Tuesday, November 26, 2019
Cancer essays
Cancer essays Of all different kinds of cancer, skin cancer is one of the most commonly diagnosed cancers in the United States. Skin cancer is a disease which cancer cells are found on the outer layers of the skin. Your skin protects the body from heat, infection, light, injury and infection. It also stores fat, water, and vitamin D. The skin has two layers and several different kinds of cells. With a certain lifestyle these cells can become cancerous.(Prodigy Web Browser: An Introduction to skin Cancer {NET}, 1997) Melanoma is associated with the highest case-fatality rate of all skin cancers.(Mortality and Morbility Weekly Report Vol. 45/No. 17 , {MMWR}, 1996) Numerous studies have delineated the natural history of skin cancers. Some cell carcinomas tend to grow and invade slowly and steadily. Certain subtypes are more aggressive, and certain sites of occurrence (scalp, shoulders and nose) are associated with worse cases. Malignant melanoma may have a thin stage, in which survival rates are excellent. The length of thin, or radial, growth phase may be months to years. If untreated at some point melanoma enters a quick growth phase. When this occurs the survival rates plummet.(Brandt, 1996) Skin Cancer can be avoided. A change in lifestyle can reduce the risk of skin cancer. This includes awareness of the reality of skin cancer, avoiding the sun, and self- Most of the time when people think of a serious disease they think of things like lung cancer, heart disease, sexually transmitted diseases, and other hot topic diseases of that nature. Skin cancer awareness and the seriousness of skin cancer is far less emphasized. The MMWR did a survey of knowledge of and awareness about melanoma in the united states in 1995. In 1996, an estimated 38,300 cases of melanoma were diagnosed, and an approximately 7300 melanoma deaths would occur . Intervention ...
Friday, November 22, 2019
8 Common Spelling Errors to Check For!
8 Common Spelling Errors to Check For! 8 Common Spelling Errors to Check For! Spelling in English can be tricky. There are tons of words that arent pronounced the way they are written, as well as pairs of words that sound the same but mean different things! Here are seven common spelling mistakes, along with rules to help you remember them. 1. I Before E Except After C In words like sieve and believe, the i comes before the e. However, in words like receive and ceiling, the e goes first since it comes directly after a c. Watch out, though! There are exceptions to this rule, such as seize, weird and caffeine. 2. Necessary Necessary has one c and a double s. You can use this mnemonic to remember how to spell this one: On a shirt, it is necessary to have one collar and two sleeves! 3. Alot This is not a word! It should always be a lot (with a space between the two words). 4. Separate Many people spell this seperate, so just remember: Theres a rat in separate! 5. Familiar Some people spell this one familier, so keep the following in mind: That liar looks familiar! 6. Exaggerate Its easy to get confused about whether there should be one g or two in exaggerate. Try using the following as a reminder: George and Graham always exaggerate! 7. Rhythm Rhythm is a tricky word because it doesnt have any vowels. Luckily, theres an acronym that helps (where the first letter of each word spells out the word we need to remember): Rhythm Helps Your Two Hips Move. 8. Affect and Effect Try to remember that affect describes the action and is a verb, whereas effect describes the result and is a noun: My early experiences affected my later choices in life. The fire had a devastating effect on London. Making up little memory aids like these can really help your spelling, especially if you always get some words wrong. However, if you want to make sure that your work is completely perfect, why not send it to the experts for checking? Well even proofread a 500-word sample for free to make sure that you are pleased with our standards of work.
Thursday, November 21, 2019
Economic impact Research Paper Example | Topics and Well Written Essays - 1250 words
Economic impact - Research Paper Example of one such nation where demand for coffee has reached an epitome so much so that it accounts for being one of the largest consumers of the commodity in the world. Annual consumption of the good is near to 4.5 kilograms per capita in USA, clearly indicating the degree of popularity that coffee has attained among Americans. Despite the downfall in the income growth rate of the nation, the nationals continue to spend an average of $165 per year on coffee with 54% of them consuming it on a regular basis (International Coffee Organisation, 2006). The present paper is a case study on how a push cart selling hot coffee and cappuccino in the industrial belts of Cleveland, Ohio and Houston, Texas will fare in its business. Objective of the paper will be to draw a conclusion about the prospects of the business in either location on the basis of the degree of demand and the economic influence it will impose. Production of coffee in USA is concentrated only within the states of Hawaii and Papua, though the nation imports a lumpsum quantity of coffee from Latin American nations, whose tropical climate are suited for its growth. In fact, as far as the data of 2001 is concerned, USA is the largest importer of coffee beans accounting for more than 25% of gross imports of the product. However in terms of production, USA produces only a fraction compared to its huge demand for coffee. Hence, a majority of the coffee being supplied in various parts of the nation comes from its imports from South American economies of Colombia and Brazil (International Coffee Organisation, 2006). Demand for coffee depends upon a number of factors which tend to vary from place to place, leading to diverse outcomes of business ventures. In Ohio for instance, these factors could be elaborated as follows. Population – According to census conducted by US Census Bureau in 2008, Cleveland comprised of 397,901 people out of whom 47.8% were males and the rest of them being females. This statistic is
Tuesday, November 19, 2019
Justice in Benito Cereno Essay Example | Topics and Well Written Essays - 750 words
Justice in Benito Cereno - Essay Example At the end, the leader of the revolt, Babo, was caught and killed. The story creates such an atmosphere where identifying the role of justice is a difficult task. However, a thorough scrutiny reveals that real justice was not ultimately done in the story. The story reveals that the purpose of the revolt for the blacks was to gain freedom, not to torture the whites. For example, after capturing the ship, the first thing Negro Babo asked was â€Å"whether there were in those seas any Negro countries where they might be carried†(Melville 64). This gives the insight that the sole purpose for the blacks was to regain their freedom and go back to a black country where they would not be subjugated to slavery. In addition, it is the fear of losing freedom that made them kill their master Don Alexandro Aranda. Negro Babo informed Don Benito of the intention in advance and gave the reason â€Å"he and his companions could not otherwise be sure of their liberty†(Meville 65). Apparently, the blacks had no intention to enslave the whites and torture them but to ensure their own liberty. In addition, the blacks used the chance to teach the whites the lesson that subjugation, torture and death are equally painful for all humans. To illustrate, on killing Don Alexandro Aranda, the ship’s proper figure-head was replaced by his skeleton. Thereafter, every white in the ship was asked, â€Å"whether, from its whiteness, he should not think it a white’s†(Melville 66). There is evident sarcasm aiming at the mentality of the whites seeing everything done by whites as virtue and blacks as vice. In simple terms, one can say that the revolt by the blacks was an effort to regain their much-valued freedom from the clutches of the whites. The readiness of blacks to risk their lives for the air of freedom is evidenced from their claim â€Å"they would do and conform themselves to everything the deponent should require as to eating and drinking†(Melville 64). Thus, the
Saturday, November 16, 2019
Cormac McCarthy’s The Road Essay Example for Free
Cormac McCarthy’s The Road Essay Life can be cruel. In most cases, it squeezes the hell out of us. Nevertheless, the challenge is to come out unscathed. But do we always achieve this? And if so, what do we get out of every excruciating pain we have to endure?            The road to recovery has so many twists and turns. It is a test of strength but more so of faith. It is about believing in something we do not even see. The kind of person we become out of life’s most ultimate test defines who we are.            How many of us could actually say that living life is a breeze? Who have not known pain? Who can claim that life was pure pleasure? Who has never cried a tear?            All of us have been tested by time at one time or the other. We have been bitten by its pangs a couple of times over. We have been bloodied at countless instances. We have cried a pail full of tears.            Yet, we continue to breathe. The sun sets and rises every single day of our lives. We battle it out today for tomorrow has a challenge of its own. We have to gain as much strength as we have lost or if possible, much greater. This is all because pain will not die at the end of day. Most probably, it will wake up the same morning we open our eyes from sleep. Throughout the course of our life’s struggle we do not usually travel alone. Someone keeps us company. Even just for a while, we journey life’s path with a companion. It makes the burden a lot easier and even more meaningful. We are reminded that life after all is about building relationships that sees us through the most trying of times. Life gives us people to guide and accompany us as we thread down the road. Sometimes they live long enough to witness our feat. But usually they do not. Nevertheless, they serve their purpose. They provide comfort whenever we are afraid. They wipe our tears dry and lull us to sleep to regain lost strength. They give us hope in the most miserable of circumstances. They teach us to see another day as a chance to turn things around.            When every one else have left, who do we turn to? When the material wealth we have is none, how can we move on? When fate turns against us, what is the chance for survival? When it seems to be the world versus one man, is success hiding beneath the clouds of doubt? Whenever life robs us of our possessions, may we find comfort in knowing that we have not lost it all. Our family will remain to be the wealth exclusively our own. Neither fate nor circumstance can take it away from us. It is something ours, and ours alone.            A father’s love can be the only thing that can make us possibly walk another mile. It could ease the pain in our hearts knowing that someone is guiding us through. Whenever doubt seems to restrict every movement we make, let us be reminded that our father’s strength runs through our veins.            The story about a father and a son is not uncommon for many of us. Universal as a literary theme is its message. It transcends age, culture, race and tradition. It speaks a language known by all. It is something that lives and outlives generations and beyond.            A father and son’s story is about strength. It is about keeping tears from falling even if you just wanted to succumb and cry. It is about learning to be a man as fate continues to challenge his ability to remain brave and undefeated. Nothing can be more painful than seeing death happen right through our very eyes. Nothing can be more frightening than the thought that the next victim could possibly be me. Nothing can be more frustrating than realizing that tomorrow will just be like any other day of violence and death. Nothing can be much harder than believing that things happen for a reason.            How can we possibly live when life on earth seems to be empty, both literally and figuratively? We all know that it would not always be a bed of roses. But why does it seem to be usually a bed of thorns? How much pain can a man endure? What is the real essence of suffering?            Cormac McCarthy’s novel entitled The Road, is dedicated to his son, John Francis McCarthy. The novel a finalist of the National Book Critics Circle Award for fiction and a recipient of both the James Tait Black Memorial Prize and the Pulitzer Price for fiction unfolds the journey of a man and a boy across a post – apocalyptic panorama. The background signifies what was left after a great cataclysm made existence on this earth almost unheard of (McCarthy, 2006). Whoever said that life must go on may not know of a lot about surviving death. Whenever we witness death, it feels like a part of us has also stopped breathing. It leaves us numb and unaware that the world around us continues to run its course. Life must go on indeed. This statement must be true after all. No matter how hard and how unimaginable it may seem we are all compelled to do it just the same. We cannot pause for a moment and recollect our lost selves before anything else. Time passes by and once lost, it can never be regained. Sometimes, we just got to keep on moving no matter what. Move on and go on and trust that life may lead us to rest right when we need it the most. Death should remind us that life is lived just once. We may not be able to control what lies on the bend of the road, but we still have to thread it, nevertheless. Death reminds us that we have to give meaning to our existence. This is the challenge we all have to face. In the dark tunnel of death, life is the light at the end of it. It may be seen as a symbol of a cycle. Every end can be the start of something new. For every chapter of life that has been told precedes another story yet to unfold. This is but the cycle of life. It is a never ending story about life and death. More importantly, it is a challenge of living a life of worth to make death as important. For death could mean something only if the life lost left a void. There may be times when giving up is all too tempting. Enduring the most painful events of life is really too exhausting. These are the moments when we beg of death. These are the times when life appears to be worthless. We are sometimes too consumed by pain that we seem to believe that life is hell on earth. Life does not come without pain.  Every once in a while or sometimes a little too often pain is thrown on our way. Whenever it does, it reminds us that we are very much alive. It makes us feel so human. It makes things so real. The sweetness of pain lies on our ability to bear its bitterness. Even so, life may not really be all about pain and suffering. We can surely get some sweetness from it when we squeeze it dry. There is some kind of balance in the world we live in. Goodness surely lies on some corner. It may take time and a lot of effort in between, but it is there as it has always been. The most challenging of all circumstances teaches a lesson or two. Things happen not to make man resolve into thinking that life is a crazy game of pessimism. While there is ruthlessness, there is goodness. Goodness comes in the most unexpected of packages. It comes during the most unanticipated of times. It comes when we have almost given up. It comes at just the right moment to remind us that it was worth it to hold on. Holding on is oftentimes the only thing left to do. It may not be the most logical but it could possibly be the most practical. Some people come into our lives and quietly go but they leave us a message that speaks so clear and sound. It is from strangers that we gain the wisdom we would not have otherwise known. And this could be the beauty of life. That after all the pain, we may be able to smile again. Just when we thought that we can never know life to be kind, someone teaches us the value of optimism. When gravity seems to pull us down while trying to hold on with all our might, a helping hand extends for the taking. Just when we get so near the end of our rope, let us find comfort that someone is at the other end to take over.   They pull us through when we might have lost all the strength that is left. They are once a stranger we crossed paths with. But before the road takes us to yet another bend, each other are no more strangers. For that walk we shared has left some of the most important lessons we can never forget. Life is hard but we are tougher. It can take away everything but we can always leave some bit of hope deep inside our hearts. We may not have anymore tears left to cry. We may be left with broken bones and battered ego. But if we continue to struggle along the road and combat every imaginable obstacle there is, we can still be hailed victors of the finest kind. May we not lose hope on the promise of yet another sunrise no matter how painful life has made known itself to man. Life takes on a whole new meaning when it is lived not for thy self. A life lived in this way is noble in all the ways that matter. References BBC.co.uk. (2007, April 17). Novelist McCarthy wins Pulitzer. Retrieved February 26, 2008, from http://news.bbc.co.uk/1/hi/entertainment/6563291.stm Chabon, M. The New York Review of Books. (2007, February 15). After the Apocalypse. Retrieved February 26, 2008, from http://www.nybooks.com/articles/19856. Conlon, M. Reuters. (2007, June 5). Writer Cormac McCarthy confides in Oprah Winfrey. Retrieved February 26, 2008, from http://www.reuters.com/article/entertainmentNews/idUSN0526436120070605?pageNumber=1. Empire. (2007, April 2). John Hillcoat Hits The Road An adaptation of Cormac McCarthy’s novel. Retrieved February 26, 2008, from http://www.empireonline.com/news/story.asp?NID=20573. Guardian.co.uk. (2007, October 30). Civilisation ends with a shutdown of human concern. Are we there already? Retrieved February 26, 2008, from http://www.guardian.co.uk/commentisfree/story/0,,2201594,00.html. Jones, M. (2006). On the Lost Highway. Newsweek. Retrieved February 26, 2008, from http://services.newsweek.com//search.aspx?offset=0pageSize=10sortField=pu bdatetimesortDirection=descendingmode=summaryq=on+the+lost+highway site-search-submit.x=33site-search-submit.y=7 Keller, J. (2007). Oprah’s selection a real shocker; Winfrey, McCarthy strange bookfellows. Chicago Tribune. Retrieved February 26, 2008, from http://pqasb.pqarchiver.com/chicagotribune/access/1246151131.html?dids=12461 51131:1246151131FMT=ABSFMTS=ABS:FTtype=currentdate=Mar+29 %2C+2007author=Julia+Kellerpub=Chicago+Tribuneedition=startpage=1 desc=Oprah%27s+selection+a+real+shocker+. Kennedy, W. (2001). Left Behind. The New York Times. Retrieved February 26, 2008, from http://www.nytimes.com/2006/10/08/books/review/Kennedy.t.html?ex=1189396800en=6d113b5a5cbaf19bei=5070 McCarthy, C. (2006). The Road. New York: Alfred A. Knopf. National Book Critics Circle. (2006). NBCC Awards Finalists. Retrieved February 26, 2008, from http://www.bookcritics.org/?go=finalists
Thursday, November 14, 2019
Organizational Development Essay -- Business, Team Intervention Model
Organizational Development (OD) has become more and more important for today’s organizations because the world is moving so fast that organizations have to find ways to be more effective, more innovation, more customer-driven, and more agile. Cumming and Worley (1997) define organizational development as â€Å"a process that applies a broad range of behavior science knowledge and practices to help organizations build their capacity to change and to achieve greater effectiveness†(p. 1). Therefore, OD will help organizations understand how people act to change and which change methods can work with the resistance to change that usually occurs in organizations undergoing change. As my concentration of SPS program is organizational development, it is important to study Organizational Intervention & Change Implementation in order to know how to operate and make use of change methods that seem to be vital in solving any problems that arise. What I First Learned about the Course In this course, I have learned that the change methods could be divided into four purposes: adaptable, planning, structuring, improving, and supportive (Holman, Devane, & Cady, 2007). In addition to the purpose, Holman, Devane, and Cady (2007) assert that individuals and organizations need to consider type of system, event size, duration, cycle, and practitioner preparation, and special resource needs. Since there are many methods to learn about, the paper of IIMT helped me to deeply understand methods that I thought they were interesting. I chose to study Appreciative Inquiry of adaptable methods, Scenario Thinking of planning methods, Participative Design Workshop of structuring methods, and The Six Sigma Approach of improving methods. In doing this assignment, ... ... experiences and information related with the issues. This was my first time to involve in fishbowl conversation and I found that it was an simple, effective technique to build trust and mutual understanding and to improve the relationship among members. Overall, the study of Organizational Intervention & Change Implementation through reading the book, attending the class, doing assignments such as IIMT and TIMPF, partaking in the process of organizational interventions, and having a fishbowl conversation help me to be very knowledgeable about change models, to effectively work in team, and to gain learning from classmates’ experiences and expertise. More importantly, I have gained ton of confidence in areas where I had little or no experience before. Now, I can have an ability to diagnose an organization’s problems and implement the appropriate change methods.
Monday, November 11, 2019
Euro Disney Essay
Introduccion The Walt Disney Company, is an American multinational corporation located in Burbank, California. It is the largest media conglomerate in the world in terms of revenue. Disney was founded on October 16, 1923, by Walt and Roy Disney and established itself as a leader in the American animation industry. Disney has created new divisions of the company in order to market more mature content than it typically associates with its flagship family-oriented brands. The company is best known for the products of its film studio, the Walt Disney Studios, and today one of the largest and best-known studios in Hollywood. Disney also owns and operates the ABC broadcast television network; cable television networks such as Disney Channel, ESPN, A+E Networks, LifeTime and ABC Family; publishing, merchandising, and theatre divisions; and owns and licenses 14 theme parks around the world. It also has a successful music division. The company has been a component of the Dow Jones Industrial Average since May 6, 1991. An early and well-known cartoon creation of the company, Mickey Mouse, is the official mascot of The Walt Disney Company. Focused on Euro Disney: Euro Disney S.C.A. is the company that owns and operates Disneyland Paris in Marne-la-Vallà ©e, France. 39.78% of shares are held by The Walt Disney Company, 10% by the Saudi Prince Alwaleed and 50.22% by other shareholders. The stock is traded on the Euronext Paris exchange. Disneyland Paris comprises Disneyland Park, Walt Disney Studios Park, Disney Village, and seven on-site Disney Hotels. Val d’Europe is a new residential and shopping development. Another seven hotels/residences have been built not far from the two Disney theme parks on land held under Euro Disney SCA’s lease, including properties from companies such as Holiday Inn, Kyriad, MyTravel and Radisson Hotels. The Resort is a result of an agreement signed on 24 March 1987 between The Walt Disney Company and the French Authorities for the development of a new tourist destination, and construction began within a year. Since opening on 12 April 1992, the Resort has created more than 30,000 jobs (both directly and indirectly) in the region to the east of Paris. Today it is the n umber one tourist destination in Europe with 14.5 million visits recorded for Financial Year. Offers/Suggestions: There are many companys which offers many packs for families. Below some examples. Esayjet: Esayjet offers the best prices on Paris Disney Area deals and get away on a Paris Disney Area holiday for less. easyJet Holidays has a fantastic range of prices and offers with a selection of easyJet flights and Paris Disney Area hotels available. http://holidays.easyjet.com/france/paris/paris-disney-area-holidays.htm Thomson: Thomson gives you the opportunity to cutomize your trip: – Accommodation in a Disney Hotel including breakfast – Tickets for both Disney Parks for each day – Access to Free Fastpass service for every member of your party: Cut down the queuing time at the most popular attractions – Extra Magic Hours: Get access to the Disneyland Park up to 2 hours before regular Park opening! http://www.thomson.co.uk/editorial/features/disneyland-paris.html Hotels inside the Amusement Park: There are many opptions for accomodation indide the park. In total there are 14 hotels. Some examples as follows: Disney’s Newport Bay Club: At Disney’s Newport Bay Club, enjoy all the style and charm of the late 19th Century New England seaside, right on the waters of Lake Disney. Disney’s Hotel Santa Fe: Disney’s Hotel Santa Fe offers you a taste of the monumental landscapes of America’s South West, along the legendary Route 66. Disneyland Hotel: If you you asked for the best. Disneyland Hotel offers the ultimate in Disney quality, service, hospitality and location! It’s right at the entrance to Disneyland Park. Location: Euro Disney is located in France (Paris). France is the largest country in Western Europe and the third-largest in Europe as a whole. It possesses the second-largest exclusive economic zone in the world. France has been a major power with strong cultural, economic, military, and political influence in Europe and around the world. France is a developed country,possessing the world’s fifth-largest and Europe’s second-largest economy. Questions A: 1) What did Disney do wrong in its planning for Euro Disney? EuroDisney made different financial ​​strategic mistakes .Taking into account the studies predicting the good economic panporama The growth would be very fast, which means good benefits for the region. But the reality was very different, It means the prediction was wrong. Maybe the will need to made two or more financial Studies befote taking a desition. Another of his errors was the European habits which had changed. From the American experience the highest assitance would be on friday’s, the opposite occurred. The company had difficulties planning the number of workers for those days. Another operational errors was the computers of the hotels. EuroDisney was based on that customers spent several days in the park. The reality was very different, customers arrived very early in the morning to spend the day in the park and get to the rooms at night to leaving the next day. Queues to pay dragged on the grounds that there was only one computer. They had to install several computers addicionales to reduce queues. 2)What recommendations would you make to Disney to deal with the problems of Euro Disney? EuroDisney uses Other Strategies to Solve the Problem of the Situation Name change to Eurodisney Disneyland Paris, so well adapted to European tastes and give a disastrous change in customer care. Through the emphasis of recognizing Paris, executives capitalize on the proximity of the park to the French capital. Keeping costs and increase revenues decreased 8.6% of its labor potential. In response to criticism of high ticket prices and hotels EuroDisney decided to introduce offers and new prices for hotels in low Seaton Disney company changed its marketing philosophy to attract customers from other countries such as Israel and Africa. Instead of offering the park as a holiday destination 3)What lessons can we learn from Disney’s problems with Euro Disney? Misunderstand food habits and customs of Europeans. They learned that for foreign market, it is necessary to conduct a comprehensive study of the customs in that country which they did not do. These results obtained in human resources can help l from this process and this be applicable everywhere in the world. The food market must require a study of economics, rights, culture, climatology, interests, customs, lifestyle, geography, work habits etc.. Questions B: 1.How should the park differentiate itself from the competitive treta posed by the growing number of European amsusement Parks? The main and most important reason is that it is the only amusement park in Europe related to Disney. In my point of view it would be important to provide prices, packs, etc. for children under 7 years, for example, for birthdays, facilitate price, queues etc†¦ Finally renovation, uptades or new attractions design quite often. 2. What target marketing strategy should be pursued in the face of the changing competitive environment? A marketing strategy that positions Euro Disney as a affordable, fully equipped and multicultural park rather than just an American import. This can be done through the following: Implementing more aspects of European culture and less American culture. Signs and ads should be multilingual Food and drinks should be fitting for European tastes. Characters and casts should be more presentable to French culture in specific and European in general. Euro Disney is for Europe and not a form of an Americanized location in Europe. 3. What branding-strategy decisions are relevant? When it comes to the branding strategy, the image of Disney as a brand needs to be maintained as an amusing and incredible experience for everyone. However, again it should be directed in a way to fit the European perceptions of Amusement parks and not the American style. Plus the brand should have the attribute of being the worlds best amusement park provider by displaying the success it has in the U.S.A and in Japan. Meaning that you can have the thrill and experience that Disney as an organization offers you but in Europe. 4. What can be done to make better use of underutilized resources (such as the Hotels) while increasing the profitability of well-patronized facilities? On the short term the most sensible idea is to have a well-fit price for the current economic situation in Europe. Disney Europe can offer packages and promotions for visitors based on the seasonality and demands of the European consumers. A combination of promotional packages can help boost the number of visitors who will find it more appealing to go to Euro Disney rather than any other park because it has a combination of facilities at a reasonable price. Conclution Disney wanted to Americanize European customs. That mistake led to the executives to build an amusement park of your dreams, but following a American model and thus strictly different from physical reality, financial and cultural center of Europe and France. To enter the European market, should make a more detailed study based on research into every applicable aspect of the economy, laws, culture, climate, interests, customs, habits in lifestyle, geography, work habits, among others. This case demonstrates the importance of taking into account the Consumer Comportamientodel when making decisions about new products or paraextender existing products to new markets. It is vitally importanciatener into account social factors such as habits, culture, customs, language, demographics, socioeconomic status, etc.. What to darsecuenta of which is the best way to reach that market.
Saturday, November 9, 2019
Alzheimer’s Disease Amyloid Precursor Protein Gene
Alzheimer’s disease, AD, is a distressing condition that involves the decline in cognition of the mind which results to psychotic disorder, and affective and behavioral disturbances (Bloom 9). It is a progressive central nervous system disorder and the main cause of dementia (Stavljenic-Rukavina 1). Alois Alzheimer in 1907 reported the case of a 51-year old Frankfurt woman who died in dementia (Bloom 9). He described the neuropathological condition of the woman with neurofibrillary tangles or NFTs and amyloid plaques or NPs (Bloom10). NPs are extracellular beta-amyloid peptide or A?Spherical deposits closely related to dendrites, reactive astrocytes, dystrophic axons, and activated microglia (Felician and Sandson 19). Thus, for several decades, collaborative efforts of experts from different scientific and medicinal endeavors were devoted for the neurological and pathophysiological characterization of this disease (Bloom 9). As such, the roles of four specified genes, as well as the mechanism of oxidative stress, tau, inflammation, hormonal changes, and inflammation on the AD’s neurodegeneration have been the central theme of scientific studies conducted on this disease (Felician and Sandson 19).As experts continuously gained insights on the mechanisms of neurodegeneration, pharmacological strategies are concurrently devised for the development of appropriate drug treatment and interventions (Felician and Sandson 19). Molecular Mechanism Early and late onset ADs are types of familial AD which are genetically heterogeneous. Familial AD is accounted for 10% of AD cases from 30-60 year old patients and ascribed to three types of genes which included APP, presenilin-1 or PSEN1 and presenilin-2 or PSEN2 (Stavljenic-Rukavina, 1).Nonetheless, the mutations in these genes also cause A? -level increase; A? is generated by proteolytic APP fragment that was also observed in the brains of AD patients (Stavljenic-Rukavina, 2). However, not all AD cases can be attributed to the three identified genes. Genes are then the most important determinant of AD development (Stavljenic-Rukavina, 2). On the other hand, there is a great chance for children with parents having history of familial AD to inherit the genetic traits and develop either early-onset or late-onset AD (Jayadev et.al. 375). As well, AD development threat in the offspring is directly related to age; the tendency of AD occurrence among children of parents with historical AD background increases as the children gain progress in their growth and development (Jayadev et. al. 375). The pathogenesis of Alzheimer’s disease, on cellular level, has been consistently observed. The pyramidal neurons are the type of cortical cells that are fundamentally deteriorated in AD pathogenesis resulting to the spread of NPs and NFTs in cortex areas (Felician and Sandson 20).Both NPs and NFTs are normally found in brain areas in the aging process but their concentrations and densities are pecu liar in the case of AD (Felician and Sandson 20). Originally, NPs are found at the amygdala and concentrated in parietal association and order temporal cortex parts (Felician and Sandson 20). In the maturity of AD, NPs can also be observed in hippocampus, in other structures of mesial temporolimbic brain, and even in cortical and meningeal blood vessels (Felician and Sandson 20).Luckily, the areas for sensorimotor and visual are remained unaffected. Meanwhile, in the early stage of AD, NFTs can be found hippocampus, amygdala, and in entorhinal cortex, the association cortex has abundance of NFTs (Felician and Sandson 20). However, NFTs are not exclusively for the cases of AD, these are also detected in the several cerebral troubles like in dementia pugilistica, postencephalitic parkinsonism, and subacute sclerosing panencephalitis (Felician and Sandson 20). The formation of NPs is attributed to the A ? peptide deposition; A ?peptide types that only differ in C-terminal are common in cerebrovascular and extracellular plaques (Felician and Sandson 19). A ? peptide, made up of 39-43 amino acids, is normally generated from APP or amyloid precursor protein. In addition, the series of hydrophobic C-terminal is crucial in its solubility and amyloid formation rate (Felician and Sandson 19). As such, A ? with 40 amino acids, A ? 40, as well as A? peptide with 42 and 43 amino acids or A? 42 and A ? 43 respectively (Felician and Sandson 19). However, in vitro, the variants of A?42 and A? 43 can easily form insoluble fibrils as compared with the A? 40 variant (Felician and Sandson 19). Furthermore, the incubation of these A? variants can immediately lead to coalescence implying the possible amyloid plaque deposition through these components. In line with this, diffuse plaques have nonfibrillary and A? soluble constituents denoting the senile plaques’ early stage (Felician and Sandson 19). Likewise, diffuse plaques have A? deposits in the absence of neuritic degener ation (Felician and Sandson 19).On the other hand, neurofibrillary tangles, comprised of abnormal bundles of intraneuronal filaments, are made up of tau microtubule-associated protein with high degree of phosphorylation (Felician and Sandson 19). The degree of phosphorylation is largely dependent on the enzymatic activities of kinases that are not yet fully understood (Felician and Sandson 19). Nevertheless, the intraneuronal abnormal filaments arrange themselves in either parallel or helical bundles in perikaryotic cytoplasm that make them in contact with the dentritic processes (Felician and Sandson 19).The amyloid precursor protein, a membrane glycoprotein, is consisted of 28 A? extracellular residues and 12 to 15 putative transmembrane residues (Felician and Sandson 20). It also occurs as 695, 751, and 770-amino acid isoform. While the 695-amino acid isoform occurs mainly in neurons, 770 and 751-amino acid forms are seen on both non-neural and neural cells along with protease in hibitor domains (Felician and Sandson 20). APPs are carried into the cell membrane by secretory vesicles and may undergo proteolytic bond breakage through the action of ?-secretase (Felician and Sandson 20). Consequently, this cleavage generates ? -APP, a soluble ectodomain and the precursor for A? peptide production through cleavage in A? domain. As the generation of soluble APP is, in vitro, ascribed with the activity of protein kinase C, uncleaved APP is inferred to take the proteolytic pathway (Felician and Sandson 20). On the other hand, APP intracerllular recycling and management are done through endocytotic or endosome-lysosome means. The endocytotic route causes proteolytic cleavages by means of ?– and ? -secratases leading to the synthesis of A? (Felician and Sandson 20). Moreover, A? production is enhanced by intracellular calcium concentration which denoted the significance of calcium-rich proteases in A? production (Felician and Sandson 20). In vivo, APP cleavage occurs at N-terminus at the A? -region through the action of ? -secretase and at the C-terminus by means of ? -secretase activity (Mohan 1). Also, APP can take a pathway facilitated by ? -secretase at the A? -peptide domain producing soluble ? -APP (Mohan 1).Ezymes can also possibly attack APP without A? -peptide generation (Stavljenic-Rukavina, 1). Since the putative ? -secretase, under the control of kinase C, regulates the generation of soluble APP, any agents that supports this metabolism may hinder the A? production (Felician and Sandson 21). As well, A? deposition may also be lessened by drugs which inhibit APP cleavage into ? – and ? -secratases (Felician and Sandson 21). Nonetheless, agents that can impede A? coalescence would decrease its neurotoxicity effects (Felician and Sandson 21).After the formation of amyloid plaques, neurofibrillary tangles and inflammation dictates the death of neurons (Stavljenic-Rukavina 1). In relation to this, microglia and astrocytes ce lls of the brain are heavily affected by inflammatory process (Stavljenic-Rukavina 1). In AD patients, astrocytes are enlarged and produce prostaglandin which in turn sends signal to activate the inflammation mediated by arachidonic acid (Stavljenic-Rukavina, 1). On the other hand, microglia generates free radicals which cause neurons’ death (Stavljenic-Rukavina 1).Meanwhile, cell nutrients as well as its regulation components are transported through the microtubules in which structural properties are mainly dependent on tau protein (Stavljenic-Rukavina 1). In AD condition, the tau lessens its capability to bind with microtubules and binds with other tau protein resulting to knots of helical filaments called as neurofibrillary tangles (Stavljenic-Rukavina 1). APP Duplication is Sufficient to Cause Early Onset Alzheimer’s Dementia with Cerebral Amyloid Angiopathy Studies showed that A? encoding through APP gene expression leads to the development of Alzheimer-type demen tia (Sleegers et.al. 2977). APP genetic expression results to elevated levels of A? 42, a 42-amino acid product of the proteolytic process (Sleegers et. al. 2977). Aside from the cleavage of APP into alpha, beta, and gamma secretases, high APP genetic expression results to elevated levels of A? 42 and A? deposition (Sleegers et. al. 2977). Meanwhile, it has been long known that APP level triplication in Down’s syndrome patients results to the development of Alzheimer type dementia at early stage; the APP excessive expression leads to neurodegeneration and A? deposition (Sleegers et. al.2977). In relation to this, it was reported that families with cerebral amyloid angiopathy and early onset Alzheimer type dementia had APP genomic duplications which implied that APP over-expression, without full trisomy 21, has triggered the Alzheimer-type dementia (Sleegers et. al. 2977). In addition, Alzheimer-type dementia patients have elevated APP mRNA levels in their brains (Sleegers et. al. 2977). Further, the variation on the transcription of APP gene due to genetic factors was believed as the underpinning factor in the pathogenesis of the disease (Sleegers et.al. 2978). In fact, three APP mutations were observed on Alzheimer-type early-onset dementia patients. These mutations, as seen in vitro by means of trisomy 21, caused a two-fold elevation of in APP transcriptions (Sleegers et. al. 2978). With the aforementioned evidences on APP elevation through APP genomic mutations or duplications which resulted to the development of early onset AD, it could logically infer that A? has a crucial role in its aetiology (Sleegers et.al. 2978). Hence, for the evaluation of APP locus duplication on Alzheimer-type dementia cases, Sleegers et. al. conducted a study on Dutch population with early onset Alzheimer-type dementia patients. Material and Methods In the approval of the University of Antwerp medical ethical committee, the respondents of this research were recruited form an epidemiological study on early onset AD in several provinces of The Netherlands and in Rotterdam (Sleegers et. al. 2978).Patients with early-onset dementia diagnosis were enlisted based on the recommendation of medical experts and healthcare providers. As such, the assessment of the patients’ conditions was done in accordance with the standards of the Stroke-Alzheimer’s Disease and Related Disorders Association, and the National Institute of Neurological and Communicative Disorders (Sleegers et. al. 2978). Medical records of the patients and their respective relative with similar trait inheritance were made available for an in-depth examination.Meanwhile, for the assessment of genetic inheritance, 111 patients with ages 33 to 65 years old of which had 75 respondents with familial background of either late or early-onset of dementia and 10 of which have autosomal dominant inheritance history for several generations of their respective clans were studied (Sleegers et . al. 2978). The genomic DNA or gDNA was derived from lymphocytes and alleles of APP were measured by means of real-time polymerase chain reaction, PCR (Sleegers et. al. 2978).Also, the PrimerExpress software was utilized for the design of ? 2-microglubulin or hB2M, exon 5, 11, and 18, ubiquitin C or hUBC, ATP5J, APP, and GABPA (Sleegers et. al. 2978). As the APP alleles were normalized for hB2M and hUBC, 20 nanograms of genomic DNA were combined with the PCR and 400 nanomoles of the respective primers (Sleegers et. al. 2978). Finally, the duplication of the samples was done by means of dosage quotients or DQs calculation through six normal individuals and dementia patients.Patients with trisonomy 21 were also included as controls (Sleegers et. al. 2978). Fluorescence in situ hybridization, FISH, was utilized to determine APP genomic duplication (Sleegers et. al. 2978). FISH was performed on both interphase nuclei and metaphase chromosomes while the Epstein-Barr virus-transformed pa tients’ lymphoblasts were taken from the metaphase period by means of 0. 1 microgram/milliliter colcemid treatment and incubated, at 37 °C for 25 minutes, in hypotonic solution of 1 molar sodium hydroxide, 30 millimolar glycerol, 0.8 millimolar magnesium chloride, 2 millimolar HEPES, and 1 millimolar calcium chloride (Sleegers et. al. 2978). This suspension then was used for 106 cells per milliliter as the chromosomes’ mechanical stretching was done through cyto-centrifugation. On the other hand, the Multiplex Amplicon Quantification, MAQ, was applied in the detection of APP locus duplication. MAQ was comprised of multiplex PCR amplification of the reference amplicons and targets which were tainted with fluorescent substance (Sleegers et. al. 2978).After MAQ, DNA fragment analysis, and comparison target amplicon DQ between control individuals and the patients were done (Sleegers et. al. 2979). Results and Discussion Real-time PCR APP measurements of 10 probands showe d heterozygous duplication (Sleegers et. al. 2982). Based on the Dutch population sample, APP duplication along with segregation pattern and neuropathology tantamount to autosomal dominant inheritance and AD with excessive CAA were identified with APP duplication in a family (Sleegers et. al. 2982).Specifically, the genomic APP locus duplication were observed in five of the 65 family cases with early onset AD autosomal dominance while APP duplication was detected in a single out of ten family cases early-onset AD autosomal dominance (Sleegers et. al. 2982). Even though these numbers are small, the data generated from this study illuminated the significance of genomic APP locus duplication assessment when simple mutations were excluded in AD known genes (Sleegers et. al. 2982). In the 65 patients with familial AD history, a single genomic duplication was identified (Sleegers et. al. 2982).In addition, the genomic duplications among the Dutch samples have 1. 8% overall frequency and 2 . 7% frequency in AD patients and family (Sleegers et. al. 2982). In contrast, duplication was failed to be detected on 36 patients with irregular early-onset AD which denoted that the duplication of de novo genomic APP is a weak cause of early-onset Alzheimer-type dementia (Sleegers et. al. 2982). Moreover, the duplication observed among the Dutch family samples has only APP which proved that genomic APP duplication, regardless of adjacent genes, has the capacity for AD and CAA mixed phenotype (Sleegers et.al. 2982). As well, duplication size differences signified the non-specific recombination substrate from the genomic attributes of APP locus; APP rather is in increased recombination region as imparted by other factors such as low transcription repeats (Sleegers et. al. 2982). Nevertheless, the mutation that affects APP expression among 4. 5% of the Dutch participants that either genomic APP duplication or APP mutation promoter carrier, are the frequent cause of Alzheimer-type de mentia (Sleegers et. al. 2982). Polymorphism in the Promoter of the Human APP GeneThe cleavage of APP produces A? with associated neurotoxicity; hence, genetic studies postulated that abnormal A? deposition neuropathologic AD conditions (Athan, Lee, Arriaga, Mayeux, and Tyco1793). The abnormal deposition of A? in AD patients has been ascribed to APP gene missence mutations and the proteolytic APP cleavage producing A? 42 which in turn triggers the development of early-onset AD (Athan, Lee, Arriaga, Mayeux, and Tyco1793). The most solid proof for this notion is the case on trisomy 21 wherein the duplication of APP gene results to increased A?peptide level and aggregation of such in the amyloid plaques of the brain (Athan, Lee, Arriaga, Mayeux, and Tyco1793). While the presenilin enyzymes enhance fibrillogenic APP conversion, the APOE or alipolipoprotein-E elevates A? coalescence and deposition (Athan, Lee, Arriaga, Mayeux, and Tyco1793). Since A? production is associated with APP con centration and on other factors in both A? and APP syntheses, it was hypothesized that the expression of APP gene is a determinant of AD development (Athan, Lee, Arriaga, Mayeux, and Tyco1793).Recently, a study reported the weak relation between AD inheritance and microsatellite sequence in the APP first intron and a tetranucleotide non-association with AD (Athan, Lee, Arriaga, Mayeux, and Tyco1794). Hence, to further scrutinize this issue, Athan et. al. anchored their study on APP promoter variant screening in tri-ethnic populations which included white, Caribbean Hispanic, and African-American as they intended to determine APP promoter identities. MethodologyThe respondents in this study were Manhattan residents of Washington Heights with ages of more than 65 years (Athan, Lee, Arriaga, Mayeux, and Tyco1794). Personal interview and medical background check, neuropsychological, physical and neurological examinations were done on the participants. In addition, individuals with quest ionable dementia, Parkinson disease, and other types of dementia were excluded in the study. Consequently, a total of 1,077 participants was successfully enlisted, whereas, 16% of them has family history of stroke (Athan, Lee, Arriaga, Mayeux, and Tyco1794).For genotyping, DNA from 1,013 respondents was taken as the panel of neuropsychologists and physicians established the criteria for the identification of AD patients along with the Clinical Dementia Rating Scale (Athan, Lee, Arriaga, Mayeux, and Tyco1794). The oligonucleotide primers used for APP promoter PCR amplification came from GenBank (Athan, Lee, Arriaga, Mayeux, and Tyco1794). From genomic DNAs and by means of Platinum Taq DNA Polymerase, the fragments were amplified while the product sequence was determined through dye terminators (Athan, Lee, Arriaga, Mayeux, and Tyco1794).Meanwhile, 15 microliter of the PCR products was introduced into WAVE fragment DNA analyzer (Athan, Lee, Arriaga, Mayeux, and Tyco1794). The haplotyp es PCR products were individually cloned through pGL3 vector in between SacI and Bg III sites (Athan, Lee, Arriaga, Mayeux, and Tyco1794). On the other hand, U-87 MG glioma cells were cultured with the solution of Earle’s balanced salt and 2 millimolar L-glutamine with 10% fecal calf serum in EMEM medium (Athan, Lee, Arriaga, Mayeux, and Tyco1794).At 70% confluence, the cells were transferred by means of FuGene 6 reagent and pGL3 vectors were added to transfected DNA to maintain a constant concentration of about 1 microgram per plate of 35 squared millimeter (Athan, Lee, Arriaga, Mayeux, and Tyco1794). While the isotonic solution of phosphate-buffered sodium chloride was used to wash the U-87 cells, the 250 microliter Reporter Lysis Buffer was applied for cell lysis (Athan, Lee, Arriaga, Mayeux, and Tyco1794).After this, the centrifugation of the cell extract was done at 10,000 g for five minutes. From the supernatant, 20-microliter aliquot was taken and combined with 100 mic roliter Luciferase Assay Buffer for luciferase activity measurement (Athan, Lee, Arriaga, Mayeux, and Tyco1794). Then, with 10-20 microliters of the lysate ? -galactosidase assays were performed. This ? -galactosidase measurement was utilized for the normalization of the luciferase data (Athan, Lee, Arriaga, Mayeux, and Tyco1794).Each allele was counted and by sample proportion calculation, the frequencies were computed (Athan, Lee, Arriaga, Mayeux, and Tyco1794). For the ethic group comparison of allele frequency, chi square analysis was applied while logistic regression was utilized for APP promoter and AD polymorphisms odd-ratio calculation (Athan, Lee, Arriaga, Mayeux, and Tyco1794). As well, for each ethnic group, logistic regression was employed as the data were classified with respect to the APOE allele’s occurrence or non-occurrence as education and age discrepancies were adjusted.Finally, Hardy-Weinberg equilibrium was analyzed through chi square analysis while the e thnic comparison of APP promoter and AD polymorphisms odd-ratio calculation as their education, age, and sex were adjusted (Athan, Lee, Arriaga, Mayeux, and Tyco1794). Results and Discussion Two types of APP promoter polymorphisms were detected and identified, with respect to the starting site of the transcription, as G>C at +37 and G>C at -9 variants (Athan, Lee, Arriaga, Mayeux, and Tyco1797).In connection to this, +37C allele was typically observed among 18% African-American respondents while European and Caribbean-Hispanic have 3% and 10% respectively (Athan, Lee, Arriaga, Mayeux, and Tyco1797). Although +37C allele was commonly observed among AD patients, the adjustment of their socio-demographic attributes with respect to this allele produced non-significant observations (Athan, Lee, Arriaga, Mayeux, and Tyco1797). Also, -9C allele was hardly detected for disease association.On the other hand, even though the adjustment with respect to socio-demographic traits was made, still a strong link was found between APOE allele and AD (Athan, Lee, Arriaga, Mayeux, and Tyco1797). Moreover, the evaluation of both +37C and -9C allele variants in U-87 glioma cells through promoter-reporter assays has resulted to non-significant promoter activity (Athan, Lee, Arriaga, Mayeux, and Tyco1797). The early onset, less than 60 years old, of AD has been ascribed to APP, PSEN1 and PSEN2 while the late stage, greater than 65 years old, AD development has not yet fully explained by the genetic model (Waring and Rosenberg 329).The development of AD in late age stage was associated with APOE and to other reported genetic variants and alleles, however, they still insufficient to plausibly explain the mechanism involved in the AD occurrence (Waring and Rosenberg 329). Summary Alzheimer ’s disease is a progressive degeneration of the capacity of the mind for cognition thus affecting the psychological and affective attributes of the inflicted individual.Based on genome-wide stu dy, children of parents with familial Alzheimer’s disease are more prone to inherit and develop this condition either as they take progress in their growth and development or at the senescence stage of their lives (Jayadev et. al. 375). The primary pointed culprit for this cognitive deterioration is the beta-amyloid peptide which is a part of amyloid precursor protein. APP passes through the fatty membrane of the cells and delineated in the different areas of the brain, even though, the normal function has not yet been fully known.As APP is attacked by enzymes, fragments are generated including A? -peptide with associated neurotoxicity. Sleegers et. al. in 2006 found the coincidence of cerebral amyloid angiopathy with Alzheimer’s disease in a Dutch multigenerational family. This genomic duplication was attributed solely to APP gene expression that was also observed in 65 Dutch families with early-onset of AD cases. However, APP locus duplication was not observed in 36 AD patients that signified the case of de novo mutation. On the other hand, Athan et. al.in 2002 reported the two types of APP promoter polymorphism which involved +37C and –9C alleles. Moreover, they found a strong link between AD inheritance and the apolipoprotein-E role. In this connection, the genetic traits of every individual should be scientifically scrutinized for an accurate determination and identification of the substance involved in the development of the disease in parallel with its molecular mechanisms. Works Cited Athan, Eleni S. , Lee, Joseph H. , Arriaga, Alex, Mayeux, Richard P. , and Tyco, Benjamin. â€Å"Polymorphism in the Promoter of the Human APP Gene.†Archives of Neurology 59 (2002): 1793-1799. Bloom, Elin. Genetic Studies of Alzheimer’s Disease. Acta Universitatis Upsaliensis. Uppsala, Sweden: Uppsala University, 2008. Felician, Olivier and Sandson, Thomas A. â€Å"The Neurobiology and Pharmacotherapy of Alzheimer’s Disease. â⠂¬ Journal of Neuropsychiatry and Clinical Neurosciences 11, 1 (1999): 19-31. Jayadev, Suman, Steinbart, Ellen J. , Chi, Yueh-Yun, Kukull, Walter A. , Schellenberg, Gerard D. and Bird, Thomas D. â€Å"Conjugal Alzheimer Disease. †Archives of Neurology 65, 3 (2008): 373-378.
Thursday, November 7, 2019
Guilded Age Essays - Economic Ideologies, Andrew Carnegie
Guilded Age Essays - Economic Ideologies, Andrew Carnegie Guilded Age There are many different views on whether or not business should be regulated during the Guilded Age. The rich who controlled the government at the time were against any kind of regulation of business. They wanted one hundred percent capitalism. The workers on the other hand wanted the business to be regulated, and the legalization of unions. I am going to support the ideas of the business owners. There were many wealthy business owners who believed in the gospel of wealth. This was the idea that God made the rich rich and the poor poor. This was a common thought process of the Guilded Age. Andrew Carnegie was a major follower of this thought. This is shown in his speech Wealth. In this speech he says that rich and poor are necessary for the race. It also describes how it is survival of the fittest. The ideas of the gospel of wealth are a scary concept today. If you look at it with a revisionist viewpoint the idea that rich are rich because God said so leaves us open for so much discrimination. The thoughts of this time were not able to see this, and the business owners wanted to keep the power in their hands. Document E also has a touch gospel of wealth in it. It talks about a preacher telling his parishioners to go out and make money. It says that it is the persons job to go out and become rich. It also talks about how the rich are the most honest of all people. That because they have money you are the least likely to lie because you dont have too. Many people of the era said that the money would be there even if the rich werent there, but Document G contradicts this idea. It says that the money is there because of the rich, along with the money that other people have. So the thoughts of the era by the rich tells point towards no regulation. The gospel of wealth was a main reason that the owners were able to keep the regulations from coming about. Without the big business of the Guilded Age we might not have developed into the superpower we did in this century.
Tuesday, November 5, 2019
Pell Grant Limits How Much Can You Get in Your Lifetime
Pell Grant Limits How Much Can You Get in Your Lifetime SAT / ACT Prep Online Guides and Tips Federal Pell Grants are great resources for students who could use more help paying for school. Like all good things, though, there are some restrictions and rules around how you can use a Pell Grant. In this post, I'll explain: Exactly how much you can get from your Pell Grant Eligibility restrictions Limits on how you can use Pell Grant money Financial Limits: What's the Most You Can Get? As you may have expected, there is a maximum annual Pell Grant award amount ("What is the Pell Grant Amount? What is the Maximum Award?"). For the 2015-2016 academic year, the most you could receive if you're a full-time student is $5775.What you might not have expected is that there is also a minimum Pell Grant award amount: again for the 2015-2016 academic year, the least you could receive if you're awarded the grant is $600. In addition to annual maximum and minimum award amount,there's also a lifetime award maximum. Every year that you apply for the Pell Grant via the FAFSA(see "How to Submit a Pell Grant Application,"coming soon), you'll be eligible for a particular amount of money. Your lifetime maximum is equal to600% of your yearly eligibility, or about 6 years' worth of grant funding. Let's go over some examples to further explain what I mean: Student A Applies for the Pell Grant for her freshman year, and is eligible to receive$5,000 in funding. She only attends school in the fall semester, though, so she only has to pay for half a year of school. As a result, she only gets $2,500, or 50%, of the annual grant money that she was eligible for. Student A can apply for the Pell Grant the next year, and she still has 550% of her lifetime max (600%) available to her. Student B Wasn't eligible for the Pell Grant his freshman, sophomore, or junior year. His family's financial situation changes his senior year when he applies for the grant, and he is glad to find out he's eligible for $1,000 in funding. All of that money goes towards paying his tuition. Student B used 100% of the annual grant money that he was eligible for, so he has 500% of his lifetime max (600%) available to him. Student B graduates at the end of his senior year; even though he didn't meet his lifetime max, he's not eligible for the Pell Grant anymore because he received his bachelor's degree. You might have noticed that this lifetime limit seems a little high. If you go to school for your bachelor's degree, it should only take you 4 years, or 400% of your lifetimemax; unless there are special circumstances that prevent you from graduating within 4 years, you likelywon't have to worry about this lifetimelimit. The more you know about financial aid, the more you can talk yourself out of feeling like this. Eligibility Restrictions Along with the financial limits above, there are also eligibility restrictions that can disqualify you from getting a Pell Grant. I've broken this section up into two main parts: family financial eligibility, and student eligibility. What about family income limits for Pell Grant eligibility? So there are family financial limits for eligibility, but they're a bit more complicated than an arbitrary income cutoff. Eligibility limits for the Pell Grant are based on your family's Expected Family Contribution (EFC).Your EFC is generated when you submit your FAFSA ("How to Submit a Pell Grant Application," coming soon). If you want to estimate your EFC before you go through all the trouble of submitting your FAFSA, you can get more information here ("What is the Pell Grant Amount? What is the Maximum Award?" coming soon). If your EFC is at or below $5081 for the 2015-2016 academic year, you will bewithin the family income limits for the Pell Grant. If you meet all the other eligibility requirements, you will receive some grant money (so, between $600-$5775). By using your EFC, you can estimate about how much Pell Grant money you may be eligible for ("Pell Grant Calculator" coming soon). Are there restrictions on what type of student can get the Pell Grant? The short answer is: yes. You can read more about eligibility criteria for the Pell Grant here ("Pell Grant Eligibility and Requirements: Do you qualify?" coming soon). In a nutshell, the Pell Grant is meant primarily for low-income students who have a high school diploma or GED, but don't have a post-secondary degree (so, a bachelor's or vocational degree). If you don't demonstrate enough financial need, or if you already have a post-secondary degree, you likely won't qualify. There is no age limit to receive the Pell Grant. It's open to people who need help funding their education at any age. Limits to using your Pell Grant money There are two logistical parameters you should be aware of if you would like to apply for a Pell Grant: there are restrictions on where and how you can spend your Pell Grant money. Where You Spend Your Pell Grant When you apply to colleges or to vocational programs, make sure they participate in the Pell Grant program. The good news is that most legitimate colleges participate; if you want to confirm, simply call the financial aid office. How to Spend Your Pell Grant In many cases,the grant money won't even be paid directly to you; it will go straight to your school. Your school will then apply the grant money to charges on your account (e.g.tuition, room, and board charges). There may be differences in how schools process federal financial aid, though, so you can contact your financial aid office if you have further questions. In some circumstances, there may be leftover grant money after your schoolpays itself. If there is leftover money, it will be passed on to you in the form of a refund. There are restrictions on how you can use this refund money.It's meant to cover school-related expenses, including: Books Lab supplies Transportation expenses (including gas or a bus pass, but NOT includinga car) Even food! These usage restrictions are pretty serious because the Pell Grant is a federally funded program. Even though it may be tempting to use refund money for, shall we say, more fun activities, be careful about using it for legitimate expenses. Perfectly sharpened colored pencils definitely count as legitimate school supplies. One Final Note About Pell Grant Limits ... If you're awarded the Pell Grant, it's super important that you stay on top of maintaining your academic performance in college. If your academic performance is deemed "unsatisfactory" (e.g. if you are failing out of your classes), you may lose eligibility for any type of federal aid, including the Pell Grant. If you're concerned that your grades are slipping and you may lose eligibility, the best thing to do is to set up a meeting with a school administrator, like your dean. What's next? The Pell Grant isn't the only source of financial aid for aspiring college grads. If you get awesome SAT scores, you could also get awesome scholarship money. Too late to bring up your SAT scores? No problem! By doing well in school, you could help yourself pay your way through. It's a win-win! Want to improve your SAT score by 160 points or your ACT score by 4 points? We've written a guide for each test about the top 5 strategies you must be using to have a shot at improving your score. Download it for free now:
Saturday, November 2, 2019
Delicate transactions Essay Example | Topics and Well Written Essays - 500 words
Delicate transactions - Essay Example In the present world scenario utmost importance is given to human rights. Under United Nations resolution human rights to every citizen of every country should be considered as an important factor. It's every country's responsibility to protect its citizen's basic human rights. Human rights violation should be considered as a serious offence, legal and appropriate action should be taken against those who violate these rights. In 1948 some states signed Universal Declaration of Human Rights. According to this men and women have equal rights but ironically none of the states that signed haven't provided any equal rights to women. Racial abuse is a serious offence and should be dealt with serious punishments.In US the Hispanics are the largest immigrants. They migrated from the neighboring country Mexico And other Latin countries. Since these countries were not as developed as US and their socio-economic structure was on decline, many of the citizens were forced to migrate to US. In US, Hispanic immigrants have less education and less skill set, even among Hispanic women also. Apart from other groups these Hispanics have less human capital, so they have very less employers in their group and it is indirectly affecting their economic status and social environment also.Gender inequality was always prevailed among the Hispanics. Since they were not the major community and further more they were immigrants, they had to face the brunt of racial abuse. One of the reasons of racial abuse was, fear among the US citizens was losing the jobs to these immigrants.
Subscribe to:
Posts (Atom)