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Everyday Use Essay Example

Everyday Use Essay Example Everyday Use Essay Everyday Use Essay Alice Walkers Everyday Use is a hurt story that illustrates heritage being diverted from the way its perceived in family values. This short story is a drama genre involving argumentative destruction in a family bond which leads to depicting social views. A now wealthy daughter (Dee), of a traditional mother, is different orientated than her sister and mother. A quilt is brought up and Dee wanes the quilt but the mom is saving it for Maggie when she gets married. Although the Moms instincts knows that the quilt to Dee wont really matter to her and just have it somewhere hanged up or see it as another profit to her pocket. While Maggie s the same like her mom that takes pride in her cultural heritage she thinks she would actually enjoy and have a special meaning to it rather than to just have laying around somewhere. Everyday Use distinguishes differences in how a family of three, Mama, Magi, and Dee using indirect direct characterization, perceive breaking change tradition. The indirect characterization of Mama leads the reader to see how she views heritage and doesnt want change. The indirect characterization is shown through a characters actions by what they say or do. In this case, Mama thinks Dee as a child is trying to brain wash her to make her believe a to of knowledge she didnt necessarily need to know. (94) Mama is afraid of change and is so stuck in the past to accept that tradition can break with this new era she is now living in. Although she didnt have education herself she isnt as aware of the changes happening now that her daughter went through when she went to school. If it isnt her way she feels like she isnt satisfied and maybe thinks she has failed as a parent due to Dee believing in other beliefs towards heritage. The direct characterization of Maggie provides the reader to see that she as well views heritage a different way and doesnt want change because shes allowing the foot steps of someone else. Direct characterization states how the actual character is with the narrator describing her, Mama, she explains how Maggie will be feel nervous until her sister leaves because she will feel ashamed and have a mixture of envy and awe. (93) Mama states Maggie this way because she is the exact same way mama is. Not because Maggie wants too but because Mama makes her this way by not letting her explore new things and not breaking traditions. Maggie was painted a picture from her mother of how she should see certain beliefs and other heritage things so she feels obligated to obey them. Since Mama is always blabbering on how Dee is different and how she got a new life, Maggie gets a sense of insecurity because she might think Well if I go against my mother maybe she as well may think I m going against her. She wants to not follow traditions and go on in the world like Dee but shes too scared as well. Also as for Dee indirect characterization shows the reader that she isnt afraid of change and sees heritage different from the others. Throughout the story the Mama makes Dee the golden child but beneath that all Dee wanted was change. Dee coming back home shes not the same Dee she was in her hill hood. Wanders, Deeds new former name after being married, said to Mama the old me is dead l couldnt bear it any longer, being named after the people who oppress me. (96) Mama sees the whole new change as a sign of Dee thinks shes better than her because she married a wealthy guy and doesnt like her old name. Although its the other way around she still is very prideful in where she comes from but is just not in the same mentality her mother still is in. Dee wanted to step out of this box her mother might of had her as AC child and explore new things now that equality is taking place during his time. She is in a whole new vibe trying to become someone in society and not be judged. Indirect and direct characterization help demonstrate the central theme by making a reader understand what the purpose of the character is. In Everyday Use three main characters were focused more than the other to analyze how breaking traditions can impact families beliefs about one another. Breaking away from heritage and traditions is perfectly fine. Imagine if the world was still in 1970 and not 2015, people would still have their mind in a closet and not as open as they do now.

Buddhism Essay Example | Topics and Well Written Essays - 750 words - 9

Buddhism - Essay Example It has also stayed conservative because aboriginalphilosophies of the nations it went to never really influenced it. Conversely, the Mahayana belief bases itself on culture, for instance, the Bon and Tibetan Buddhism. Theravada’s philosophy is straightforward. All worldly phenomena possess three traits, which are transient, impermanent, unsatisfactory and no one owns them. Elements that are compound contain both the material and non-material part. Further, they contain nothing but five compounds such as the material quality and non-material qualities such as consciousness, sensations, mental formatives, and perception (Duiker 225). The Theravada belief has remained intact since inception by the elders who heeded to the customof the abbots of the initial Buddha council. Theravada exhibits no hierarchical authority framework. However, the Sangha respects seniority, and the Pali canon, Sanskrit’s Tripitaka and Pali’s Tipitakaare the authoritative scripture, which contains the entire teachings of the Buddha (Saibaba 122). Based on understanding, it is the best thing to venerate Buddha and obey his teachings devoid of biastowards any tradition. This may prove intricate depending on a person’s culture. However, the pronounced teachers from all civilizations avoid any possible bias. The Theravada routeis captivating because it sticks to the fundaments. It is a live tradition with an uninterruptedancestry, which traces back to the ancient Buddha. Theravada Buddhism is the chief religion in the South East Asian dispensations such as Cambodia, Sri Lanka, Burma, and Thailand. Mahayana Buddhism depicts much of the teachings by Buddha’s,but it is churned with additional philosophical conceptions so that it appears to have a different view and leading to a dissimilarobjective. Both Mahayana and Theravada traditions honor and follow ShakyamuniBuddha. Theravada followers do not venerate the various celestial gods and Buddha as

PRESENTATION REPORT Essay Example | Topics and Well Written Essays - 750 words - 1

PRESENTATION REPORT - Essay Example History proves that the Gospel of John was written on the polite demand of the Bishops of Asia so that the history of Jesus remains alive in the eyes of Christian people. His writing also proves that it is solely for the Greek readers (Smith 1988, p. 433). John describes the whole story and shows the different viewpoint as compared to previous writers. The purpose of the writing of the Gospel of John was not to add materials in the previous Gospels. For that reason, he added authentic information in the fourth Gospel. His purpose of writing was also not to negate the Cerinthian heresy. In his writing, he just stated the truth in a different or unique way. He also not intended to resolve the problems of the harsh parties by giving them a lesson of unity, just like the Tubingen school did not disapprove Jewish opposition and criticism. This viewpoint is so much famous among scholars (Von Wahlde 1995, p. 381) The purpose of writing the fourth Gospel is to prove that Jesus is the Christ and he is the son of God and one should have a spiritual association with him. He also explains that he has a close relationship with his father. In this case, any other person who is spiritually close to Jesus is automatically close to God. In that time period, Cerinthian heresy was famous among Christians, but because of the Gospel of John, Christians were again attracted towards their own religion and followings. The author of the fourth Gospel was a Palestinian Jew. In his writing he shows that he is closely attached and follows the Jewish customs. He knew the Jews religious customs and followership entirely (De Jonge, 1993, p. 349). He also knew, it is entirely an illegal and non-religious thing to alter the pious book and he could face the bad circumstances. He knew there were strict thoughts and rules, that were followed in the Jewish world and it was unlawful to change the Sabbath, 5: 1 ff.; 9:14 ff. He knew the hopes of Jewish

Huntington Disease: An overview

Huntington Disease: An overview Huntington Disease Huntington disease (HD) is an autosomal-dominant disorder, characterized as disease of progressive brain degeneration in late adulthood with subsequent brain atrophy. The affected areas of degeneration are the basal ganglia, which play an important role in the control of movement. This degeneration causes various motor problems such as behavioral abnormality, chorea, incoordination and dystonia (Folstein, 1989). George Huntington was the first man that described HD in the 19th century in detail especially its hereditary nature of chorea (Huntington, 1872). New findings have shown that HD involves the mutant protein huntigtin. This protein is translated from a CAG repeat forming a polyglutamine strand of variable length at the N-terminus. The molecular mechanism of HD is not fully understood but new findings using animal models have provided valuable information. The gene associated with HD is termed the HD gene and can be found on the short arm of chromosome four. As the disease is autosomal dominant, only one HD gene is sufficient to cause the disorder. The HD gene is composed of a trinucleotide CAG repeats.The alleles of the HD gene are grouped as normal, intermediate or HD-causing. Each group has a characteristic number of CAG repeats. The normal alleles have 26 or fewer CAG repeats whereas intermediate alleles have 27-35 CAG repeats (Potter et al., 2004). Carriers of normal alleles and intermediate alleles are not at risk of developing HD. However, individuals with intermediate alleles are at risk of giving birth to a child with an allele of HD-causing characteristic (Semaka et al., 2006). Thus, intermediate alleles are also termed mutable alleles as they may mutate to cause HD phenotype in the offspring. The reason for the mutation lies in the instability of the replication. The longer the number of trinucleotides, the greater the insta bility. In 73% of the cases, the instability leads to an expansion of the trinucleotide repeats and thus an increase in the risk of developing HD whereas only 23% show a contraction of the number of repeats associated with a low risk of developing HD (Chattapadhyay et al., 2005; Djousse et al.,2004, MacDonald et al., 1999). HD-causing alleles usually contain 36 or more CAG repeats and pose the carrier at an increased risk of developing HD. HD-causing alleles have been categorized into two groups: Reduced-penetrance HD-causing alleles and Full-penetrance HD-causing alleles. Reduced-penetrance or incomplete HD-causing alleles are composed of 36-39 trinucleotide CAG repeats (Rubinsztein, 2003; Rubinsztein et al., 1996; McNeil et al., 1997). Carriers of this allele may be asymptomatic and not show the symptoms. On the other hand, full-penetrance HD-causing alleles are characterized by 40 or more CAG repeats and carriers of this allele have a high probability of developing HD (Rubinsztein et al., 1996; McNeil et al., 1997; Langebehn et al., 2004). The instability of the trinucleotide repeats occurs more often in males (spermatogenesis) than in females (oogenesis). This phenomenon can also be observed in the offspring with paternal inheritance of the HD gene where the onset of HD is more potent and occurs in the early youth. In addition, families with no history of HD may develop HD via new mutations arising by the amplification of trinucleotide CAG repeats and most of these new mutations come from the paternal side (Anca et al., 2004; Squitieri et al., 2003). Somatic instability of CAG repeats can also arise and have been observed in human beings as well as animal models. Furthermore, identical twins demonstrate different clinical syndromes and have almost a similar age of onset. Twins that are carriers of homozygous alleles have no difference in the age of onset (Georgiou et al., 1999). Carriers of the HD allele are clinically healthy before the onset of the HD disease symptoms. However, in the so called presymptomatic phase, there are slight changes occurring in motor skills, cognition and personality (Walker, 2007). The onset of HD disease symptoms usually occurs in the mean age of onset which is 35 to 44 years (Bates et al., 2002). In 66%, initial symptoms are abnormalities in the neurological function or psychiatric changes. Other symptoms are minor involountary movements, difficulty in mental planning, depression and slight changes in the eye movement. In 25% of HD carriers, the appearance of initial symptoms such as chorea, dysphagia and gait disturbance is delayed until after 50 years with the disease symptoms taking a more prolonged and gentle course. At the same time, the lifestyle of the affected individuals does not change and they can still continue with their current employment. The initial onset of the symptoms is followed by an increased symptomatic chorea, difficulty in controlling voluntary movement as well as exacerbation of dysarthria and dysphagia. As a result of the worsening symptoms, the affected individuals must leave employment and may require additional help to cope with some activities in their daily life. The final stage of HD demonstrates severe motor disability. The symptoms have worsened so much that so that the carriers cannot deal with their impairment at all and require the assistance of other people. The carriers are mute and incontinent and show a median survival time of 15 to 18 years after the first onset of HD related symptoms. The life expectancy is suggested to be at 54 to 55 years (Harper, 2005). The diagnosis of HD is based on mutation analysis. For this purpose, PCR based methods can be utilized which spots alleles up to about 115 CAG repeats. Likewise, southern blot is employed for alleles with more than 115 CAG (Potter et al., 2004). Such large expansions are linked with juvenile-onset of HD triggered by homozygous HD genotypes. Moderate-to-severe Huntingtons disease illustrate larger frontal horns of the lateral ventricles and deficiency in striatal volume when routine MRI and CT scans are performed (Stober et al., 1984). However, scans are not helpful for the diagnosis of early disorder. Functional MRI studies and data from PET have displayed that affected brains started to alter before the onset of symptoms (Kunig et al., 2000, Paulsen et al., 2004). Using these techniques, it is possible to recognize caudate atrophy as easrly as 11 years before the expected onset of the disease, and it is possible to recognze putaminal atrophy 9 years before the expected onset (Aylwar d et al., 2004). Tensor-based magnetic resonance morphometry demonstrates increasing loss of striatal loss in individuals who are presymptomatic carrying the HD gene and do not show evidence of progresson by clinical or neuropsychological tests over 2 years (Kipps et al., 2005). Genetic testing for HD is only considered by 5% of HD risk carriers due to family planning and employment. Many HD risk carriers do not undergo testing as there is no efficient treatment for HD available (Laccone et al., 1999). Moreover, predictive testing can have psychological consequences for HD risk carriers leading to suicide due to mental depression (Almqvist et al., 2003). Therefore, it is crucial to identify suicidal patterns in young HD risk carriers and give pretest counseling. Epidemiological studies suggest that HD is most prevalent in the white Caucasian population with 5-7 people affected per 100000. There are also exceptions in areas where the entire population is derived from a few founders 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 reason for the various distribution of HD incidence lies in the CAG repeats. White Caucasians have a much higher frequency of HD alleles that are composed of 28-35 CAG repeats (Kremer, 2002; Harper Jones, 2002). The high frequency of this HD alleles in the white population is not fully understood. The HD gene may give a health benefit as in other genetic disorders such as sickle cell trait. It is thought that the HD gene is associated with a lower risk of developing cancer, possibly due to the upregulation of TP53 in HD disease (Bae et al., 2005; DiFiglia etal., 1995). The pathogenesis of HD involving the protein huntingtin is poorly understood. Even though orthologs of that protein have been detected in zebrafish, drosophilia and slime moulds, the role of the protein is still unknown (Jones, 2002). Huntingtin has a high dominance in all human cells. Most of it is expressed in the brain and testes whereas heart, lungs and liver show moderate amounts of it (DiFiglia et al.,1995). One hypothesis suggests that happloinsufficiency plays an essential role in the pathogenesis of HD. This would mean that insufficient amounts of huntingtin protein are generated for the cells to function properly (Ambrose et al.,1994). However, this hypothesis also have been refuted by other findings which suggest that a deficiency of HD gene in man does not cause HD in man (Rubinsztein, 2003; Ambrose et al., 1994). This is also supported by transgenic mouse models. One allele of the HD gene does not cause HD in transgenic mouse models and complete absence of the HD gene is linked to mortality in mouse embryos (Squitieri et al., 2003). Thus, new findings explain the pathogenesis of HD as a toxic gain of function derived from the mutant HD gene. Likewise, this phenomenon can also be observed in other genetic diseases such as muscular atrophy or dentatorubropallidoluysian (Ambrose et al., 1994; Andrew et al., 1993). There is not sufficient evidence to support the claim of happloinsufficiency in any of these genetic disease but an accumulation of polyglutamines with subsequent neurodegeneration. This is further supported by the relationship between length of polyglutamine repeat and age of onset. Longer polyglutamine repeat chains are associated with more aggressive progression of HD disease symptoms and the juvenile onset of HD (Mahant et al., 2003; Squitieri et al., 2002; Forproud et al., 1999). The biological structure of polyglutamine gives more insight into the toxic gain of function in HD. Experiments performed in vitro show that polyglutamine aggregates by forming dimmers, trimers and oligomers. For this aggregation to be efficient, a minimum number of 37 glutamine residues in sequence is required. The rate of aggregation increases as more glutamine repeats are added to the long chain of glutamine polypeptide. This in vitro observation may be an explaination why some individuals experience late onset of HD while others have a juvenile onset of HD. Some key points have been discovered in the mechanism explaining how aggregated polyglutamine leads to neuronal dysfunction. The mutant huntingtin protein is more prone to proteleolysis than its wild type counterpart. This higher risk of protein degradation creates truncated proteins, which lead to the formation of aggregates of truncated huntingtin. Additionally, shorter glutamine repeats are less likely to form steric clashes than longer ones. It is believed that these aggregates are toxic and locate in the cell nucleus. (Saudou et al., 1998; Peter et al., 1999; Wellington et al., 2000). Eventually, the rate of aggregation overcomes the rate at which proteosomes or autophagic vacuolization degrade the proteins in the cell. This further exacerbates the formation of aggregated protein in conjunction with the ability of aggregates to recruit normal body proteins to their matrix. Examples of normal body proteins are those proteins that interact with the wild type form of huntingtin dir ectly (Mills et al., 2005). Some papers also propose that the protein huntingtin may exert not only a toxic gain of function but also a dominant negative effect on the typical function of the wild type protein huntingtin. This way, mutant huntingtin could interfere with proteins that regulate transcription, apoptosis, tumor suppression or axonal transport (Bae et al., 2005; Busch et al., 2003; Charrin et al., 2005; Gauthier et al., 2004 , Hickey Chesselet, 2003). Lastly, one other hypothesis states that mutant huntingtin may interfere in neuron-neuron interaction. This has been illustrated in mice where the mutant protein huntingtin disrupts the axonal transport and vesicle release of neurotrophic factor in neurons leading to intrinsic dysfunction of striatal neurons (Pulst et al., 1996; Komure et al., 1995). References Almqvist EW, Brinkman RR, Wiggins S, Hayden MR. Psychological consequences and predictors of adverse events in the fi rst 5 years after predictive testing for Huntingtons disease. Clin Genet 2003; 64: 300-09. Ambrose CM, Duyao MP, Barnes G, et al. Structure and expression of the Huntingtons disease gene: evidence against simple inactivation due to expanded CAG repeat. Somat Cell Mol Genet 1994; 20: 27-38. Anca MH, Gazit E, Lowewenthal R, Ostrovsky O, Frydman M, Giladi N. Diff erent phenotypic expression 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) repeat length and clinical features of Huntingtons disease. Nat Genet 1993; 4: 398-403. Aylward EH, Sparks BF, Field KM, et al. Onset and rate of striatal atrophy in preclinical Huntington disease. Neurology 2004; 63: 66-72. Bae BI, Xu H, Igarashi S, et al. P53 mediates cellular dysfunction and behavioral abnormalities in Huntingtons disease. Neuron 2005; 47:29-41. Bates G, Harper P, Jones L (2002) Huntingtons Disease. Oxford University Press, New York. Busch A, Engemann S, Lurz R, et al. Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin: a potential mechanism for loss of huntingtin function in Huntingtons disease. J Biol Chem 2003; 278: 41452-61. Charrin BC, Saudou F, Humbert S. Axonal transport failure in neurogenerative disorders: the case of Huntingtons disease. Pathol Biol 2005; 53: 189-92. Chattapadhyay B, Baksi K, Mukhopadhyay S, Bhattacharyya NP. Modulation of age at onset of Huntingtons disease patients by variations in TP53 and human caspase activated DNase (hCAD) genes. Neurosci Lett 2005; 374: 81-86. DiFiglia M, Sapp E, Chase K, et al. Huntingtin is a cytoplasmic protein association with vesicles in human and rat brain neurons. Neuron 1995; 14: 1075-81. Djousse L, Knowlton B, Hayden MR, et al. Evidence for a modifier of onset age in Huntington disease linked to the HD gene in 4p16. Neurogenetics 2004; 5: 109-14. Foroud T, Gray J, Ivashina J, Conneally PM. Differences in duration of Huntingtons disease based on age at onset. J Neurol Neurosurg Psychiatry 1999; 66: 52-56. Folstein S. Huntingtons disease: a disorder of families. Maryland: The Johns Hopkins University Press, 1989. Gauthier LR, Charrin BC, Borrell-Pages M, et al. Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport 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 function in a pair of monozygotic twins with Huntingtons disease. Mov Disord 1999; 14:320-25. Harper PS, Jones L. Huntingtons disease: genetic and molecular studies. In: Bates G, Harper P, Jones L, eds. Huntingtons 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 Huntingtons 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 preclinical Huntingtons disease: a tensor based morphometry study. J Neurol Neurosurg Psychiatry 2005; 76: 650-55. Kunig G, Leenders KL, Sanchez-Pernaute R, et al. Benzodiazepine receptor binding in Huntingtons disease: [11C]fl umazenil uptake measured using positron emission tomography. Ann Neurol 2000; 47: 644-48. Kremer B. Clinical neurology of Huntingtons disease. In: Bates G, Harper P, Jones L, eds. Huntingtons disease. New York: Oxford University Press, 2002: 3-27. Komure O, Sano A, Nishino N, et al. DNA analysis in hereditary dentatorubral-pallidoluysian atrophy: correlation between CAG repeat length and phenotypic variation and the molecular basis of anticipation. Neurology 1995; 45: 143-49. Jones L. The cell biology of Huntingtons disease. In: Bates G, Harper P, Jones L, eds. Huntingtons disease. New York: Oxford University Press, 2002: 348-62. Laccone F, Engel U, Holinski-Feder E, et al. DNA analysis of Huntingtons disease: fi ve years experience in Germany, Australia, and Switzerland. Neurology 1999; 53: 801-06. Langbehn DR, Brinkman RR, Falush D, Paulsen JS, Hayden MR.A new model for prediction of the age of onset and penetrance for Huntingtons disease based on CAG length.Clin Genet.2004;65:267-77. MacDonald ME, Vonsattel JP, Shrinidhi J, et al. Evidence for the GluR6 gene associated with younger onset of Huntingtons disease. Neurology 1999; 53: 1330-32 Mahant N, McCusker EA, Byth K, Graham S. Huntingtons disease: clinical correlates of disability and progression. 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 Huntingtons 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 nuclear hormone receptors. J Cell Biol 2005; 170: 191-200. Paulsen JS, Zimbelman JL, Hinton SC, et al. fMRI biomarker of early neuronal dysfunction in presymptomatic Huntingtons 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 standards and guidelines for Huntington disease testing.Genet Med.2004;6:61-5. Pridmore SA. The large Huntingtons disease family of Tasmania.Med J Aust 1990; 153: 593-95. Pulst SM, Nechiporuk A, Nechiporuk T, et al. Moderate expansion of a normally biallelic trinucelotide repeat in spinocerebellar ataxia type 2. Nat Genetics 1996; 14: 237-38. Rubinsztein DC. Molecular biology of Huntingtons disease (HD) and HD-like disorders. In: Pulst S, ed. Genetics of movement disorders. 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 characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats.Am J Hum Genet.1996;59:16-22. Rubinsztein DC. Molecular biology of Huntingtons disease (HD) and HD-like disorders. In: Pulst S, ed. Genetics of movement disorders. California: Academic Press, 2003: 365-77. Rubinsztein DC, Leggo J, Coles R, et al. Phenotypic characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats. Am J Hum Genet 1996; 59:16-22. Saudou F, Finkbeiner S, Devys D, Greenberg ME. Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions. Cell 1998; 95: 55-56. Squitieri F, Cannella M, Simonelli M. CAG mutation eff ect on rate of progression in Huntingtons disease. Neurol Sci 2002;23 (suppl 2): S107-08. Squitieri F, Gellera C, Cannella M, et al. Homozygosity for CAG mutation in Huntingtons disease is associated with a more severe clinical course. Brain 2003; 126: 946-55. Stober T, Wussow W, Schimrigk K. Bicaudate diameter: the most specifi c and simple CT parameter in the diagnosis of Huntingtons disease. Neuroradiology 1984; 26: 25-28. 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Travelling: Culture and Travel

Why do people insist in taking their holidays in the same locations year after year? This is always something that puzzled me as surely the whole reason behind travelling is to experience different cultures and their unique lifestyles? Sure, you may have had a great time on your holiday to (insert destination! ) when you first visited five years ago but, does it surely the adrenalin fuelled excitement has started to wane with each passing year when you have visited? Of course you probably still haven't even done half of what is possible at your holiday hotspot but that still doesn't gauge the interest quite like going somewhere unique. Take for example your everyday life. If you have ever moved to a new location it can be an exciting time for some. There are endless possibilities of new things to see, people to meet and, daily excursion. But, over time this excitement erodes although you probably haven't done as much as you really could! There are so many things to learn from visiting new places that it would be a shame to go to the same location. You can see the pyramids of Gaza, the Taj Mahal, or the Great Barrier Reef. Sure, going to Disneyland is probably a great thrill but you're not going to learn about Arabic culture there! Travel is a valuable tool in educating oneself on other cultures and lifestyles. And, what's more, it will sure make the gifts you bring back for people more exciting. Those who like to lie on the beach all day and sunbathe would probably like to do just that. But for those of us interested in learning about other cultures, there's no excuse for not travelling elsewhere! Travel broadens the mind' Travel does broaden the mind. However it is what ‘travel' means to the individual. Is it is the consequence of travel where the true expansion is achieved. Travel opens a doorway for the individual to seek the experiences and be open to the absorption of those experiences. Allowing to take from those to build on and develop. These journeys could be far afield or a walk to the corner shop- Muslims praying to the West or the tired eyes of the lady passed in the street Each experience opening a spectrum of further questions. It is the travellers personal reflection, interpretation and conclusion that ‘broadens the mind'. Travel presents experiences of other lifestyles, cultures, values and convictions. Expansion is gained by personal deliberation reflected in their own lives. Travel teaches diversity. The value of that cannot fail but to broaden the mind. ravelling enables many people to broaden their minds in certain respects. When you travel you gain new ideas and experience new things. However you do not have to travel miles to expand your horizons, and there are many disadvantages associated with travelling. Travelling makes it possible to experience new cultures; for example, observing different religions and customs, even if it just means traipsing round an Indian mosque, or visiting an Egyptian temple. While travelling, you an learn new languages, which may increase your confidence. If you learn a few basic phrases, you are given the chance to interact with the native people. Also you are more likely to experience the friendliness of the locals because language barriers are broken. This may lead to prejudice ideas being destroyed. A new language gives a different outlook on life. Travel also teaches you independence, because it allows you to escape the familiar surroundings of home and stay in a strange or alien place. Just arranging travel and accommodation can give you new responsibilities. Often when people travel they leave everyday commodities behind and have to learn to cope without them. Improvising or making do without them teaches patience and determination, and when you return home you become more grateful for the things you left behind. Not only does travelling allow you to see new cultures, it also often allows you to learn the roots of your own cultures. Travelling enables you to become aware of differences in lifestyle – whether they are regional or national – and to learn how different people interact and generally what they base their ideas on. Travelling lets people explore their own customs and way of life, and appreciate their countries’ history and traditions. Travelling introduces new ideas that can change your opinions on different topics and help you to become more open minded about things you would normally disapprove of. Such as exploring different political situations in countries you visit. By experiencing life in different social systems or under different governments, you can see how successful they are and form intelligent opinions. Travelling an also make you more aware of other traditions and help you understand different views and perceptions that foreign people have. Our neighbours in France, a mere twenty-two miles from our shores live diverse lives from our selves, socially, politically and legally. By visiting new places you are introduced to new etiquette, which you may be expected to abide by. This provokes awareness in many people on the correct rules of behaviour in society and broadens the m ind. The opportunities of travel are expanding. Package holidays are becoming more popular. And travelling to new countries is being made more accessible, and cheaper. In the future there will be orbital hotels in space offering ‘out of this world’ holidays. Ordinary holidaymakers will be able to travel to space and back. How could travelling to a different planet not broaden the mind? Space travel could put a new perspective on life and change the way you think and the way you live your live. However, travelling has many disadvantages and it is possible to take the view that it does not broaden the mind. Travelling can be very expensive and you may have to be inconvenienced by having to get visas or a passport. Why would you want to go to all this bother when you are able to experience new cultures through media, such as television programmes, newspaper articles or the Internet? There are numerous travel programmes on the television and radio, and it is much easier and cheaper to see new places by this method. Also England is very international and there are many foreign people living and studying here. So you do not have to go abroad in order to learn new languages or see different traditions. An example of this is ‘China Town’ in London. Here in this bustling town are many Cantonese and Mandarin speaking people. There are a variety of restaurants offering a taste of the eastern culture. There are also many dangers associated with foreign cultures. There are the hazards of diseases and you may have to go to the trouble of getting injections and taking malaria tablets. You are relatively safe in England as there is no risk of wars or terrorist attacks. Some people could feel going abroad daunting because of the different laws and punishments for crimes. Also some might argue that there is no point in going abroad, as everywhere is becoming the same and homogenised. An example of this is the fact that in many countries there are ‘McDonalds’ restaurants situated everywhere. Moreover many countries’ cultures are modified to suit English tastes. So in fact you are not really experiencing the true way of life in that country. Also when you go travelling you often don’t meet people of new nationalities. As Laurence Sterne expressed it ‘ As an English man does not travel to see English men, I retired to my room’. Guests staying in many resorts are urged to remain in the safety of the complex of the hotel, and urged not to venture out, because of disturbing sights of poverty or fear of the unaltered world outside the hotel. Many tourists are reluctant to venture forth and so seldom see the real country, and its people, which they are visiting. However I feel that it is much easier to broaden the mind by travelling than watching travel programmes. It is also much more enjoyable.

Beyond Band of Brothers The War Memoirs of Major Dick Winters

Retired US Army Major Richard â€Å"Dick† Winters’ quiet life as a civilian ended in 1992 with the release of historian Stephen Ambrose’s best-selling book titled Band of Brothers, which tells of hishis comrades’ experience serving during the World War II . The limelight on Winters increased a hundredfold when famed Hollywood director Steven Spielberg and veteran actor Tom Hanks teamed up to bring his story to tens of millions in the highly acclaimed, award-winning HBO miniseries Band of Brothers. This mass exposure transformed Winters and his companions into cultural icons for generations far removed from World War II.In his autobiographical book titled Beyond the Band of Brothers, Major Richard â€Å"Dick† Winters speaks candidly about his life during the war with Company E, 506th Parachute Infantry Regiment, 101st Airborne Division, which he commanded from Normandy to Berchtesgaden. He tells the E-Company story in his own words and shares lessons about leadership in life and death in the crucible of war. Lastly, he pays tribute to the men with whom he served his country and those who lost there lives in the battles of the Second World War. Virtually all this material is being released for the first time.This paper is divided in three sections. The first section summarizes how Winters ended up in a military career and his life with the Easy Company. The second section explains the leadership lessons that Winters gleaned from leading a band of men to survive in the bloodiest conflict of the 20th century. The Beginnings of a War Hero Fresh out of college, Dick Winters entered the United States Army on August 25, 1941 as a private to complete his one-year military service. After finishing boot camp, he stayed behind at Camp Croft, SC to assist in training newly enlisted soldiers.Any thoughts that he harbored about getting out of the army after just one year vanished with the bombing of Pearl Harbor in December 1945. After the P earl Harbor bombing, Winters contemplated about becoming an officer. Hence, when one of his commanders asked if he was interested in attending OCS (Officers Cadets School), he grabbed the chance immediately. It is while at OCS when he met and became friends with Lewis Nixon and Harry Welsh. After cadet school, Winters was assigned to the newly formed 506th Parachute Infantry Regiment (PIR).Friction rose between Winters and the company commander Herbert Sobel. Nevertheless, Winters attributes a large part of E-Company’s success to Sobel’s training. The Easy Company When Lieutenant Meehan, Sobel's successor, was killed during the D-Day invasion in Normandy, Dick Winters became the company's new commander. He parachuted into France and assumed leadership of the Band of Brothers and was regarded as â€Å"the best combat leader in World War II† by his men. The Easy Company suffered 150% casualties while liberating Europe—an unparalleled record of bravery under fire.Winters led them through the Battle of the Bulge and into Germany, where and at a time each member was wounded. They liberated an S. S. death camp from the horrors of the Holocaust and captured Berchtesgaden, Hitler’s Alpine retreat haven. Even though it was Winters who was greatly recognized and rewarded for his actions on the battlefield, he never failed to thank or forget the men who served under him. Furthermore, Winters showed remarkable compassion and concern for his men's well being, so much that it sometimes overrode his rank's duty.In Haguenau, a second patrol was ordered over the Rhine to catch more German prisoners. Survival was next to impossible. Winters told the men that where supposed to go on the patrol to get a good nights rest. After his discharge from the U. S. Army, Major Richard Winters returned to civilian life. He worked for a while for the family firm of his wartime friend Louis Nixon. Following a brief tour of duty during the Korean War, he retu rned to Pennsylvania and embarked on a successful business career, raised a family, and lived the quiet life he had promised himself after his first day in combat.Though out this book you will find three common themes the first is what he calls the â€Å"Leadership at the Point of the Bayonet Ten Principals of Success† , which he summarizes in the last section of the book. The second is the fact that he is very humble about he success, he is very much aware that the men contributed a lot to Easy Companies success as he did, and lastly he gives credit to the men who served under him and helped make Easy Company one of the best companies on the 506th. ConclusionWinters reveals the Easy Company's story in a rich, refreshing, and more personal way than how it has been depicted in its famous HBO miniseries. From the stationing of companies in Toccoa, GA in July 1942 until its deactivation in November 1945, Winters takes us every step of Easy Company's journey, and also includes hi s comrades’ untold stories. This book also has value as a tool on leadership. It was Winters ten principals on leadership that help Easy Company grow as a company and helped Winters rise thought the ranks.It is not a mystery why these men have become the embodiment of millions of American servicemen who marched off to war as ordinary men but achieved extraordinary things. References Alexander, Larry (2005). Biggest brother: the life of Major Dick Winters, the man who led the band of brothers. New York: NAL Caliber. Anderson, Christopher (2004). Dick Winters: Reflections on the band of brothers, D-Day and leadership. American History Magazine: August Issue http://www. historynet. com/magazines/american_history/3029766. html