird of prey† represents something sly, dominating and warlike. The story continues with oxymoronic inverted syntaxes of line two, that helps to emphasize that the creatures have contradicting personas and that their union could never last as it was based on confusion. Just as in the prose fiction, Silla thought she could turn Deighton into someone he wasn’t, and failed. The diction used in the first stanza such as; â€Å"vicis†, â€Å"Jay† and â€Å"Night†, aid in displaying the theme of conflict in relationships. ‘Vicis’ is the Latin word for change, in reference to the context it highlights Silla’s need to change her husband’s persona and fight to create a life for them that he never wanted. The capitalization diff words such as Jay and Night, personify these nonhuman objects, in the case of the Jay it helps to emphasize this being a character trait of Deighton, while the Night highlights Silla’s character as bright cold and heartless, but at that time seeming beautiful and peaceful . Lines three and four of the first stanza also help to concretize the theme of contradictory persons in relationships, displayed in the first stanza. Stanza two is a rhetorical question sestet, it constantly asks questions the ‘Jay’ is obviously unable to answer, and these are symbolic of the time where the relationship between Silla and Deighton was confusing. He didn’t know where she stood, whether still in love with him or hating h for the injustice she believes he did to their son, the first line emphasizes this. It follows with a reference to the brownstone house Silla spent a majority of the text fighting to obtain. The use of diction such as â€Å"prison†, â€Å"brown†, and â€Å"stones† was a slight pun as a Jay would find a house made of stones a prison, and juxtaposed with the text, it can be said that Deighton saw the house his wife fought so much for was like a prison to him, and a symbol of his failures in his relationships and providing for his family. Line two is the first and only mention of their children in the poem. This is symbolic as it shows that not only did Deighton not spend enough time  with them and focused more on himself, but he also failed as a father in that he couldn’t protect them from the â€Å"snow† which is a personified symbolism of his wife. The personification of the ‘light’, at the end of the stanza references all the happiness and innocence still in the family. When the persona asks about the moaning light that ‘she’ has trapped it means that he was unable to prevent the happiness and life from leaving their family, this aids in uncovering the themes of failing one’s family and loosing things that are important. The third stanza has the most textual allusions, the stanza opens with a pun, â€Å"window silla†. As a bird a sill is somewhere you can rest, be at peace like a home, in this means Deighton no longer feels at home in the browns stones. Silla is also the name of his wife so it can mean that he is also no longer feeling happy in his marriage, as shown in the text queen he began going you the house form his mistress in the nights. â€Å"They’ve clipped your wings† line two of the stanza refers to when he almost got his arm amputated due to his indolence. This is symbolic as it is a physical representative and slight foreshadowing of how his time was ending. The next line refers to the song they sang to him at the wedding. The ‘f’’, ‘s’, ‘th’ and ‘b’ fricative and plosive so funds of the fourth line in the third stanza, emphasizes the running and the drama happening in that scene of the text. The ‘swim home’ in the last line of that stanza references the Caribbean since Islands in the Caribbean are surrounded by water. The last sestet refers to the last actions before Deighton’s death. It starts with a pun, on Deighton’s childhood, as he dived for the coins white men through at him, and also an allusion to him diving to his death. The ‘new light’ is symbolic for Deighton’s religious period, where the movement of the new light helped him to finally discover himself, though completely swiping his personality. ‘winter’s clock’ is symbolic for Deighton’s attempts at going back in time to rectify the problems mainly caused by his relationship with his wife. The couplet, single line and septet, is after his death. People have pained cries due to morning Deighton’s death. The mansion of Prayers refer to his newfound beliefs and Eulogy is the speech given at a funeral. The final stanza is technically the omnipresence’s eulogy for Deighton, though it shows that he is not someone people will remember with respect. It speaks of how he could have had a life if he’d made different choices. It gives an image of his death at sea, and  its connection to his past in the Caribbean. It then shows the general sadness surrounding his death, and accentuates the theme of death in the text. The poem changes from a tone of observation, to unease, to sadness. Hopefully bringing out an overall sympathy for the persona. Though it is not a total rhyming poem, it still has a flowing rhythms that showcases the life cycle of Deighton, as shown in the text. Conclusion The text Brown girl, brownstones, is an excellent depiction of women and men in immigrant communities. Most persons generally sympathize with the women of these communities, however this poem has hopefully garnered a positive response to men in these communities, and those shown in the text. This may help persons to recognize that women were not the only ones with problems in the text. The blame for these conflicts also, should not be solely the fault of males like Deighton, in the prose, but equally shared between each individual, and characters in the prose fiction.