Huntington Disease Essays

Huntington Disease Essays Huntington Disease Essay Huntington Disease Essay Huntington Disease Huntington disease ( HD ) is an autosomal-dominant upset, characterized as disease of progressive encephalon devolution in late maturity with subsequent encephalon wasting. The affected countries of devolution are the basal ganglia, which play an of import function in the control of motion. This devolution causes assorted motor jobs such as behavioural abnormalcy, chorea, incoordination and dystonia ( Folstein, 1989 ) . George Huntington was the first adult male that described HD in the nineteenth century in item particularly its familial nature of chorea ( Huntington, 1872 ) . New findings have shown that HD involves the mutant protein huntigtin. This protein is translated from a CAG repetition organizing a polyglutamine strand of variable length at the N-terminus. The molecular mechanism of HD is non to the full understood but new findings utilizing carnal theoretical accounts have provided valuable information. The cistron associated with HD is termed the HD cistron and can be found on the short arm of chromosome four. As the disease is autosomal dominant, merely one HD cistron is sufficient to do the upset. The HD cistron is composed of a trinucleotide CAG repeats.The allelomorphs of the HD cistron are grouped as normal, intermediate or HD-causing. Each group has a characteristic figure of CAG repetitions. The normal allelomorphs have 26 or fewer CAG repetitions whereas intermediate allelomorphs have 27-35 CAG repetitions ( Potter et al. , 2004 ) . Carriers of normal allelomorphs and intermediate allelomorphs are non at hazard of developing HD. However, persons with intermediate allelomorphs are at hazard of giving birth to a kid with an allelomorph of HD-causing characteristic ( Semaka et al. , 2006 ) . Thus, intermediate allelomorphs are besides termed changeable allelomorphs as they may mutate to do HD phenotype in the progeny. The ground for the mutant lies in the instability of the re production. The longer the figure of trinucleotides, the greater the instability. In 73 % of the instances, the instability leads to an enlargement of the trinucleotide repetitions and therefore an addition in the hazard of developing HD whereas merely 23 % show a contraction of the figure of repetitions associated with a low hazard of developing HD ( Chattapadhyay et al. , 2005 ; Djousse et al.,2004, MacDonald et al. , 1999 ) . HD-causing allelomorphs normally contain 36 or more CAG repetitions and present the bearer at an increased hazard of developing HD. HD-causing allelomorphs have been categorized into two groups: Reduced-penetrance HD-causing allelomorphs and Full-penetrance HD-causing allelomorphs. Reduced-penetrance or uncomplete HD-causing allelomorphs are composed of 36-39 trinucleotide CAG repetitions ( Rubinsztein, 2003 ; Rubinsztein et al. , 1996 ; McNeil et al. , 1997 ) . Carriers of this allelomorph may be symptomless and non demo the symptoms. On the other manus, full-penetrance HD-causing allelomorphs are characterized by 40 or more CAG repetitions and bearers of this allelomorph have a high chance of developing HD ( Rubinsztein et al. , 1996 ; McNeil et al. , 1997 ; Langebehn et al. , 2004 ) . The instability of the trinucleotide repeats occurs more frequently in males ( spermatogenesis ) than in females ( oogenesis ) . This phenomenon can besides be observed in the progeny with paternal heritage of the HD cistron where the oncoming of HD is more powerful and occurs in the early young person. In add-on, households with no history of HD may develop HD via new mutants originating by the elaboration of trinucleotide CAG repetitions and most of these new mutants come from the paternal side ( Anca et al. , 2004 ; Squitieri et al. , 2003 ) . Bodily instability of CAG repetitions can besides originate and hold been observed in human existences every bit good as animate being theoretical accounts. Furthermore, indistinguishable twins demonstrate different clinical syndromes and have about a similar age of oncoming. Twins that are bearers of homozygous allelomorphs have no difference in the age of oncoming ( Georgiou et al. , 1999 ) . Carriers of the HD allelomorph are clinically healthy before the oncoming of the HD disease symptoms. However, in the so called preclinical stage, there are little alterations happening in motor accomplishments, knowledge and personality ( Walker, 2007 ) . The oncoming of HD disease symptoms normally occurs in the average age of oncoming which is 35 to 44 old ages ( Bates et al. , 2002 ) . In 66 % , initial symptoms are abnormalcies in the neurological map or psychiatric alterations. Other symptoms are minor involountary motions, trouble in mental planning, depression and little alterations in the oculus motion. In 25 % of HD bearers, the visual aspect of initial symptoms such as chorea, dysphagia and pace perturbation is delayed until after 50 old ages with the disease symptoms taking a more drawn-out and soft class. At the same clip, the life style of the affected persons does non alter and they can still go on with their current employment. The initial oncoming of the symptoms is followed by an increased diagnostic chorea, trouble in commanding voluntary motion every bit good as aggravation of dysarthria and dysphagia. As a consequence of the deterioration symptoms, the affected persons must go forth employment and may necessitate extra aid to get by with some activities in their day-to-day life. The concluding phase of HD demonstrates terrible motor disablement. The symptoms have worsened so much that so that the bearers can non cover with their damage at all and necessitate the aid of other people. The bearers are tongueless and incontinent and demo a average endurance clip of 15 to 18 old ages after the first oncoming of HD related symptoms. The life anticipation is suggested to be at 54 to 55 old ages ( Harper, 2005 ) . The diagnosing of HD is based on mutant analysis. For this intent, PCR based methods can be utilised which musca volitanss alleles up to about 115 CAG repetitions. Likewise, southern smudge is employed for allelomorphs with more than 115 CAG ( Potter et al. , 2004 ) . Such big enlargements are linked with juvenile-onset of HD triggered by homozygous HD genotypes. Moderate-to-severe Huntington s disease illustrate larger frontal horns of the sidelong ventricles and lack in striatal volume when modus operandi MRI and CT scans are performed ( Stober et al. , 1984 ) . However, scans are non helpful for the diagnosing of early upset. Functional MRI surveies and informations from PET have displayed that affected encephalons started to change before the oncoming of symptoms ( Kunig et al. , 2000, Paulsen et al. , 2004 ) . Using these techniques, it is possible to acknowledge caudate wasting every bit easrly as 11 old ages before the expected oncoming of the disease, and it is possible to re cognze putaminal wasting 9 old ages before the expected oncoming ( Aylward et al. , 2004 ) . Tensor-based magnetic resonance morphometry demonstrates increasing loss of striatal loss in persons who are preclinical transporting the HD cistron and do non demo grounds of progresson by clinical or neuropsychological trials over 2 old ages ( Kipps et al. , 2005 ) . Familial proving for HD is merely considered by 5 % of HD hazard bearers due to household planning and employment. Many HD hazard bearers do non undergo proving as there is no efficient intervention for HD available ( Laccone et al. , 1999 ) . Furthermore, prognostic testing can hold psychological effects for HD hazard bearers taking to suicide due to mental depression ( Almqvist et al. , 2003 ) . Therefore, it is important to place self-destructive forms in immature HD hazard bearers and give pretest guidance. Epidemiologic surveies suggest that HD is most prevailing in the white Caucasic population with 5-7 people affected per 100000. There are besides exclusions in countries where the full population is derived from a few laminitiss such as in Lake Maracaibo in Venezuela or Tasmania ( Pridmore, 1990 ) . Across most of Asia and Africa the incidences of HD are much lower. The ground for the assorted distribution of HD incidence lies in the CAG repetitions. White Caucasians have a much higher frequence of HD allelomorphs that are composed of 28-35 CAG repetitions ( Kremer, 2002 ; Harper A ; Jones, 2002 ) . The high frequence of this HD alleles in the white population is non to the full understood. The HD cistron may give a wellness benefit as in other familial upsets such as reaping hook cell trait. It is thought that the HD cistron is associated with a lower hazard of developing malignant neoplastic disease, perchance due to the upregulation of TP53 in HD disease ( Bae et al. , 2005 ; DiF iglia etal. , 1995 ) . The pathogenesis of HD affecting the protein huntingtin is ill understood. Even though orthologs of that protein have been detected in zebrafish, drosophilia and sludge molds, the function of the protein is still unknown ( Jones, 2002 ) . Huntingtin has a high laterality in all human cells. Most of it is expressed in the encephalon and testicles whereas bosom, lungs and liver show moderate sums of it ( DiFiglia et al.,1995 ) . One hypothesis suggests that happloinsufficiency plays an indispensable function in the pathogenesis of HD. This would intend that deficient sums of huntingtin protein are generated for the cells to work decently ( Ambrose et al.,1994 ) . However, this hypothesis besides have been refuted by other findings which suggest that a lack of HD cistron in adult male does non do HD in adult male ( Rubinsztein, 2003 ; Ambrose et al. , 1994 ) . This is besides supported by transgenic mouse theoretical accounts. One allelomorph of the HD cistron does non do HD in transgenic mouse theoretical accounts and complete absence of the HD cistron is linked to mortality in mouse embryos ( Squitieri et al. , 2003 ) . Therefore, new findings explain the pathogenesis of HD as a toxic addition of map derived from the mutant HD cistron. Likewise, this phenomenon can besides be observed in other familial diseases such as muscular wasting or dentatorubropallidoluysian ( Ambrose et al. , 1994 ; Andrew et al. , 1993 ) . There is non sufficient grounds to back up the claim of happloinsufficiency in any of these familial disease but an accretion of polyglutamines with subsequent neurodegeneration. This is farther supported by the relationship betwe en length of polyglutamine repetition and age of oncoming. Longer polyglutamine repetition ironss are associated with more aggressive patterned advance of HD disease symptoms and the juvenile oncoming of HD ( Mahant et al. , 2003 ; Squitieri et al. , 2002 ; Forproud et al. , 1999 ) . The biological construction of polyglutamine gives more insight into the toxic addition of map in HD. Experiments performed in vitro show that polyglutamine sums by organizing dimmers, trimers and oligomers. For this collection to be efficient, a minimal figure of 37 glutamine residues in sequence is required. The rate of collection additions as more glutamine repetitions are added to the long concatenation of glutamine polypeptide. This in vitro observation may be an explaination why some persons experience late oncoming of HD while others have a juvenile oncoming of HD. Some cardinal points have been discovered in the mechanism explicating how aggregative polyglutamine leads to neural disfunction. The mutant huntingtin protein is more prone to proteleolysis than its wild type opposite number. This higher hazard of protein debasement creates truncated proteins, which lead to the formation of sums of abbreviated huntingtin. Additionally, shorter glutamine repetitions are less likely to organize steric clangs than longer 1s. It is believed that these sums are toxic and locate in the cell nucleus. ( Saudou et al. , 1998 ; Peter et al. , 1999 ; Wellington et al. , 2000 ) . Finally, the rate of collection overcomes the rate at which proteosomes or autophagic vacuolisation degrade the proteins in the cell. This farther exacerbates the formation of aggregative protein in concurrence with the ability of sums to enroll normal organic structure proteins to their matrix. Examples of normal organic structure proteins are those proteins that interact with the wil d type signifier of huntingtin straight ( Mills et al. , 2005 ) . Some documents besides propose that the protein huntingtin may exercise non merely a toxic addition of map but besides a dominant negative consequence on the typical map of the wild type protein huntingtin. This manner, mutant huntingtin could interfere with proteins that regulate written text, programmed cell death, tumour suppression or axonal conveyance ( Bae et al. , 2005 ; Busch et al. , 2003 ; Charrin et al. , 2005 ; Gauthier et al. , 2004, Hickey A ; Chesselet, 2003 ) . Last, one other hypothesis provinces that mutant huntingtin may interfere in neuron-neuron interaction. This has been illustrated in mice where the mutant protein huntingtin disrupts the axonal conveyance and cyst release of neurotrophic factor in nerve cells taking to intrinsic disfunction of striatal nerve cells ( Pulst et al. , 1996 ; Komure et al. , 1995 ) . Mentions Almqvist EW, Brinkman RR, Wiggins S, Hayden MR. Psychological effects and forecasters of inauspicious events in the fi rst 5 old ages after prognostic testing for Huntington s disease. Clin Genet 2003 ; 64: 300-09. Ambrose CM, Duyao MP, Barnes G, et Al. Structure and look of the Huntington s disease cistron: grounds against simple inactivation due to spread out CAG repetition. Somat Cell Mol Genet 1994 ; 20: 27-38. Anca MH, Gazit E, Lowewenthal R, Ostrovsky O, Frydman M, Giladi N. Diff erent phenotypic look in monozygotic twins with Huntington disease. Am J Med Genet 2004 ; 124: 89-91. Andrew SE, Goldberg YP, Kremer B, et Al. The relationship between trinucleotide ( CAG ) repetition length and clinical characteristics of Huntington s disease. Nat Genet 1993 ; 4: 398-403. Aylward EH, Sparks BF, Field KM, et Al. Onset and rate of striatal wasting in presymptomatic Huntington disease. Neurology 2004 ; 63: 66-72. Bae BI, Xu H, Igarashi S, et Al. P53 mediates cellular disfunction and behavioural abnormalcies in Huntington s disease. Neuron 2005 ; 47:29-41. Bates G, Harper P, Jones L ( 2002 ) Huntington s Disease. Oxford University Press, New York. Busch A, Engemann S, Lurz R, et Al. Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin: a possible mechanism for loss of huntingtin map in Huntington s disease. J Biol Chem 2003 ; 278: 41452-61. Charrin BC, Saudou F, Humbert S. Axonal conveyance failure in neurogenerative upsets: the instance of Huntington s disease. Pathol Biol 2005 ; 53: 189-92. Chattapadhyay B, Baksi K, Mukhopadhyay S, Bhattacharyya NP. Transition of age at oncoming of Huntington s disease patients by fluctuations in TP53 and human caspase activated DNase ( hCAD ) cistrons. Neurosci Lett 2005 ; 374: 81-86. DiFiglia M, Sapp E, Chase K, et Al. Huntingtin is a cytoplasmatic protein association with cysts in human and rat encephalon nerve cells. Neuron 1995 ; 14: 1075-81. Djousse L, Knowlton B, Hayden MR, et Al. Evidence for a qualifier of onset age in Huntington disease linked to the HD cistron in 4p16. Neurogenetics 2004 ; 5: 109-14. Foroud T, Gray J, Ivashina J, Conneally PM. Differences in continuance of Huntington s disease based on age at oncoming. J Neurol Neurosurg Psychiatry 1999 ; 66: 52-56. Folstein S. Huntington s disease: a upset of households. Old line state: The Johns Hopkins University Press, 1989. Gauthier LR, Charrin BC, Borrell-Pages M, et Al. Huntingtin controls neurotrophic support and endurance of nerve cells by heightening BDNF vesicular conveyance along microtubules. Cell 2004 ; 118: 127-38. Georgiou N, Bradshaw JL, Chiu E, Tudor A, OGorman L, Phillips JG. Diff erential clinical and motor control map in a brace of monozygotic twins with Huntington s disease. Mov Disord 1999 ; 14:320-25. Harper PS, Jones L. Huntington s disease: familial and molecular surveies. In: Bates G, Harper P, Jones L, eds. Huntington s disease. New York: Oxford University Press, 2002: 113-58. Harper B.Huntington disease.J R Soc Med.2005 ; 98:550. Hickey MA, Chesselet MF. Apoptosis in Huntington s disease. Prog Neuropsychopharmacol Biol Psychiatry 2003 ; 27: 256-65. Huntington G. On chorea. Med Surg Rep 1872 ; 26: 317-21 Kipps CM, Duggins AJ, Mahant N, Gomes L, Ashburner J, McCusker EA. Progression of structural neuropathology in presymptomatic Huntington s disease: a tensor based morphometry survey. J Neurol Neurosurg Psychiatry 2005 ; 76: 650-55. Kunig G, Leenders KL, Sanchez-Pernaute R, et Al. Benzodiazepine receptor binding in Huntington s disease: [ 11C ] Florida umazenil consumption measured utilizing antielectron emanation imaging. Ann Neurol 2000 ; 47: 644-48. Kremer B. Clinical neurology of Huntington s disease. In: Bates G, Harper P, Jones L, eds. Huntington s disease. New York: Oxford University Press, 2002: 3-27. Komure O, Sano A, Nishino N, et Al. Deoxyribonucleic acid analysis in familial dentatorubral-pallidoluysian wasting: correlativity between CAG repetition length and phenotypic fluctuation and the molecular footing of expectancy. Neurology 1995 ; 45: 143-49. Jones L. The cell biological science of Huntington s disease. In: Bates G, Harper P, Jones L, eds. Huntington s disease. New York: Oxford University Press, 2002: 348-62. Laccone F, Engel U, Holinski-Feder E, et Al. DNA analysis of Huntington s disease: fi ve old ages experience in Germany, Australia, and Switzerland. Neurology 1999 ; 53: 801-06. Langbehn DR, Brinkman RR, Falush D, Paulsen JS, Hayden MR.A new theoretical account for anticipation of the age of oncoming and penetrance for Huntington s disease based on CAG length.Clin Genet.2004 ; 65:267-77. MacDonald ME, Vonsattel JP, Shrinidhi J, et Al. Evidence for the GluR6 cistron associated with younger oncoming of Huntington s disease. Neurology 1999 ; 53: 1330-32 Mahant N, McCusker EA, Byth K, Graham S. Huntington s disease: clinical correlatives of disablement and patterned advance. Neurology 2003 ; 61:1085-92. McNeil SM, Novelletto A, Srinidhi J, Barnes G, Kornbluth I, Altherr MR, Wasmuth JJ, Gusella JF, MacDonald ME, Myers RH.Reduced penetrance of the Huntington s disease mutation.Hum Mol Genet.1997 ; 6:775-9. Mills IG, Gaughan L, Robson C, et Al. Huntingtin interacting protein 1 modulates the transcriptional activity of atomic endocrine receptors. J Cell Biol 2005 ; 170: 191-200. Paulsen JS, Zimbelman JL, Hinton SC, et Al. fMRI biomarker of early neural disfunction in preclinical Huntington s disease. AJNR Am J Neuroradiol 2004 ; 25: 1715-21. Peter MF, Nucifora FC Jr, Kushi J, et Al. Nuclear targeting of mutant Huntingtin increases toxicity. Mol Cell Neurosci 1999 ; 14: 121-81. Potter NT, Spector EB, Prior TW.Technical criterions and guidelines for Huntington disease testing.Genet Med.2004 ; 6:61-5. Pridmore SA. The big Huntington s disease household of Tasmania.Med J Aust 1990 ; 153: 593-95. Pulst SM, Nechiporuk A, Nechiporuk T, et Al. Moderate enlargement of a usually biallelic trinucelotide repetition in spinocerebellar ataxy type 2. Nat Genetics 1996 ; 14: 237-38. Rubinsztein DC. Molecular biological science of Huntington s disease ( HD ) and HD-like upsets. In: Pulst S, erectile dysfunction. Geneticss of motion upsets. California: Academic Press, 2003: 365-77. Rubinsztein DC, Leggo J, Coles R, Almqvist E, Biancalana V, Cassiman JJ, Chotai K, Connarty M, Crauford D, Curtis A, Curtis D, Davidson MJ, Differ AM, Dode C, Dodge A, Frontali M, Ranen NG, Stine OC, Sherr M, Abbott MH, Franz ML, Graham CA, Harper PS, Hedreen JC, Hayden MR.et al.Phenotypic word picture of persons with 30-40 CAG repetitions in the Huntington disease ( HD ) cistron reveals HD instances with 36 repetitions and seemingly normal aged persons with 36-39 repeats.Am J Hum Genet.1996 ; 59:16-22. Rubinsztein DC. Molecular biological science of Huntington s disease ( HD ) and HD-like upsets. In: Pulst S, erectile dysfunction. Geneticss of motion upsets. California: Academic Press, 2003: 365-77. Rubinsztein DC, Leggo J, Coles R, et Al. Phenotypic word picture of persons with 30-40 CAG repetitions in the Huntington disease ( HD ) cistron reveals HD instances with 36 repetitions and seemingly normal aged persons with 36-39 repetitions. Am J Hum Genet 1996 ; 59:16-22. Saudou F, Finkbeiner S, Devys D, Greenberg ME. Huntingtin acts in the karyon to bring on programmed cell death but decease does non correlate with the formation of intranuclear inclusions. Cell 1998 ; 95: 55-56. Squitieri F, Cannella M, Simonelli M. CAG mutant eff ect on rate of patterned advance in Huntington s disease. Neurol Sci 2002 ; 23 ( suppl 2 ) : S107-08. Squitieri F, Gellera C, Cannella M, et Al. Homozygosity for CAG mutant in Huntington s disease is associated with a more terrible clinical class. Brain 2003 ; 126: 946-55. Stober T, Wussow W, Schimrigk K. Bicaudate diameter: the most specifi degree Celsius and simple CT parametric quantity in the diagnosing of Huntington s disease. Neuroradiology 1984 ; 26: 25-28. OHearn E, Holmes SE, Calvert PC, et Al. SCA-12: shudder with cerebellar and cortical wasting is associated with a CAG repetition enlargement. Neurology 2001 ; 56: 299-303. Walker FO.Huntington s disease.Lancet.2007 ; 369:218-28. Wellington CL, Leavitt BR, Hayden MR. Huntington disease: new penetrations on the function of huntingtin cleavage. J Neural Transm Suppl 2000 ; 58: 1-17.

The Abolitionists, Who They Were And How They Became Influential

The Abolitionists, Who They Were And How They Became Influential The term abolitionist generally refers to a dedicated opponent to slavery in the early 19th century America. The abolitionist movement developed slowly in the early 1800s. A movement to abolish slavery gained political acceptance in Britain in the late 1700s. The British abolitionists, led by William Wilberforce in the early 19th century, campaigned against Britains role in the slave trade and sought to outlaw slavery in British colonies. At the same time, Quaker groups in America began working in earnest to abolish slavery in the United States. The first organized group formed to end slavery in America began in Philadelphia in 1775, and the city was a hotbed of abolitionist sentiment in the 1790s, when it was the capital of the United States. Though slavery was successively outlawed in the northern states in the early 1800s, the institution of slavery was firmly entrenched in the South. And agitation against slavery came to be regarded as a major source of discord between regions of the country. In the 1820s anti-slavery factions began spreading from New York and Pennsylvania to Ohio, and the early beginnings of the abolitionist movement began to be felt. At first, the opponents to slavery were considered far outside the mainstream of political thought and abolitionists had little real impact on American life. In the 1830s the movement gathered some momentum. William Lloyd Garrison began publishing The Liberator in Boston, and it became  the most prominent abolitionist newspaper. A pair of wealthy businessmen in New York City, the Tappan brothers, began to finance abolitionist activities. In 1835 the American Anti-Slavery Society began a campaign, funded by the Tappans, to send anti-slavery pamphlets into the South. The pamphlet campaign led to enormous controversy, which included bonfires of seized abolitionist literature being burned in the streets of Charleston, South Carolina. The pamphlet campaign was seen to be impractical. Resistance to the pamphlets galvanized the South against any anti-slavery sentiment, and it made abolitionists in the North realize that it would not be safe to campaign against slavery on southern soil. The northern abolitionists tried other strategies, most prominently the petitioning of Congress. Former president John Quincy Adams, serving in his post-presidency as a Massachusetts congressman, became a prominent anti-slavery voice on Capitol Hill. Under right of petition in the U.S. Constitution, anyone, including slaves, could send petitions to Congress. Adams led a movement to introduce petitions seeking the freedom of slaves, and it so inflamed members of the House of Representatives from the slave states that discussion of slavery was banned in the House chamber. For eight years one of the main battles against slavery took place on Capitol Hill, as Adams battled against what came to be known as the gag rule. In the 1840s a former slave, Frederick Douglass, took to the lecture halls and spoke about his life as a slave. Douglass became a very forceful anti-slavery advocate, and even spent time speaking out against American slavery in Britain and Ireland. By the late 1840s the Whig Party was splitting over the issue of slavery. And disputes which arose when the U.S. acquired enormous territory at the end of the Mexican War brought up the issue of which new states and territories would be slave or free. The Free Soil Party arose to speak out against slavery, and while it didnt became a major political force, it did put the issue of slavery into the mainstream of American politics. Perhaps what brought the abolitionist movement to the forefront more than anything else was a very popular novel, Uncle Toms Cabin. Its author, Harriet Beecher Stowe, a committed abolitionist, was able to craft a tale with sympathetic characters who were either slaves or touched by the evil of slavery. Families would often read the book aloud in their living rooms, and the novel did much to pass abolitionist thought into American homes. Prominent abolitionists included: William Lloyd GarrisonFrederick DouglassAngelina Grimkà © and her sister Sarah Grimkà ©Wendell PhillipsJohn BrownHarriet TubmanHarriet Beecher Stowe The term, of course, comes from the word abolish, and particularly refers to those who wanted to abolish slavery. The Underground Railroad, the loose network of people who assisted escaped slaves to freedom in the northern United States or Canada, could be considered part of the abolitionist movement.

HI 325C The Frontier Essay Example | Topics and Well Written Essays - 1000 words

HI 325C The Frontier - Essay Example Kit Carson uses those virtues and skills to overcome challenges and hardships in the Rocky Mountains. One, he uses his keenness to protect himself and other traders. One instance when Kit Carson’s promptness of action is tested is the night when an inexperienced guard alerts them of invading Indians. Kit Carson is seen to be on his feet in an instant with a pistol on his hand (Abbott 12). It is asserted that the loss of a single second may give an enemy the opportunity to launch its attack and disappear in the dark night. Kit Carson reacts quickly and shoots his mule. Nevertheless, it is a false alarm. Two, his persistence enables him to hunt for food and find a suitable location to set camp. Carson travels for over fifty miles with his mule and horse, looking at every stream and creek, being on the lookout for any indication of a beaver. Kit Carson selects a location for his camp after travelling past a meandering stream circling through the centre, which he believes has a la rge number of beavers (Abbott 17). Finally, his acquaintance of the Spanish language becomes a beneficial investment to him. It enables him to retain everything that the expert ranger of the woods convey in respect to the topography of the Far West, the challenges to be encountered, and the ways of dealing with them. Part 2 Last of the Mohicans This part will discuss whether the movie Last of the Mohicans portray the Trans-Appalachian frontier of the 1750s as a bloody â€Å"no-man’s-land† between clashing empires, or as a â€Å"middle ground† in which settlers and natives interact peacefully and exchange culture on equal terms. It will also evaluate whether it portrays Indians as bloodthirsty and savage or as peaceful and virtuous, and look at how the British and French officials in this film differ in their attitude toward Indians and colonial settlers. The movie portrays the Trans-Appalachian frontier of the 1750s as a bloody â€Å"no-man’s-land† between clashing empires. From the start of the movie there is a battle for the control of colonial America by the French and British troops. The British troops seek military assistance from a number of Native American war groups who are not willing to leave their residence undefended. As the French and British soldiers fight for the control of the North America, the natives and the settlers are compelled to take sides. In recruiting Native Americans for their military battles, the

Annotated Bibliography for Organizational Analysis Essay

Annotated Bibliography for Organizational Analysis - Essay Example The Political Frame recognizes the power play within and between institutions. The Symbolic Frame believes that schools produce symbols to create commitment and meaning. This article is important, because it describes different forms of leadership. However, it does not consider that some school leaders may be integrating these different frameworks. This source is important to my field of study, because it will help me analyze and prescribe the best frameworks for different goals and conditions in the Training and Doctrine Command. Managementhelp.org. (no date). What is an open system? Retrieved from http://managementhelp.org/misc/orgs-open-systems.pdf This article describes the main elements and concepts of an open system. An open system is a system that interacts with its external environment through feedback processes. Some of the important components of an open system are inputs, processes, outputs, goals, assessment, and learning. This article is a good source of the basics of an open system, but further research on its real-life applications is needed to understand its strengths and limitations further. This source is important to my field of study, because I want to know how the Training and Doctrine Command works as an open system and what can be done to exploit the advantages of this system. I also want to learn the issues with an open system, especially in how the external environment affects the internal system. Nadler, D.A., & Nadler, M.B. (2000). The Congruence framework - a roadmap for understanding organizational performance. Mercer Management Journal, (13), 4-10. Retrieved from http://www.oliverwyman.com/deu-insights/MMJ13-OrganizationalTrans.pdf Nadler and Nadler (2000) argued that the congruence framework analyzes the roots of organizational performance. They described that it is not a prescriptive model, but an analytical framework that helps leaders understand the interaction between social and technical factors that affect the performance of each organization, so that people can design and execute their own solutions to their organization’s distinctive performance problems. The strengths of the article are its explanation of the components of the congruence model and its application of the model on the Harley-Davidson’s case. Its weakness is that it was not tested empirically using other companies and industries. This source is important to my field of study, because it will help me analyze the best way to implement large-scales changes to the Training and Doctrine Command. McLeod, S. (2007, June 25). Bolman & Deal frameworks. Big think.com. Retrieved from http://bigthink.com/ideas/bolman-deal-frameworks McLeod explains the Bolman & Deal frameworks. These frames are different on their main beliefs about schools as organizations, and the means in achieving their goals. The strength of this article is that it underlines that it is possible to use all frames in understanding and resolving school problems and in implementing organizational changes. It is not an academic source, however, and it will help to do more research on these frameworks and how they are actually used or changed during design and implementation changes. This source is important to my field of study, because I am interested in knowing different ways of analyzing issues in the Training and Doctrine Command and in determining the best leadership approaches. Bolman & Deal fr

Eddie and beatrice created and sustained Essay Example for Free

Eddie and beatrice created and sustained Essay Throughout the play Beatrice and Eddie have contrasting views about various issues.Eddie has strong veiws on masculinity which leads him to reject effeminate behaviour and be aggressive when he is challenged. Beatirce on the other hand is a more laid back personality. Miller uses this friction between husband and wife to create and sustain tension by making the issues gradually more serious as the play progresses At the opening of act one, Eddie and Cathrine appear to be almost flirting. (Eddie is pleased and therefore shy about it.)This type of relationship is surprising because Cathrine is Eddies niece and proves to be a source of friction between Eddie and Beatrice. This is openly shown at the end of the play when Beatrice tells Eddie you can never have her.  Further disagreement comes from Eddies protectiveness of Cathrine. He feels that as an uncle it is his duty to protect her from the world; he tells her that her revealing clothes attract unwanted attention, and he is not keen for her to get a job. Beatrice thinks that Eddie is over protective of Cathrine and convinces him that she is old enough. Look, you got to get used to it, shes no baby no more. Miller continues to increase the tension between Beatrice and Eddie when later they begin to argue about Rodolpho; his sexuality and his relationship with Cathrine. Eddies affection for Catherine leads him to dislike Rodolpho and find faults in him, at every opportunity. He interprates Rodolphos effeminate behaviour ( singing, cooking and stiching dresses) as homosexuality and tells Cathrine that Rodolpho is decieving her, in order to gain an American passport ( Rodolpho is an illegal immigrant ) . The tension in the play is fueled further as Beatrice openly tells Eddie that he is being too protective of Cathrine and harsh on Rodolpo. Miller uses these arguments to create a sense of mounting tension between the couple as the arguments become gradually more serious.This climaxes when Beatrice asks Eddie to forgive Marco for acussing Eddie of turning the two imigrants in. This argument is very heated and long before a lull when Marco appears.  MARCO: Eddie Carbone!   all stand transfixed for an instant  Miller uses this to create the effect of a fuse reaching its end before the explosive finale of Eddies death at the hands of Marco.At this point Miller turns the tables on the relationship between Eddie and Beatrice. EDDIE: Then why of B!  BEATRICE: Yes, yes!  EDDIE: My B!  (He dies in he arms..)  This shows their ultimate unity.  Miller could be trying to sustain the tension by showing the audience that Eddie refuses to acknowledge his attration to Cathrine upto his last breath.  As this play is a tragedy reminiscent of the Greek style, Miller could be trying to redeem the tragic hero by showing that despite all of Eddies shortcomigs, he is ultimately devoted to and in love with Beatrice.

Effects of Hydraulic Fracturing :: Energy

Advanced technology created the possibility to extract a natural gas beneath the earth which has never been possible before. Oil industries are once again booming deploying hydraulic fracturing method to access the natural gas lies beneath the earth, specifically the Marcellus Formation which contains limestone beds that is black shale or black rock due to presence of iron pyrite and siderites. Marcellus shale formation lie under New York, Pennsylvania, Maryland, West Virginia, Ohio and other parts of the US states according to Parks & Recreation Journal (Dolesh 57). Its vast richness of natural gas is no doubt that it will help America’s energy demand but using hydraulic fracturing to bring that energy to the surface is disturbing the already troubled environment. Although my opponents claim that hydrocracking create jobs and reduce oil imports but it also poses environmental disaster that outweighs its profits which could be irreversible. Environmental disaster such as pollu tion increase, water contamination and risk to the public health in inevitable if gas companies are allowed to continue for drilling America’s soil. As energy demand is increasing throughout the world, America is not least, its demand for energy is increasing and energy supply dependability is at risk. The calls for cleaner energy is at its momentum with production of natural gas using hydrocracking method are deployed vast major cities across America. According to Analysis environment journal released on May 2011 has stated that new Environmental Protection Agency have â€Å"found that greenhouse gas emissions from fracturing are almost 9,000 times higher than previously calculated† this is no surprising because there are no federal regulation on hydraulic fracturing techniques (Nelson 24). Fracking products account 25% in oil industries which will increase in the near future as we are turning to other sources of alternative energy. According to EPA on â€Å"recent research into the complete life cycle of natural gas emissions raises questions about its relative cleanliness† which means as we see the increase of extracting natural gas as means of hydrocracking the pollution will drastically increase. The main component of natural gas is methane â€Å"which leaks from fractured wells or is otherwise released during natural gas drilling, transportation and power-plant accord to CQ Researcher (McGlynn 1054). It’s clear and not concise that emission of methane escaped to the earth’s atmosphere will increase as drilling of hydraulic fracture increases which will create havoc to our already ailing environment. Our existence depends on the accessibility of clean water which our life depends on.

Explication of Phllip Larkin’s “Cut Grass” Essay

In Cut Grass, Philip Larkin uses onomatopoeia, color and flower symbolism, and punctuation to show that death is inevitable, and is unaware of specific circumstances. By contrasting the cut grass with the typically vibrant, lively month of June, Larkin shows the harsh nature of death, and its disregard towards its surroundings, while simultaneously providing a sense of hope once death does arrive. In the first stanza, Larkin uses onomatopoeia to create a vivid image of mown grass. The sharp sounds of â€Å"cut grass† imply fierceness, while the next phrase â€Å"lies frail,† is reminiscent of helplessness and weakness. He continues to parallel sounds by using phrases such as â€Å"brief is the breath,† and â€Å"exhale,† whose sounds resemble their respective actions. Through his use of onomatopoeia, Larkin connects the reader to the grass, and thus evokes sympathy. While the reader is sensitive towards the death, it nonetheless continues, regardless of the liveliness of â€Å"young-leafed June.† Larkin also contrasts the â€Å"brief breath† with â€Å"long death† to show that life is relatively brief when compared to the eternity of death. He makes the majority of the poem, in describing death, one sentence, from â€Å"long, long†¦Ã¢â‚¬  until the end, in order to illustrate the prolonged and slow dying. He describes the death â€Å"at summer’s pace;† a lazy and dawdling movement that disregards its blooming surroundings. He shows that death is unavoidable, and is continually occurring, even at supposed joyful moments. However, Larkin also ends the poem with movement, to show that death, although inevitable, is not necessarily final, and that there is potential for an afterlife. The repeated reference to white also serves to show the two sides of death; while it is pure and innocent, it is also melancholy. By personifying death, Larkin shows that though one can evaluate death from different perspectives, it inevitably returns to the unfair and merciless nature of death. He also mentions â€Å"chestnut flowers,† â€Å"white lilac,† and â€Å"Queen Anne’s lace,† three white flowers, to represent the two sides of death. Larkin personifies the white lilacs, which are typically symbolic or youthful frankness, to bow to death to show that death is unyielding to its subordinate, youth. However  Ã¢â‚¬Å"white hours,† â€Å"and chestnut flowers† serve to depict a luxurious, pleasant atmosphere, which also describes death. Thus, Larkin shows a glimmer of hope for a future after death, and allows the reader relief and relaxation when approaching death. In using the symbolism of white and flowers, onomatopoeia, and relevant punctuation, Larkin is able to portray death as both eternal and hopeful, and to restore a sense of relief around death’s depressing nature.