Ikea Hotel: Business Environment and Position

Ikea Hotel: Business Environment and Position Xeroderma Pigmentosum (XP): Causes and Treatment Xeroderma Pigmentosum (XP): Causes and Treatment Xeroderma Pigmentosum is a rare autosomal recessive disease affecting about 1 in 250,000 people in Europe which greatly reduces the quality of life of its sufferer. XP patients have a much greater chance of developing skin neoplasms, internal organs neoplasms or even neurological disorder due to a defective Nucleotide Excision Repair (NER) pathway. In this report, I found out that most experts in this field do believe that reactive oxygen species which can cause DNA lesions that can only be repaired by the NER pathway is the main cause of the neurological disorder in XP patients. However, modern technology can not yet prove this is the case. The treatments for XP are mainly preventive rather than interventionist. However, more new treatments have been proved to be effective in helping XP patients with the aid of modern technology. The bacterial enzyme T4 Endonuclease V has recently been put in use for treating XP and gene replacement therapy might be a possible treatment for the futu re. The aim of this article is to gain a general overview of Xeroderma Pigmentosum (XP), to understand the possible causes of neurological disorder in XP patients as well as the current and possible treatments for XP. To achieve my aim, I have first researched using various textbooks to understand DNA repair and damage. After that, I set my focus on Xeroderma Pigmentosum and used two online databases Medline and PubMed to look for review articles on XP in order to have a basic understanding of XP. I used two keywords Xeroderma Pigmentosum and Neoplasm to achieve the goal (Table 1). After having some basic knowledge of XP, I found that the neurodegeneration and the current treatments for XP are quite interesting so I decided to set my aim of these two topics. By searching for Xeroderma Pigmentosum and Neurodegeneration on Medline, I was able to look for some useful articles on my first aim (Table 2). I also searched for Xeroderma Pigmentosum and Gene Therapy for my second aim (Table 3). Cancer which can be considered as an uncontrolled growth and spread of cells is one of the top three causes of mortality in the world.(1) With the WHO predicting that it is going to be the top killer by 2010(2), it is vital for the public and medical professions to understand its aeitiology and pathogenesis in order to fight against it. Generally, the incidence of cancer is increased with aging as the chances of DNA mutation increases with age for lots of different reasons and we now understand that our DNA needs at least 5-6 mutations in order for cancer to develop(3). However, there are some other risk factors which might increase the susceptibility such as smoking, alcohol, radiation and so on. One of the most interesting factors is probably the cancer-prone DNA repair deficiency syndrome, for example Xeroderma Pigmentosum, Cockaynes Syndrome, Werner Syndrome. Patients with these syndromes are characterised by not being able to repair the DNA damage precedes the mutation and thus enhance the chances of getting cancer(4). The aim of this article is to discuss the genetic disorder Xeroderma Pigmentosum (XP). To understand this disorder, we have to first look into the types of DNA damages, their causes and their specific repair mechanism. DNA damage Mutation happens for lots of different reasons. It can occur spontaneously or naturally, for example DNA strand looped out during replication, hence causes a deletion of base. The other main types of spontaneous mutation are Depurination (Fig.1) i.e. detachment of Adenosine or Guanine from its deoxyribose sugar due to the hydrolysis of water and deamination (Fig.2) i.e. oxidation of bases by an oxidising agent e.g. nitrous acid. Spontaneous mutation occurs at a rate varies between and 4ÃÆ'- per gene per generation.(5-7) Another type of mutations could be elicited by the exposure of organisms to substantial mutagens, like chemicals or radiation.(7) The focus of this report is mainly on radiation. Radiation is probably the most well-known type of mutagen and there are three different types of radiation, each of which has its specific effects. The first type is ionising radiation which generates reactive oxygen species (ROS) e.g. H2O2, OHÂÂ · when passing through cells. These oxygen species oxidise DNA bases and thus causes base mispairing. The second type of radiation is the ultraviolet light. It has a wavelength ~ 260nm and is greatly absorbed by the bases. The absorbed energy causes the fusion of adjacent pyrimidine dimers on the same DNA strand and will mainly affect thymine (Fig.3). The results of this type of mutation are stoppage of DNA replication and transcription, which affects the normal function of cells significantly. Ionising radiation such as X-Rays can have a direct effect on DNA strand as well. It reacts directly with deoxyribose backbone and causes double-strand breaks in the DNA and may in turn completely stop DNA replication because of the significant d amage induced.(6-7) The Cell Cycle There are 4 main stages in the cell cycle, G1 (Gap 1), S (Synthesis), G2 (Gap 2) and M (Mitosis) and the duration for each cell cycle is around 24 hours. As from the diagram, each stage has its particular functions. There are two important checkpoints between G1 and S phase and G2 and M phase and they are called G1-to-S checkpoint and G2-to-M checkpoint respectively. These checkpoints are important as they detect the existing DNA damage and generate signals for DNA repair. If the DNA damage is too severe and beyond repair, tumour suppressor like p53 will come into action. This prevents the mutated cell from dividing and developing into cancer cells and the cell either goes into apoptosis or senescence.(5, 7) DNA Repair As previously mentioned, each type of mutation has its own specific repair mechanism and this paper is to focus on nucleotide excision repair (NER) (Fig.5), which is the only relevant mechanism to XP. NER helps repairing pyrimidine dimers and bulky DNA adduct to bases. This repair system works by detecting distortion to the double helix shape of the polynucleotide strand such as thymine-thymine dimers. This distortion triggers a series of events to restore the stability of the DNA. Firstly, XPC is the protein responsible for recognising the distortions. Then XPA and XPD generate a bubble (Fig.5) a ring-like structure formed by unwinds of DNA double-strand around the damaged site. The bubble creates two cleavage sites for ERCC1-XPF (5side) and XPG (3side) to act on. The cleavage sites are exactly 24 nucleotides away from the lesion on the 5side and 5 nucleotides from the 3end. Finally, DNA helicase releases the fragment that has been cut out, and once again DNA polymerases and ligase fill in the gap and repair the lesion. It is important to understand this repair mechanism as several genetic disorders like Xeroderma Pigmentosum, Cockaynes syndrome and trichothiodystrophy are connected with defects in the nucleotide excision repair.(6-7, 12) Brief introduction of XP XP was first described by two dermatologists in Vienna, Ferdinand Ritter von Hebra and Moritz Kapozi in the year 1870. The term xeroderma denotes parchment skin while pigmentosum was added later to indicate and emphasize the characterised pigmentation abnormalities(14-15). At that time, no one knows exactly what causes XP and the link between XP and defective NER was established by Cleaver in 1968(14, 16). Researchers have identified that there are 8 complementation groups of XP and they are XP-A-G and XP variant group. XPA-G are known as the classical forms of XP while the XP-V which is not associated with a defective NER, constituting 20% of the cases of XP. Instead of having a defective NER pathway, XP-V patients have gene coded for a defective form of DNA polymerase, causing a thymine-thymine dimers bypass during replication. Each complementation group represents a mutated form of a specific gene, i.e. complementation group A means the patient has a mutated version of the XP-A ge ne, etc.(14, 17) Patients with XP have a high photosensitivity to UV radiation as their cells have a defective nucleotide excision repair pathway. As a result, those cells exposed to UV radiation will have a high mutation rate and causes a high occurrence of skin cancer as well as affecting ocular tissues. XP can also cause neurodegeneration or neurological diseases and it would be discussed later.(14-15) Prevalence of XP XP is a rare autosomal recessive disease, which means that the disease will only be developed in patients with two mutated form of XP genes, XP will not develop in patients with a normal and a mutated gene as the mutated gene is recessive and wouldnt be expressed but he/she would be a carrier of XP. XP has a dispersed worldwide distribution, varying from 1 in 40,000 in Japan and 1 in 250,000 in Europe and USA. Symptoms of XP can start as early as first exposure to sunlight but the average age of onset of symptoms is around 2 years. There is also a greater than 1000-fold increased risk of skin cancers development connected with XP and the average age of onset of the foremost skin cancer or neoplasm is 8 years, around 50 years earlier comparing with the public. The life spans of XP patients are reduced by around 30 years as many of them die of neoplasia. As mentioned before, NER also removes bulky DNA adduct to bases, such lesions are induced chemically by chemicals like alkylating age nt rather than UV radiation. This explains why XP patients also have a 10 to 20- fold higher risk of forming internal neoplasms below the age of 20.(7, 12, 14, 17) Neurodegeneration of XP It is quite easy and straight forward to understand why XP patients are prone to skin cancers and even internal organs neoplasms. However, there is one interesting clinical feature that is still unexplained and remains puzzling and this is the neurodegeneration of XP patients, which is affecting approximately 20% of the XP patients. Since UV radiation cannot penetrate through our skull, thymine-thymine dimers would not be the type of mutation occurring in the neurological tissues e.g. brain tissues, neurons and so on. Thus, damages in the neurological tissues are more likely to be caused by chemicals like alkylating agents, ROS which damages DNA by oxidising DNA bases or adding bulky adducts to it and are also repaired by the NER pathway(14, 19). The following section will discuss some of the symptoms as well as possible causes of this interesting feature. The first symptom of the XP neurological disorder is reduced tendon reflexes, possibly as a result of peripheral nervous system and ataxia degeneration. With the progression of the disease, the patient will also develop hearing loss and other motor anomalies and become wheelchair bound eventually. Dementia and progressive cognitive decline are also the possible outcomes of the XP neurological disorder.(19) There are several candidates for the causes of neurodegeneration in XP patients but there are yet to be a confirmation of the ultimate cause of those symptoms. ROS is a possible cause for neurodegeneration in XP patients. These species react with our DNA bases or deoxyribose sugar and generate some form of lesions which should be repaired by our NER pathway, for example, hydroxyl radical, a ROS which reacts with deoxyribose sugar and produces a lesion called cyclopurine-deoxynucleosides (Fig.7). This type of lesion can only be repaired by NER and will accumulate in our cells if not repaired.(19) Aldehydes and thymine glycol are some other possible reagents that might cause neurodegeneration in XP patients. Aldehydes react with DNA, forming a DNA lesion called Propano-deoxyguanosine lesion (PdG) which might block transcription by RNA polymerase. Thymine glycol causes oxidative damage to the DNA and produces Nonbulky oxidatively-induced lesion, which could be repaired by the NER pathway as well.(19-20) It is important to understand the fundamental cause of neurodegeneration in XP patients, by doing so; we can develop a possible treatment, not only for reducing the incidences of neurological disorder in XP patients, but for improving the patients quality of life as well. For example if H2O2 is the cause of the neurodegeneration, we can develop a pathway which reduces the level of H2O2 in patients body and reduces the level of H2O2 in their cells.(19) Diagnosis for XP XP can be diagnosed in different ways. Diagnosis can be made clinically by examining eye, skin and nervous system, a detailed family history could also aid in the diagnosis. As XP cells have a defective NER, a functional test for DNA repair on living cells may also be used for diagnosis. Nowadays, genetic testing of XPA and XPC genes is available clinically but the testing for the other genes is only available on a research basis.(21) Treatment for XP At the moment, there is no cure for XP. Primary care for XP is probably more important than secondary care in terms of prevention and regulation of the disease. Once the patient is diagnosed with XP, he/she should avoid exposure to sunlight and other mutagens like cigarette smoke or alcohol immediately. XP patients should also wear protective clothing like UV suits, sunglasses and gloves in order to get minimum exposure to UV radiation, reducing the chances of getting further DNA damage. UV radiation levels should also be measured routinely at in-door environment for safety reasons. XP patients should also consume sufficient vitamin D in their diet to compensate for the insufficient production of vitamin D by their body.(21) As the disease progresses, XP patients might develop small lesions in the skin which could be treated using liquid nitrogen or topical 5-fluorouracil. Skin cancers, neoplasms of the eyelids, conjunctiva and cornea developed could be removed surgically. In patients with multiple skin cancers, high-dose oral isotretinoin may be used to prevent the formation of new neoplasms. X-radiation therapy can also be used to treat cancer with close monitoring as most XP patients are not hypersensitive to therapeutic X-rays.(21) Gene replacement therapy, i.e. replacing the mutated gene by insertion of a normal set of gene might also be a possible treatment in the future but very few research groups are working on that(22). In 2001, a study showed that the insertion of the bacterial DNA repair enzyme T4 Endonuclease V (also known as denV T4 endonuclease, an enzyme which removes the glycosyl bond of the pyrimidine dimer(23)) in liposomes into XP patients can actually increases the rate of repair of UV induced lesion, lowering the chances of new skin neoplasms development and it is now one of the treatments of XP. (21, 24) A research on gene replacement therapy published in 2003 was supportive for the XP patients(25). The result was quite promising as the researchers successfully restore the DNA repair capacity of XP cells after the insertion of gene(25). Although the efficacy of the treatment is high, its reliability is relatively low and there are definitely some limitations in the study. Firstly, it was an in vitro experiment; results shown in test tube would not be necessarily the same as in mammals or humans. Secondly, the research only focused on the XP-C cells so it is still unsure whether gene replacement therapy would work on other XP genes. Thirdly, the research was only done on cells from 2 patients; a larger sample size, preferably samples from different ethnicity or a more comprehensive study is needed to confirm the effectiveness in clinical practice. The bacterial enzyme T4 Endonuclease V was proved to be a quite effective treatment for XP as mentioned previously. The study that I looked into was a randomised study and involves 30 patients, with 20 in the intervention group and 10 in the placebo group(24). Overall, the study is quite reliable as it was a randomised double-blind study which minimise the bias that might affect the final outcomes of the study. However, some issues do present in the trial and should be addressed for future research. Firstly, the sample size is relatively small; a larger sample size is needed to confirm the effectiveness of the bacterial enzyme. Secondly, the ratio of patients in the two study groups varies, which might affect the statistical outcome significantly, especially for a small-sized study. Conclusions, limitations and further study To conclude, with the progression of technology and more time and resources spent on XP, we have now got much more understanding of XP, comparing with the first discovery of the disease. However, we shouldnt be satisfied with it and stop here as there is still a long way to go to get a full understanding of this genetic disorder. From my research, I found out that majority of the researchers favour ROS as the underlying cause of the neurodegeneration in XP patients. Firstly, our nervous system has a high demand for oxygen and ROS produced during respiration could potentially accumulate in our nervous system, causing damages to our DNA. Secondly, ROS causes DNA lesion that might only be repaired by the NER pathway. Thirdly, ROS can generate lesions that could block the RNA transcription, contributing to the loss of proteins and eventually cell death(19). All of these evidences suggested that ROS are possible causes of the neurological disorder in XP. At the moment, the resources are not available to prove that it is the case and there might be some other DNA damages that cause neurodegeneration which have not been discovered yet. However, I am sure with all the hard-work, and the advancement of technology, this mystery would soon be solved. In my opinion, with the lack of treatment for XP at the moment, preventive measures would be the most important things. As a result, diagnosis of XP should be made as quickly as possible. Genetic screening for new born baby might be a method for early diagnosis of XP. However, XP is a rare genetic disorder which is not so cost-effective for genetic testing as it is still relatively costly to diagnose XP in a molecular level and we should probably look for a cheaper alternatives and an easier way for diagnosis of XP. As for the future treatment, as I have previously mentioned, understanding the underlying cause of neurodegeneration is important for reducing the incidences of neurological disorder in XP patients and would improve the patients quality of life. My opinion on gene replacement therapy is that it is viable as the technology is available but not practical yet. First of all, although our skins are quite easy to reach, we should bear in mind that the skin has got a large surface area and would be quite difficult to insert replacement genes into the majority of the skin cells. We have now developed a method of inserting genes by genetically modified retrovirus, which could deliver genes into our cells quite easily. However, the technology for this is still premature and it is quite hard to monitor the viruses and might generate side effects like escape of viruses to the nature, mutation of the viruses and so on. I think that the information on gene replacement therapy for XP patients is qu ite limited; a lot more need to be done to address this issue. Finally, I do believe that with the advance of technology and as our knowledge of gene therapy progresses, a cure for XP should soon be found.

A Literature Review Identifying Group of Learners Within Society and Providing Reasons for Their Possible Underachievement Essay

Those could include students who do not perform well in a specific subject area, do not show interest in gaining qualifications or perhaps are limited by poor language skills or culture from doing well academically at school. There have been many explanations for low attainment and some of them include: * Natural differences between sexes, * Natural intelligence, * Home background, * Type of schooling, * Different teaching styles (stereotyping by teachers), * Material factors (Hammersley-Fletcher, Lowe & Pugh, 2006). Halsey performed a survey of the working class and found that material factors were central to whether learners stayed at school beyond the age of 16 (Halsley cited in Hammersley-Fletcher, Lowe & Pugh, 2006). Department for Education also states that the gap between the best and worst performers in our system actually widens as they go through education; and it is both significantly wider and more closely related to socio-economic status in this country than anywhere else (DFES, 2004). In education, the relationship between schools and social inequality is often explored by looking at the test and examination scores achieved by different groups of children and young people, and other monitoring data. According to Molly Warrington by the age of 11, girls in many primary schools are performing better than boys, particularly in English, and this pattern of differential achievement is sustained and exacerbated throughout secondary education (Warrington and Younger, 2006). This is a particular concern for white working class boys which is the reason why we should evaluate it further trying to establish possible reasons for their underachievement. BBC reported that government figures from January 2008 show only 15% of white working class boys in England getting five good GCSEs including maths and English. (BBC News, 2008). Above view is also supported by the chief inspector of schools who stated that white boys from poor families were worst affected and achieved the worst results aged 16 at school. White British boys who qualify for free school meals achieve the worst results of any apart from gypsy and traveller children – with just 29 per cent getting good marks. (Daily Mail, 2012) Why is this happening then in a modern world where we seem to have unlimited access to books, resources and other forms of help towards achievement? There is no doubt that to be able to achieve we must have the desire to learn and aspirations to perform well academically. Maslow’s Hierarchy of Needs outlines the necessity of satisfying the basic physiological and safety needs before the ones on upper levels like achievement, understanding and approval make students realise their potential. Unfortunately white working class households often undermine the values of schooling, academic achievement and aspirations. Boys from very early age associate manual labour with ‘masculinity and toughness’ therefore do not find academic learning relevant to them as it is not based on what they have been told or taught at home. Department for Education confirms that ‘schools where socio-cultural strategies were most transformative were those where head teachers recognised that there were sometimes conflicts between the cultural contexts of home and school, and that such conflicts might lead to disengagement and potential underachievement’ (DfES, 2005) Paul Willis performed a case study through a detailed ethnographic account of school lives of white working class boys who were ‘destined’ for labour. Boys showed lack of commitment to schoolwork and an acceptance of the authority of the teacher at the same time associating manual labour with ‘masculinity and toughness’. Willis argued that the boys were drawing upon cultural constructions of masculinity which idealised manual workers strength, so becoming a source of higher self-esteem. The ‘lads’ asserted their masculinity in the stories they told about resisting mental work (Willis, 1977). Most schools in Britain are dominated by the anti-education and anti-aspiration culture which has much more pronounced effects on boys. They believe that it is not ‘cool’ to learn, that real men work with their hands, not their minds, and that school does not matter (Telegraph, 2011). All of the above are deeply ingrained in our culture therefore boys like acting tough or hard, for example, by fighting or publicly denying adult authority; using humour and wit, sometimes as a confrontational device against teachers; wearing fashionable clothes and trainers or possessing culturally acclaimed knowledge, for example, being able to talk knowledgeably about the latest computer game (Swain, 2003, 2004). There are many reasons for this behaviour but Connell claims that working class communities in some parts of England are those most affected by the collapse of the traditional local manufacturing industry base and deindustrialization. These working-class boys can no longer rely on work for their traditional status of power and see little point in gaining qualifications, therefore are more likely to reject values that are conducive to academic success such as work ethic or punctuality. For the same reason they do not value academic success and admire peers challenging school’s authority (Connell cited in Younger, 2005). How do we change that? What do schools need to provide the best possible progress and the highest attainment for all pupils? Practical suggestions for educational organisations to better meet the needs of these pupils. Given the amount of literature talking about the underachievement of working class white boys, it appears that the reading material available, suggesting solution to the growing problem is limited. The suggestions on how to better meet the needs of these boys have been based on the literature review. Main points however, have been developed through discussions with school staff, parents and pupils from a local primary school where most pupils are White British with a few from minority ethnic groups. The proportion of pupils with special educational needs and/or disabilities and with a statement of special educational needs is below that found in most schools. Those discussions gave an insight into successful practices that minimise the impact of barriers to achievement for white working class boys. After careful consideration of the subject, improving achievement of boys appears to be a very complex process linked to many factors playing important parts. They include factors like leadership and vision, the curriculum and language support, behaviour management, parental engagement, targeted support including the role of the learning mentor in supporting white working class pupils. Successful transition to Year 7 from Year 6 has proven to also have a positive impact on white working class pupils. ‘These factors are significant in all schools, whether mixed or single-sex, maintained or independent. Senior managers play a crucial role in determining the most appropriate strategy for school improvement, based on close examination of the school situation and identification of the barriers to improving boys achievement’ (OFSTED, 2003). The quality of management and leadership within the schools plays a major part in developing successful strategies. Head teachers who keep their students at the heart of the school’s ethos and everything they do, find it easier to engage staff and parents. Strong leadership can be the driving force behind change, new expectations and inspirational success. They should: * Create a culture of achievement with a positive can do attitude. * Have high expectations and the provision of intensive support should be expected of all * Allocate a lot of time to being in the classroom with teachers and pupils * Make sure that diversity of pupil’s backgrounds and circumstances are celebrated. * Make sure that all children are encouraged to achieve their potential and stereotypical expectations are not made. * Make sure that books used, displays and worksheets avoid stereotypical images, sexist language and represent our multicultural society. The curriculum and language support also plays a major part in tackling underachievement. The Guardian (2013) agrees that barriers to learning faced by white working class boys are mostly concerned with language and literacy: ‘Many of these young people have a limited vocabulary and grasp of standard English and have a limited higher order reading skills such as skimming, scanning, synthesis, and empathy. Pupils with low levels of literacy rarely read at home, and their development in this area stalls when they get into their teens’. Our school believes that the curriculum should be accessible to all children whatever their age, race, gender, ability or social background. The use of appropriate reading materials gives the teachers the ideal opportunity for tackling stereotypical views, as well as widens their knowledge and understanding of things that middle class pupils already know and understand. Considering the above it was interesting to find that Schools and Communities Research Review (2010) suggests, it is unlikely that changing textbooks or curriculum content will in itself lead to improved outcomes in reading or mathematics. It is believed that professional development and coaching in effective teaching strategies make much more of a difference. Continuing, extensive professional development to teachers is likely to improve academic attainment for poor pupils therefore teachers need extensive, engaging workshops to learn new strategies and then coaching to be able to successfully implement and maintain them in their classrooms. Behaviour management also plays a major part in raising achievement of working class boys, and involves using successful strategy which requires a planned approach and subsequently dedication from all parties involved specially educators, pupils and parents. Ofsted reinforces this view by stating that behaviour is significantly better in settings which have a strong sense of community and work closely with parents and carers. In these settings learners feel safe and are confident that issues such as bullying are dealt with swiftly and fairly (Ofsted, 2005). Involvements of parents in the school life of their children, and their aspirations for them, have been also acknowledged as some of the most important factors associated with lower educational achievement. This appears to be particularly relevant to children from low-income families as parental aspirations and attitudes towards education vary significantly according to socio-economic status (Goodman and Gregg 2010). Young working class boys lack self believe and aspirations which results in having difficulties in understanding its importance and relevance. A lot of working class parents have had poor experience of education and believe that there is nothing to be gained from it as their children are likely to end up unemployed, or perhaps have achieved a lot in life through hard work despite having no formal qualifications. In both cases parents do not believe in education therefore pass that view and lack of aspirations onto their children (The Guardian, 2013). The head teacher of the local school reported that the white working class families were the hardest to engage within the life of the school and their children’s learning. School staff expressed frustration at the mismatch between the high aspirations of the school and low aspirations of the parents for their children’s learning, and therefore have to work hard on strategies to engage white parents with a view to raising achievement. School staff are aware that they have to draw parents in for positive reasons as a counter balance for the negative experiences that many had at school themselves. Younger ;amp; Warrington (2005) suggested that a combination of a strong learning ethos in school and increased involvement of parents in their children’s education could raise aspirations and achievement. There are number of reasons why white working class pupils should be able to do well academically despite challenging socio-economic circumstances in the areas served by schools. The evidence presented by the teachers from our local school mentioned earlier, enables the conclusion to be drawn that this school demonstrates the many ways in which they work to support pupils through a wide range of imaginative and inclusive strategies. Their success in raising the achievement of their pupils is a tribute to their vision, and to the very hard work that is needed to make it a reality. WORD COUNT: 2028 References BBC News Channel. (2008). White working class boys failing. Available: http://news. bbc. co. uk/1/hi/education/7220683. stm. Last accessed 28th Feb 2013 Centre for Excellence and Outcomes in Children and Young People’s Services . (2011). Effective classroom strategies for closing the gap in educational achievement for children and young people living in poverty, including white working-class boys. Available: http://www. c4eo. org. uk/themes/schools/classroomstrategies/files/classroom_strategies_research_review. pdf. Last accessed 3th March 2013. Daily Mail. (2012). White working-class boys are consigned to education scrapheap, Ofsted warns. Available: http://www. dailymail. co. uk/news/article-2159616/The-anti-school-culture-condemns-white-boys-failure. tml. Last accessed 28th Feb 2013. Department for Education and Skills. (2004). Five Year Strategy for Children and Learning. Putting people at the heart of public services. Available:https://www. education. gov. uk/publications/eOrderingDownload/DfES-5%20Year%20Plan. pdf. Last accessed 21st February 2013. Department for Education and Skills. (2005). Raising Boys’ Achievement. Available: https://www. education. gov. uk/publications/eOrderingDownload/RR636. pdf. Last accessed 28th Feb 2013. Goodman, A. , Gregg, P. (2010). POORER CHILDREN’S EDUCATIONAL ATTAINMENT: HOW IMPORTANT ARE ATTITUDES AND BEHAVIOUR?. Available: http://www. jrf. org. uk/publications/educational-attainment-poor-children. Last accessed 3th March 2013. Hammersley-Fletcher, L. , Lowe, M. and Pugh, J. (2006) The Teaching Assistant’s Guide, an essential textbook for foundation degree students. Oxton, Routledge. OFSTED. (2003). Boys’ achievement in secondary schools. Available: http://www. ofsted. gov. uk/resources/boys-achievement-secondary-schools. Last accessed 28th February 2013. OFSTED. (2005) Managing challenging behaviour. Available: http://www. ofsted. gov. uk/resources/managing-challenging-behaviour. Last accessed 15th February 2013. Swain, J. (2003). How young schoolboys become somebody: the role of the body in the construction of masculinity. British Journal of Sociology of Education, 24: 299-314. Swain, J. (2004). The resources and strategies that 10-11-year-old boys use to construct masculinities in the school setting. British Educational Research Journal, 20: 167-85. The Guardian. (2013). Working class boys: schools must work with parents to raise their attainment. Available: http://www. guardian. co. uk/teacher-network/teacher-blog/2013/jan/17/working-class-boys-raise-attainment. Last accessed 3th March 2013. The Telegraph. (2011). Why are poor white boys doing so badly at school? It’s about culture, and we’ve got to change it. Available: http://blogs. telegraph. co. uk/news/neilobrien1/100102225/why-are-poor-white-boys-doing-so-badly-at-school-its-about-culture-and-weve-got-to-change-it/. Last accessed 28th Feb 2013. Warrington, M. , Younger, M. (2006) Raising Boys’ Achievement in Primary Schools. Berkshire, McGraw-Hill Professional Publishing. Willis, P. (1977). Learning to Labour: How Working Class Kids Get Working Class Jobs. Aldershot: Saxon House. Younger, M. , McLellan, R. , Warrington, M. (2005). Raising Boys’ Achievement in Secondary Schools. Birkshire: McGraw-Hill Professional Publishing.

Linguistics Essay Essay

Some key terms: cultural, social, situational meaning; language; phonetics; the vocal apparatus; the vocal cords; voiced-voiceless sounds; place of articulation; stress or accent; pitch or tone; morphology; morpheme (singular-plural, tense). Assignment # 1: Essay on â€Å"what can the way a person speaks tell us about that person?† (due 1/18 at lecture time). Week 2: Jan. 18 The structure of language. [Assign. 1 (essay) due today at lecture time] Some key terms: syntax: subject, verb, object; language types; semantics (†Colorless green ideas†¦Ã¢â‚¬ ); pragmatics. Jan. 20 Language structure analysis. Language, Culture, and Cognition. (hdt. #3.0 & 3.01) Readings: Bonvillain, Chaps. 2-cont. (pp. 22-27, 37-39) & 3 (pp. 41-63) Some key terms: Sapir-Whorf hypothesis; semantic or vocabulary domain; color language and color cognition; lexical classifications and ethnoscientific domains; focal meaning and fuzzy membership; cultural presupposition; metaphor, metonymy; metaphors of kinship, other metaphors; proverbs. Week 3 Jan. 25 Language, Culture, and Cognition. (Hdt. 3.1, 3.2- metaphors & new words) â€Å"Metaphors We Live By†. Readings: Bonvillain, Ch. 3 (pp. 64-71) Jan. 27 Language and Culture: New Words in American English. Readings: Handouts: â€Å"Dictionary adds terms like chick flicks†; â€Å"Blog-blogger explained† â€Å"Words banned,† newspaper article. Project Explained: Profile of an ethno-linguistic group in the Los Angeles area. CHEM 105B Chapter 13 – 7 hours Chapter 14 – 7 hours Mastering Chemistry -8 hours Problems in Book – 2 hours Calculus 5.6 # 1,2,9,13,21,25 5.7 # 1,2,13,18*,35,39,45,48 5.8 # 1,11,13,16,21,27,29,32,35,41,49 * – use a computer program 6.1 # 1,2,3,7,9,13,16,18,20,27,33,44 6.2 # 1,3,5,14,19,23,37,39,40,43,48,49,53,54 7 hours

The Comedy of Errors

The Comedy of Errors â€Å"The Comedy of Errors† was written in early 1590ies and is considered to be one of William Shakespeare’s earliest plays. Being both the shortest and the most farcical, the play is characterized by unusual for Shakespeare humorous devices, as the humor mainly comes from slapstick and mistaken identity, as well as from traditional for him puns and play on words. â€Å"The Comedy of Errors† is one of very few plays in the creative heritage of Shakespeare which observes the classical unities of time, place and action. The latter can probably be explained by the fact that the basis for it was taken from two Roman comedies. The play is the story of two sets of identical twins that were accidentally separated at birth. Antipholus of Syracuse and his servant, Dromio of Syracuse, arrive in Ephesus, which is the home of their twin brothers, Antipholus of Ephesus and his servant, Dromio of Ephesus. When the Syracusans encounter the friends and families of their twins, a series of strange and unusual misunderstandings based on mistaken identities lead to wrongful fights and adultery, which almost happens, the arrest of Antipholus of Ephesus, and accusations of infidelity, theft, insanity. For centuries, scholars considered â€Å"The Comedy of Errors† to be the work of a slightly superficial nature. It was often stated that Shakespeare created the light comedy, making it much less serious than his histories, tragedies or later comedies. Recent research, however, used a different approach. They consider the play to be a series of social relationships, such as master-servant, husband-wife, parent-child, native-alien, buyer-seller and monarch-parliament, which, if rooted in a Roman past, acquire special significance in the transition to early modernity that constantly guides Shakespeares drama.