Franz Joseph Haydn The Founder And Developer Of The...

The 18th Century composer, Franz Joseph Haydn, was arguably the founder and developer of the formal and structural principles of classical style. His work included hundreds of symphonies, string quartets, and instrumental sonatas. Haydn’s innovation and style created a model for many composers after him. FOUNDATIONS On March 31, 1732, Franz Joseph Haydn was born in the charming village of Rohrau, Lower Austria which is on the Hungarian border. Joseph, called Sepperl by his German parents, was born a peasant boy. Haydn’s father helped the village head to build and repair wooden wheels. His mother worked as a cook in the Palace of Count Harrach before she married. Remarkably, neither of Haydn’s parents could read music, but his father was a self-taught harpist. Hadyn’s father and mother had 12 children. Anna Maria died in 1754 and Mathias remarried and had five more children, all of whom died in childhood. Luckily, Haydn’s parents recognized and supported his talent for music. At age five, he became the music students of a schoolmaster at Hainburg, Johann Matthais Frankh. At 8 years old, he worked at the Cathedral of St. Stephen s in Vienna as a choirboy. By 1749 his voice had changed and he was no longer able to sing high choral parts. When Haydn played a joke on a f ellow classmate by cutting off her ponytail, he was met with a severe lashing and dismissal from school. After being dismissed, Haydn had no place to stay, and his family could not help him financially.Show MoreRelatedThe Austrian Composer : Franz Of The Formal And Structural Principles Of Classical Style1259 Words   |  6 PagesThe Austrian composer Franz Joseph Haydn (1732-1809) was arguably the founder and developer of the formal and structural principles of classical style. His work included hundreds of symphonies, string quartets, and instrumental sonatas. Haydn was an innovator and many composers after him, modeled his style. FOUNDATIONS On March 31, 1732, Franz Joseph Haydn was born in the charming village of Rohrau, Lower Austria which is on the Hungarian border. Joseph, called Sepperl by his German parents, was

Factors Affecting Successful ERP Implementation

Question: Read the case study Using a Case Study to test the three key social enablers in ERP implementation.The key findings are shallow clichs. They are: Strong and committed leadership at the top level Open and honest communication Balanced and empowered teams Do some research on ERP implementation. Identify other factors which may account for the success of ERP implementation. Discuss the factors you have identified and explain why they are more reliable than the clichs in the original article. In other words Compare other research articles with the 3 points (shallow clichs mentioned in the case). Why they are better factors than the points mentioned in the case? Answer: Introduction The systems of Enterprise Resource Planning may well be accounted as the most relevant development within the corporate utilization of information technology. The implementation of ERP are mostly complex and large projects that involve groups of large size with a number of resources, who work together within considerable pressure of time and face a number of unforeseen developments(Calaway 2000). The case provided has three key findings that are shallow clichs. In comparison with the three key findings identified, this report will be identifying other factors that may have the accountability towards the successful implementation of ERP System. Factors affecting ERP Implementation Based on the case study provided, the key findings have been found are shallow clichs. These shallow clichs are committed and strong leadership at the top- most level, honest and open communication, and empowered and balanced teams. These particular items contribute in disclosing the biases of the researchers, and will be doing little assistance in order to understand the success of ERP projects. Apart from these factors, it is important to understand that there are other factors that affect the success of the ERP Implementation as well(Godla 2009). Some of these factors include good management of project, appropriate vision and plan of business, appropriate systems of legacy and business, and culture and program for the management of change. Further ahead in this report, these factors will be discussed in a way stating that these are better factors affecting the success of ERP Implementation. Culture and Program for the Management of Change Management of change is relevant, to start at the phase of project and continuously in the entire cycle of life. Change in the structure and culture across the enterprise should and has to be managed in an appropriate manner. These include the change amongst culture, organization and people (Calaway 2000). This is extremely important as if appropriate management of change is not done then there will be a major impact over the future smooth functioning of the business. Appropriate systems of legacy and business Appropriate systems of law and business are relevant within the initial phase of chartering the project. A successful and stable setting of business is important. The systems of IT and business involving the present processes of business, structure of organization, information technology and culture affect the success of ERP Implementation (Swanson 2007). This is important as it helps in determining the change in the organization and IT needed for the appropriate level of success. Hence, it can be argued that success within other areas of business is important for the success in implementation of ERP. Good Project Management Good management of project is important. A single person or a group of individuals should be holding the responsibility for driving the level of success within the management of project. Firstly, it is important for establishing and controlling the scope in a significant manner. There must be clarity in defining the scope and be restricted as well. This should be including the value for the implementation of systems, units of business being involved, and value of the need to reengineer the process of business (Davenport 2007). There is an increased need for evaluating the appropriate changes being proposed against the benefits of the business, and the implementation being done at the phase later to come. In addition to this, there is an increased need for assessing the requests for the expansion of scope with respect to the extra duration of time and amount of cost related to the changes being proposed. Appropriate Vision and Plan for Business Clarity in the vision and plan of the business for steering the need of directing the projects in the entire life cycle of ERP. A plan of business that outlines the strategy being proposed and the tangible advantages, timeline, risks, costs and resources is crucial. This will be extremely helpful for focusing on the benefits of the business. The model of business should be having clarity with respect to the fact as to how the operations of organization can be conducted by the effort of implementation (Gibson 2009). There is an increased need for justifying the investment being made on the basis of an issue and the change directly related to directing the organization. The mission of project should be in relation with the needs of business and there must be clarity in stating it. Expectations from the System of ERP Clarity in the objectives of management and the level of expectations from the system of ERP should be clearly expressed with the vendors. This results in believing the fact that the power of system for the integration of the actual functions of the business. In accordance with the vendor, expectation of management for availing return on investment quickly which might not have been practically appropriate for noticing any specifically significant return on investment. In context with these factors, it can be stated that apart from the shallow clichs, it is extremely important for considering the other factors of ERP implementation as well, because these affect the success in a significant manner (Godla 2009). Apart from the three clichs, the above stated factors help in ensuring effective implementation of ERP and helps to realize the promised benefits. However, the three clichs do provide the same advantages but the benefits being realized cannot be considered as being extremely and accurately promising. However, support from the top most management has to be considered as the most important factors of all. Hence, it can be stated that the implementation of ERP should be done in alignment with the each and every factor stated above and the related clichs involved. Conclusion Based on the case study provided, the key findings have been found are shallow clichs. These shallow clichs are committed and strong leadership at the top- most level, honest and open communication, and empowered and balanced teams. In context with these factors, it can be stated that apart from the shallow clichs, it is extremely important for considering the other factors of ERP implementation as well, as these affect the success in a significant manner (Swanson 2007).Some of these factors include good management of project, appropriate vision and plan of business, appropriate systems of legacy and business, and culture and program for the management of change. References Calaway, E. 2000.Enterprise Resource Planning Integrating Application and Business Processes Across the Enterprise. Computer Technology Research Corporation, Charleston, SC. Davenport, T.H. 2007. Puting the enterprise into the enterprise system. Harvard Business Review, pp. 121-31. Gibson, N. 2009. A critical success factors model for enterprise resource planning implementation,Proceedings of the 7th European Conference on Information Systems, 1, pp. 273-97. Godla, J. 2009. Critical issues affecting an ERP implementation. Information Systems Management, pp. 7-14. Nemec, J. 2008. Making ERP succeed: turning fear into promise. IEEE Engineering Management Review, pp. 116-23. Swanson, D. 2007. A recipe for ERP success. Beyond Computing, pp. 44-5.

East of Eden free essay sample

East of Eden deplores many religious matters, specifically, the concepts of sibling rivalry and the age old battle between good and evil. In the biblical Book of Genesis, the brothers Cain and Abel offer God the father a sacrifice. God favors the shepherd Abels sacrifice of his best lamb over the farmer Cains grain. Subsequently, in a Jealous rage, Cain kills his brother Abel, only to be marked by God and banished to wander the earth. Stanford dropout, John Steinbeck applies the story of Genesis heavily in East of Eden; the concepts of this iblical allusion are evident in both generations of brothers. In each generation, one of the Trask brothers is moral and good while the other brother behaves badly and immorally, already we see how the Trask family parallels Genesis. Because the good Trask brothers are favored, the bad Trask brothers develop envious tendencies and a recurrent theme of sibling rivalry appears throughout the book. We will write a custom essay sample on East of Eden or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page The first generation of Trask brothers, Charles and Adam, follow the Cain and Abel biblical model from the very beginning. .. its awful not to be loved. Its the worst thing in the world t makes you mean, and violent, and cruel. (Steinbeck 347). This quote epitomizes the root of all evil in the Trask generations- lack of recognition to one of the sons. When their deadbeat father Cyrus favors Adams birthday gift of a puppy over Charles expensive knife, Charles nearly beats Adam to death. Although Charles does not kill Adam, he is a clear allusion to Cain. While Adam wanders the Earth in the army, it is Charles who remains on the farm, where like Cain, he becomes marked with a dark brown scar. Adam therefor, is reflected as Abel. Humans are caught†in their lives, in their thoughts, in their hungers and ambitions, in their avarice and cruelty, and in their kindness and generosity too†in a net of good and evil. (127). This quote is a clear representation of the Adam and Charles relationship throughout the novel. The incident that occurred over a simple birthday gift sparked a Jealous rage that caused Charles and Adam to remain at odds with each other throughout their entire lives despite their love for each other. The next generation of Trask brothers, the dark haired Cal and fair-haired Aaron, also carry out the dynamics of the Cain and Abel tale. Cals Jealousy towards Aron is due to the favoritism that Aron receives from their father Adam; this is especially seen through an episode that resulted in Aarons death. For some reason, Adam favors Aron over Cal and when Cal offers his father a birthday present of $1 5,000 to help him recover his financial losses, Adam scorns him for making the money during a war-time economy. In a rage, Cal takes his brother to isit the notorious prostitute that birthed the two boys. Emotionally traumatized, Aaron runs away to the army during World War l, and dies soon after. Cal lies to Adam when asked about Aarons whereabouts. Where is he? How do I know? said Cal. Am I supposed to look after him? (p. 562). This sequence between Cal and Adam portrays the emotional barrier between the two that seems to bring out the untruthfulness in Cal that reflects his ancient parallel, Cain. Thus, the biblical tale plays out with Cal, although inadvertently, killing his brother. It might be the most important word in the world. That says the way is open. That throws it right back on a the concept of timshel. While psychologically shattered Adam reminisces over Cathy, Lee and Samuel share philosophical discussions over the ancient Hebrew word timshel. Timshel defies the pattern in the Cain and Abel tale, rather than condemning the less favored brother to a life of sin it pursues the issue of free will and grants Cal the strength to depart from the inherently bound evil motives that ossessed him at an early age. East of Eden free essay sample This paper is an analysis and review of the many topics that are presented in John Steinbecks book, East of Eden. This paper is a detailed examination of the different themes that John Steinbeck raises in his book, East of Eden. The author discusses the significance of the storys setting and the different family themes that are dealt with throughout the story as the many different family members history are detailed. The author breaks down the individual characters, their symbolism and relevance to the continuity of the family saga. As life progresses for the three men, all three separate themselves, which brings a peace treaty of sorts. My sympathies are still toward Adam, who deals with the emotional problems he has gotten from his childhood. Charles has turned into a more likeable person, and the evil that was once so dominant in him has almost disappeared by the time the brothers are reunited in chapter seven. We will write a custom essay sample on East of Eden or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page The evil has died with Cyrus, and the interaction between the two brothers reflects that. I almost breathed a sigh of relief when Cyrus is finally dead, but it is amazing how quickly fate takes over the story again, and how Steinbeck weaves a new loop into the story.

Taxation Law Question free essay sample

Part 2Advise Crowbar Ltd as to which value of closing stock it should choose at 30 June 2010 on the basis that the company wishes to minimise its taxable income. Would your answer be different if Crowbar Ltd had carry-forward losses from a prior income year? Part 3 What difference would it make to your answer if Crowbar Ltd had an average annual turnover over the previous 4 years of $800,000? Part 1: As Crowbar Ltd has remaining stock on hand at the year-end, it is necessary for the company to take into account any unsold trading stock which is held by the taxpayer at the time as stated under Section 70-35 of ITAA 1997. Trading stock provisions allow a deduction for the cost of stock that is actually sold. Under Section 70-35(2), ITAA97, where the value of the closing stock at the end of the year exceeds the value of the opening stock at the beginning of the year, the difference is assessable income. We will write a custom essay sample on Taxation Law Question or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page Furthermore under s70-35(3), where the value of the opening stock exceeds the value of the closing stock, the difference is a deduction. Part 2: It is in the best interest for Crowbar to select a method of stock valuation that minimises its taxable income. Under Section 70-45(1), ITAA (1997) 31(1), the taxpayer has the option to value trading stock on hand at the end of the year either cost price, market selling value, replacement price or as stated under s70-50, ITAA (1997) {31(2)}, a lower value in special circumstances if commissioner is satisfied. Crowbar Ltd Unit of StockValuation MethodLowest Cost ($) ACost Price$10,000 BMarket Selling Value$2,000 CReplacement Price$7,000 Total$19,000 Opening Stock Unit A + B + C -$48,000 Stock Value-$19,000 Claim Deductions $29,000 If Crowbar Ltd had carry-forward losses from a prior income year: In this situation, it is advisable for Crowbar Ltd to maximise the value of its closing stock. For companies with carry-forward losses, it can offset those losses against its income for the current year. Crowbar Ltd (with Carry-Forward Losses) Unit of StockValuation MethodLowest Cost ($) AMarket Selling Value$14,000 BCost Price$10,000 CMarket Selling Value$18,000 Total$42,000 Part 3 What difference does it make to your answer if Crowbar Ltd had an average annual turnover over the previous 4 years of $800000? An entity that is carrying on a business that has an annual turnover of less than $2 million s328-110 of ITAA 1997 is considered a small business entity therefore it shows that Crowbar Ltd is a small business entity as it has an average annual turnover of $800000 in the 4 previous years. This leads to meeting the criteria under Section 328-285(1) where you can choose not to account for changes in the value of your trading stock for an income year and the difference between the value of your trading stock on hand at the start of an income year and the reasonably estimated value at the end of the income year is not more than $5,000. Crowbar Ltd can choose replacement cost at end of the year, which is 11,000 + 3,000 + 7,000 = 21000. The difference between opening which is $48,000 and end which is $21,000 is $27,000 which more than 5,000. Therefore Crowbar Ltd needs to: * Value each item of trading stock on hand at the end of the income year, or * Â  Account for any change in the value of trading stock on hand. * If a SBE taxpayer chooses to account for changes in the value of trading stock for an income year, the taxpayer will have to do a stocktake and account for changes in the value of trading stock.

Writing a Sample Extended Response Essay For the GED

Writing a Sample Extended Response Essay For the GEDWriting a sample extended response essay for the General Education Diploma or GED is usually a very simple process. A lot of schools will also supply you with an essay sample and so it should be the same.For many students, the written work is too much and they require some guidance in the form of a sample response essay. The sample is not meant to imitate someone you see in a magazine and on television, but rather a sample extension response essay for the GED test. Students want a response that is unique to them.The sample essay should be representative of your personality and the style you are best at writing. It must be interesting and reflective. The use of statistics, concrete examples and generalizing examples are all helpful in making your responses compelling. Your final written work must not be littered with adverbs and excessive use of nouns.In preparing for the GED essay exam your chosen choice of writing sample will be an extension of the writing style you choose for your other writing assignments. This essay writing sample will serve as a mirror to reflect back on to help you get an understanding of your own writing and style. Not only will this enable you to prepare a much better response but you will also be able to keep the consistency of your writing from one course to the next.Most students don't consider using a sample essay for their GED test because they fear they may look boring or repetitive. This can happen, but you can avoid it. Many students don't find anything about their writing odd or repetitive and this will help you avoid this common issue.When you select your essay writing sample, make sure it is easy to read and also easy to understand. Because many students have trouble reading long essays, most writing samples are shorter and will accommodate this. It doesn't make sense to write an essay on the Moon landing if you have never been to the moon and don't know if the moon exists.U sing your essay writing sample will give you a firm base for the beginning of your response essay. It will help you improve your writing and also helps you identify your writing style. This is a very powerful tool that will help you if you need to improve your essay writing to pass your test.You can prepare for this test by using a sample response, which makes it easier for you to learn how to write a response essay on your own. It's a great idea to use a sample of another student's response, or take a class for it.

Pathogenesis of measles virus infection The WritePass Journal

Pathogenesis of measles virus infection Introduction Pathogenesis of measles virus infection IntroductionSymptomsVaccinationSubacute Sclerosing Panencephalitis  ConclusionRelated Introduction Often dismissed in the developed world as a common childhood infection, measles are in fact a worrying contributor to childhood morbidity and mortality worldwide. In the UK alone, approximately 10% of cases result in complications requiring hospitalisation, 1 in 5,000 could be fatal [1]. This is much higher for the developing world where infection spreads rapidly in children that are living in close quarters, are malnourished and unable to avail of the vaccine. In 1994, under the national schools vaccination campaign all school children aged 5-16 were offered the mumps-measles-rubella (MMR) vaccine. An uptake of 92% under this campaign resulted in measles being all but eradicated from England and Wales [2]. Unfortunately a fall in immunisation uptake over the last decade, amid fears of a link between MMR vaccine and autism, now means that the number of susceptible children is such that measles are once again endemic in the UK [3]. Epidemics are prevalent throughout European countries including Italy, Austria Switzerland. Controlling a measles epidemic can be difficult, despite the availability of a safe and effective vaccine, as it is a highly infectious disease that spreads rapidly between susceptible individuals. Infection Spread The measles virus (MV) is single stranded RNA Morbillivirus from the paramyxovirus family that results in an acute infection of respiratory and lymphoid tissues. It is a highly contagious disease transmissible via respiratory droplets that can remain viral on surfaces for up to two hours [1]. Although it’s spread via the respiratory route and symptoms are well established little is actually known of the cellular events underlying the disease. Figure 1: Schematic diagram of measles structure [4] To better understand the process of infection and spread we must take a closer look at the measles virus (MV). MV is single negative-strand enveloped RNA Morbillivirus that contains 15,894 base pairs encoding 8 proteins. As shown in figure 1 hemagglutinin (H) and fusion (F) proteins are transmembrane envelope proteins and as such their primary role is to initiate infection. Antibodies to these proteins may render the virus inactive [4].   The RNA genome is encapsidated by the nucleotide (N) protein forming a ribonucleocapsid complex which acts as the substrate for transcription and regulation [5]. The large protein (L) and phosphoprotein (P) are also associated with the ribonucleocapsid complex and hence replication and transcription.   The matrix protein (M) links the ribonucleocapsid complex to the envelope proteins during virus assembly [6]. There are also two non-structural proteins, C V encoded within the P gene that act as regulators of infection by interacting with cellul ar proteins. As previously mentioned binding of H to susceptible cells is an important instigating step in measles pathogenesis. Three viral receptors for H are identifiable, CD46 a low affinity protein present on all nucleated cells, an undetermined receptor on epithelial cells and SLAM / CD150, a high affinity receptor present on subsets of lymphocytes, thymocytes, macrophages and mature dendritic cells (DCs). SLAM/CD150 is the preferential receptor for wild type strains of MV. Initially it was thought that MV infected respiratory epithelial cells which would in turn infect monocytes resulting in spread of infection to lymphoid tissues. However, this has been found not to be the case as monocytes only express CD46 low affinity receptors. Since then it has been demonstrated in vivo that lymphocytes expressing CD150 recpetors are the primary infected cells during measles in macaques [7]. However lymphocytes are not commonly found at respiratory epithelial cell surfaces hence MV target cells at transmission and throughout pathogenesis of MV are unclear. It is thought that professional antigen presenting cells (APCs) known as dendritic cells may have a dual role in mediating transmission of the measles virus [8]. Although the expected role of DCs is to capture and present MV antigens for degradation, some escape degradation and are actually protected by DCs for transportation to lymphoid tissues. Here they encounter and infect CD150+ lymphocytes allowing replication of the virus. From the primary lymphoid tissue, infected cells enter circulation. Infected peripheral blood mononuclear cells (PBMCs) are evident in the blood 7-9 days after infection [9].   From here the infection spreads to distal lymphoid tissues and to the epithelial and endothelial cells of multiple organs. Less is known about receptors used to infect these cells. There is however a number of cell surface molecules that interact with MV and as such may play an important role in MV pathogenesis, including receptor clustering, fusion, entry, cell-to-cell spread or cytokine production.   These include DC-SIGN, Toll like receptor 2 (TRL2), neurokinin-1 and Fc-ÃŽ ³ receptor II. DC-SIGN (C-type lectin dendritic cell-specific ICAM-3 grabbing non-integrin) for example is credited with binding of MV to DCs. The role of which has been previously described for HIV1 [10] and has been demonstrated in MV infected macaques [7].   TRL2 interacts with H envelope protein to induce interleukin-6 (IL-6) wh ich in turn stimulates the expression of CD150. TLR2 interaction with CD46 also inhibits IL-12 production. Symptoms Measles typically have an incubation period of 7-14 days. During the prodrome period of day 4-7 characteristic clinical symptoms of measles appear which include fever (often 104 °F), cough, conjunctivitis and photophobia. Koplik spots, which are white buccal opposite the first and second upper molars, appear 2-3 days later followed by the maculopapular rash that lasts on average of 3-5 days [11] The rash is a manifestation of the adaptive immune response, and marks the start of viral clearance. Activated T cells and MV specific antibodies are present in circulation at this time and CD4+ and CD8+ cells have infiltrated sites of virus replication. Immunocompetent individuals will be successful in clearing the virus from these sites of replication and confer life long immunity to re-infection. Interestingly, MV appears to have a contradictory effect on the immune system with acute infections predominantly linked to periods of transient immunosuppression, often lasting weeks after the disappearance of characteristic symptoms [8]. It is these periods of immunosuppression that leaves an individual susceptible to many associated secondary complications and ultimately MV related deaths. The risk of complications may increase in densely populated areas, in children infected under the age of two, pregnant women, malnourished individuals particularly those lacking in vitamin A and in individuals who have existing immunodeficiency. Complications include respiratory complications such as bronchopneumonia and giant cell pneumonitis, neurological complications such as acute demyelinating encephalitis, subacute sclerosing panencephalitis and measles inclusion body encephalitis, gastrointestinal complications like diarrhoea or clinical hepatitis and vitamin A deficiency which may manife st as xerophthalmia a leading cause of blindness worldwide [1]. The mechanisms that result in immunosuppression are not clearly understood but a number of methods are hypothesised. For example, there is noted decrease in the numbers of T cells and B cells during the rash which for the most part is attributed to an increase in CD95 mediated and lymphocyte apoptosis [9]. This may contribute to lymphopenia, however lymphocyte numbers generally return to normal as the rash clears. It is also thought that suppression of lymphocyte proliferation may be associated with G1 arrest of the cell cycle after infection with MV [12].   Similarly T-cell proliferation may be suppressed as a result of direct inhibitory signalling by the H and F1-F2 membrane viral complex which when in contact with a cell will delay S phase entry of T cells by several days leading to accumulation of cells in the G0-G1 cell cycle phase [9]. Yet another mechanism of immune suppression is type 2 skewing of CD4+ T-cells. During infection of APCs with MV there is marked decrease in production of IL-12, which plays an important role in T-cell production of type 1 cytokines [12]. Altered CD4+T production leads T cells that fail to proliferate. Immunosuppression is characterised by lymphopenia, defective response to new antigens and a loss in the delayed type hypersensitivity responses to recall antigens. Vaccination A combined live attenuated mumps, measles and rubella (MMR) vaccine is the vaccine of choice against measles in more the 90 different countries worldwide. [13] Since its introduction in the 1970s the MMR vaccine has proven its capability to eliminate its target diseases from a number of countries. Following a national vaccination programme it was reported in 1996 that measles had all but been eradicated from the UK [2]. The US had similar success prior to this in 1993 [13] as did many other countries. Numerous strains of the MMR vaccine are produced worldwide, many of which are derived from the Edmonston strain [14]. Four non Edmonston strains including Leningrad 16, Shanghai-191, CAM-70 and TD-97 are also in use [13]. The virus is generally cultured in chick embryo cells. Most vaccines also include a small dose of antibiotic. A number of combinations of these virus, mumps virus and rubella virus are used to produce a commercial MMR vaccine. There are five commonly used MMR vaccines on the market today including M-M-R by Merck, Morupar by Chiran, Priorix by Glaxo-Smith Klein, Trimovax by Pasteur Merieux Serums and Triviraten Berna. Current US guidelines regarding vaccination with MMR recommend first dose at 12 months and a second dose to be administered before the age of 4, leaving at least 28 days between doses [15]. One dose and two dose vaccination strategies have been tried and tested in many countries [16, 17]. Although one dose strategies may achieve as much as 85% efficacy a second dose is essential to achieve eradication. Unfortunately erroneous claims linking the MMR vaccine to autism and Crohn’s disease have led to a decline in uptake of MMR vaccine and as a result countries like the US, Germany, Austria and Italy are once again facing a measles epidemic [18]. Subacute Sclerosing Panencephalitis Subacute sclerosing panencephalitis (SSPE) is an incurable complication of measles virus that presents itself 1-15years following acute MV infection [1]. It is most common in boys who under the age of two become infected with MV and is a far less common when MV infection occurs in adulthood [12]. SSPE occurs at the rate of 10,000-300,000 in acute MV infections. A disease affecting the central nervous system (CNS), SSPE initially presents as subtle cognitive changes, progressing to overt cognitive dysfunction, motor dysfunction, seizures, organ failure and eventual death. Neurons are initially targeted but as the disease progresses infected oligodendrocytes, astrocytes and endothelial cells have also been noted. Histologically it is characterised by cellular inclusion bodies, loss of neurons, inflammation, glial activation and deterioration of the blood brain barrier [12]. High numbers of MV specific antibodies are found in both blood and cerebrospinal fluid of SSPE patients.   Conclusion Little is actually known of how MV may cause SSPE and other associated MV complications. Early studies using brain biopsies of SSPE patients did however show that infected neurons were unable to release budding virus. Since then extensive sequencing of such cells have lead to the conclusion that point mutations of envelope associated genes, namely as H, M, and F, could result in defective protein expression and therefore do not allow infected neurons to complete the viral process [19]. How this impacts on the development of SSPE is unclear. Pathogenesis of measles virus infection Introduction Pathogenesis of measles virus infection IntroductionInfection1. Attachment2. Fusion3. RNA replication and Assembly of viral particles4. Release of virusSpread1. Changes in lymphocyte number and function2. Shift in cytokine profile3. Impaired antigen presentationSymptomsImmunosuppressionVaccinationSubacute sclerosing panencephalitis (SSPE)BibliographyRelated Introduction Measles is a highly contagious disease caused by an enveloped RNA virus of the genus Morbillivirus in the family of Paramyxoviridae (Griffin et al, 1994). It is a major cause of child morbidity and mortality, particularly in developing countries, despite the introduction of attenuated measles virus vaccines which have greatly reduced the incidences since the 1960s (WHO, 2009). The window period of infection for infants lies between the disappearing maternal antibody protection and vaccine administration (Manchester and Rall, 2001). In 2008, 164,000 measles deaths were reported and majority was children under five years old (WHO, 2009). Affected individuals combat measles by generating cell mediated immunity to clear the virus and humoral immunity to provide long-term protection (Manchester and Rall, 2001). However, measles virus (MV) induces immunosuppression during infection and for weeks after recovery, rendering infected individuals susceptible to secondary infections (Griffin et al, 1994). The evidence of immunosuppression caused was first recognized in 1908 when von Pirquet reported that children lost positive skin test for tuberculin antigen during MV infection (von Pirquet, 1908). Research has been carried in vitro and in vivo in order to define the pathogenesis pathways of MV. Immune responses to MV have been described on transgenic mice and cynomolgus monkeys models (Sato et al, 2007) suggesting that multiple potential mechanisms are linked to the virus-induced immunosuppression (Schneider-Schaulies et al, 2002). Infection Measles is transmitted via airborne exposure from coughing and sneezing or close contact with nasal and throat secretions. MV remains active in the air for up to two hours. It enters the body through the respiratory system and spread systemically by infecting lymphoid cells. Infection and spread is a complex process. The structure and proteins of MV are important determinants of virus tropism and pathogenesis (Yanagi et al, 2006). Measles virus consists of a non-segmented single negative-strand RNA genome (16,000 ribonucleotides) with a diameter of 150 to 300 nm. The outer envelope comprises with the inner matrix protein to form a lipid bilayer surrounding the viral genome. It encodes six structural proteins and two nonstructural proteins which are important for attachment of the virus to the host, replication and spreading of the virus in the body (Horikami et al, 1995). Table 1 briefly describes the functions and locations of structural components and Figure 1 illustrates the structure of a measles virus. Table 1: Locations and functions of Measles virus structural proteins Structural proteins    Locations Functions 1. Haemagglutinin(H) Both H and F proteins are surface transmembrane glycoproteins. They project from the lipid bilayer and traverse the internal matrix. Responsible for the initiation of infection. H protein: receptor binding and cell fusion F protein: cell fusion and viral entry. 2. Fusion proteins (F) 3. Nucleoprotein (N) Surround the RNA strand Form a ribonucleocapsid. 4. Phosphoprotein (P) Both P and L proteins are associated with the ribonucleocapsid The ribonucleoprotein complex acts as RNA polymerase and is responsible for RNA replication and transcription. 5. Large polymerase protein (L) 6. Matrix protein (M) Attaches to the inner surface of the envelope Assembly of the viral particles. Virus budding. Adapted from (Yanagi et al, 2006) The nonstructural protein C and V are encoded on the P gene by RNA editing and alternative translation. Patterson et al (2000) showed that C and V proteins functioned as virulence factors in CNS measles infection using YAC-CD46 transgenic mice. In addition, C protein is capable to inhibit viral transcription and enhancing MV particles assembly. These proteins have shown to be involved in inhibition of interferon production (Naniche et al, 2000). The infection process involves four steps: 1. Attachment When measles virus enters the respiratory tract, the initial infection begins with viral attachment to host cellular receptors by the haemagglutinin (H) protein. The most studied receptors are CD46 and signaling lymphocytic activation molecule (SLAM/ CD150) (Ferreira et al, 2010). CD46 is a complement regulatory molecule and is present on all nucleated human cells whereas SLAM is only expressed on thymocytes, mature dendritic cells and T and B lymphocytes (Hsu et al, 2001). Other cell surface proteins such as moesin and substance P receptor were also proposed in MV binding (Kehren et al, 2001). The primary target for early stage infection has not been clearly defined. It was originally thought that respiratory epithelial cells were firstly infected (Griffin, 2001) but following the discovery of SLAM, some studies suggested that SLAM-positive immune cells should be the initial targets (Yanagi et al, 2002). Leonard et al. (2008) suggested the presence of a basolateral epithelial recept or (EpR) is necessary for entry of MV into respiratory epithelium and infection of the epithelial cells is required for shedding and transmission. Figure 1: a) Structure of a measles virus   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   b) Measles virus genome   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   c) Membrane fusion and replication of measles virus in a cell   Take from the wed-site nature.com/nrmicro/journal/v4/n12/box/nrmicro1550_BX1.html (Moss Griffin, 2006) 2. Fusion The interaction of both H and F proteins with human receptors is important for the virus to gain access into the host cell. Fusion (F) protein mediates the fusion of viral envelop with cell membrane. Figure 1 (c) demonstrated the fusion process. When the tetramer H protein binds to its receptor, it generates a conformational change within the F protein which is composed of two subunits F1 and F2 linked by a disulphide bond. The activated F protein inserts the hydrophobic fusion peptide into the target cell membrane and provides entry of the viral genome into the host cell interior (Weidmann et al, 1999). 3. RNA replication and Assembly of viral particles The polymerase allows replication and transcription of the genome within the cell. The negative sense RNA is copied into a complementary positive strand which, in turn, acts as a template for the negative strand. Viral components are translated in the cell and are assembled at the cell surface (Yanagi et al, 2006). 4. Release of virus MV leaves the host cell in a budding form (Yanagi et al, 2006). Spread The viremic spread from the respiratory tract is carried out by infected immune cells including monocytes, dendritic cells, B and T cells which travel through the local lymphatics and are transported to the secondary lymphoid tissue where further viral replication occurs. A secondary viremia occurs when infected cells enter the circulation and viral replication continues in the endothelia and epithelia of other organs including skin, gastrointestinal tract, liver, kidney and central nervous system (Ferreira et al, 2010). A systemic spread is favored by the immunosuppression following infection. Multiple mechanisms are involved in the development of immunosuppression and a brief description below focuses on some of the important pathways. 1. Changes in lymphocyte number and function Lymphopenia of B and T cells during viremic and post-clinical recovery stages is demonstrated by many studies. Bieback et al. (2002) showed that MV can bind to Toll-like receptor (TLR) 2 on monocytes, inducing SLAM expression and interleukin-6 (IL-6) production. In addition, binding of SLAM can induce Fas (CD95)-mediated apoptosis of uninfected CD4+ and CD8+ T lymphocytes. The extracellular composition of CD46 is characterized by four short consensus repeat (SCR) and a STP domain. SCRs 2, 3 and 4 are binding regions for C3b and C4b, thereby preventing them from causing autologous complement lysis. The attachment of MV to SCRs 1 and 2 alters the normal signaling pathway resulting in down-regulation of CD46, eventually leading to increased C3b-mediated complement lysis (Manchester and Rall, 2001). MV also inhibits lymphoproliferation by causing cell cycle arrest in the G0/G1 phase in dividing lymphocytes (Niewiesk et al, 1999) and interferes with NF-kB signaling pathways and anti-apoptotic B cell lymphoma 3 (Bcl-3) proteins (Bolt Berg, 2002). Furthermore, Nucleoprotein of MV binds to the Fc-gamma receptor on antigen presenting cells and impairs their ability to stimulate T cell proliferation (Hehren et al, 2001). Figure 2 summarized the main pathways leading to immunosuppression. Figure 2: Mechanisms of immunosuppression following measles virus infection Adapted from (Moss et al, 2004) 2. Shift in cytokine profile Early evasion of the innate immune responses is the interference of interferon-alpha/beta signaling pathways (Naniche et al, 2000) due to inhibition of STAT1 and STAT2 phosphorylation by proteins V and C. However, IFN-gamma production is not affected in the acute phase of measles (Takeuchi et al, 2003). Cross-linking of CD46 by MV and direct binding of MV to CD46 on monocytes and dendritic cells inhibit the production of IL-12 (Karp et al, 1996) and hence suppress macrophage activation, T cell proliferation and delayed-type hypersensitivity (Atabani et al, 2001). The loss of IL-12 also decreases type 1 cytokines TNF-alpha and IL-2, leading to transition to type 2 cytokines IL-4, IL-5 and IL-10 by CD4+ T cells (Moss et al, 2002). Th1 to Th2 shift leads to a change of cell-mediated immunity to a dominant humoral immunity which is not sufficient to combat new infections (Kemper et al, 2003). 3. Impaired antigen presentation Dendritic cells are critical for the antigen presentation to naà ¯ve T lymphocyte. MV infected dendritic cells fail to undergo differentiation to become mature effector cells and some of them are susceptible to Fas-mediated apoptosis (Servet-Delprat et al, 2000). Marttila et al (2001) reported that antigen processing of other viruses such as rubella virus and coxsackie B4 virus is compromised in MV-infected human mononuclear cells, suggesting impaired antigen presentation to T cells. Symptoms The clinical presentation is induced by the immune responses. The initial encounter of the virus activates the innate immunity with high levels of IFN-ÃŽ ³ and IL-8 but it is not efficient to clear the virus, leading to rapid multiplication of virus (Sato et al, 2008). Figure 3 illustrates the timeline of viremia and appearance of symptoms. Figure 3: Pathogenesis of measles virus and immune responses of host. Obtained from http://pathmicro.med.sc.edu/mhunt/mump-meas.htm (Hunt, 2008) The early symptoms of measles, listed below, usually appear after an incubation period of 10 to 12 days and last for 2 to 4 days due to inflammatory reactions affecting the respiratory tract and conjunctiva (Griffin, 1995). Fever Malaise Coryza Cough Small white spots in the oral cavity (Koplik’s spots) Conjunctivitis Rash The appearance of maculopapular rash reflects the immune complex formation in the skin. It correlates with viremia and onset of adaptive immune responses. The rash starts on the face and upper back after 14 days of exposure and spreads to the entire body over the next 3 days and finally fades after 5 to 6 days indicating that Cytotoxic T lymphocytes destroy infected host cells and clear the virus. Measles antibodies also appear in the circulation around this time with IgM at day 10 and IgG at day 14. They reduce measles viral load through serum neutralization. IFN-ÃŽ ³ and IL-8 levels decrease at convalescent as cytotoxic T cells decline (Heffernan and Keeling, 2008). Immunosuppression The most important pathologic feature of measles virus is immunosuppression. Most measles-related deaths are caused by secondary bacterial and viral infections. Malnourished children with weakened immune system and vitamin A deficiency are at high risk of developing complications which include blindness, diarrhoea, bronchitis, encephalitis, ear infection and pneumonia. Patients with impaired cell-mediated immunity may not develop the rash and they are susceptible to giant cell pneumonia (Manchester and Rall, 2001) Vaccination There is no antiviral therapy for measles although medications can reduce complications. Vaccination is currently the best method to prevent the disease. The first MV called Edmonston strain was isolated in 1954 on primary human kidney cells and it was subsequently adapted to chicken embryo fibroblasts and become the progenitor for currently used attenuated live vaccines. Composition of vaccines is important to elicit long-term protective immunity but not immunologic reactions and clinically significant immunosuppression. Measles vaccine is now usually given as part of a trivalent combined vaccine, MMR which is also against mumps and rubella (Hilleman, 1999). The World Health Organization has recommended infants should have the first administration of measles vaccine at 9 to 12 months because immunity requires Th1-type response. For countries with high measles transmission, a second dose should be given at age 15 to 18 months (WHO, 2009). Vaccination campaigns are effective in promoting the use of vaccination and reducing measles deaths. Between 2002 and 2008, measles vaccination has significantly reduced 78% of measles deaths from an estimated 733 000 in 2000 to 164 000 in 2008. However, many developing countries, particularly parts of Africa and Asia, still suffer from this preventable infection due to the poor access to vaccinations and lack of facilities to properly store vaccines (Manchester and Rall, 2001). Ohtake et al (2010) has reported a spray drying method was successful to produce heat-stable measles vaccine powders. However, further tests are required to demonstrate the feasibility of these dry vaccines. Molecular epidemiology is a useful tool to monitor measles and genomic study of measles virus can provide insight in the development of new and safe vaccines (Ohtake et al, 2010). The World Health Organization is making an effort to monitor outbreaks and increase immunization coverage and hopefully can ev entually eradicate the virus in the future. Subacute sclerosing panencephalitis (SSPE) SSPE is a fatal disease caused by a persistent infection with a defected form of measles virus in the brain. The common mutated components are the matrix (M), the fusion (F) and the haemagglutinin (H) proteins. Mutations can be point mutations, deletions and biased hypermutations and are mostly found in the M gene (Gutierrez et al, 2010). SSPE has a slow progression and usually develops in an interval of 5 to 10 years after the initial infection. It is very rare. Incidence rate varies between countries but the average is about one per million. Age and sex of infected individuals can affect the frequency of SSPE. Infection before the age of 2 years is associated with higher occurrences and boys are 2 times more likely to acquire SSPE (Gutierrez et al, 2010). The development of SSPE is caused by an imcompleted eradication of MV due to inadequate cell-mediated responses caused by genetic polymorphisms (Yentur et al, 2005) and high level of IL-4 but low levels of IL-12. These cytokines favour humoral response and predispose to viral replication (Hara et al, 2006). MV enters neurons by binding to host receptors CD46 and CD9 using the F protein. It replicates inside the cells and spreads to neighbouring neurons by neurokinins synaptic receptors (Makhortova et al, 2007). In addition, sequence analysis of viral RNA showed that the virus was entered from one point and disseminate throughout the brain. The defective structural envelope proteins assist them to escape from the immune system as the mutated M, F and H proteins failed to assemble and bud out the cells. Thus, the viral particles are not recognized for many years. However, inflammatory responses are finally triggered when the virus damages the host DNA and induces apoptosis (Oldstone et al, 2004). Histological examination of the brain tissue shows evidence of widespread demyelination, infiltration of immune cells and blood brain barrier damage. Glia cells and astrocytes may be activated with increased expression of MHC class II molecules and tumor necrosis factor-ÃŽ ±. Appearance of inclusion bodies in brain tissue is also common (Akram et al, 2008). Patients are often diagnosed based on presentation and clinical findings of electroencephalography, magnetic resonance imaging and CSF serology (Koppel et al, 1996). SSPE has four clinical stages (Table 2) and most patients died within 3 years of diagnosis (Gutierrez et al, 2010). Table 2: Clinical stages of SSPE Stage Clinical manifestations I Personality changes Behaviour abnormalities II Seizures Motor decline III Rigidity Progressive unresponsiveness IV Coma Akinetic mutism (Loss of ability to speak and move) Adpated from Gutierrez et al, 2010 Word count: 2421 excluding references and plagiarism statement. Bibliography Akram M, Naz F, Malik A et al. (2008) Clinical profile of subacute sclerosing panencephalitis. J Coll Physicians Surg Pak. 18, 485-488. Atabani SF, Byrnes AA, Jaye A et al. (2001) Natural measles causes prolonged suppression of interleukin-12 production. Journal of Infectious Diseases,184, 1-9. Bolt G Berg KB (2002) Measles virus-induced modulation of host-cell gene expression. Journal of General Virology,83, 1157-1165. Ferreira CSA, Frenzke M, Leonard VHJ et al. (2010) Measles virus infection of alveolar marcrophages and dendritic cells precedes spread to lymphatic organs in transgenic mice expression human signaling lymphocytic activation molecules (SLAM, CD150). Journal of Virology, 84(6), 3033-3042. Griffin DE (1995) Immune responses during measles infection. Curr Top Microbiol Immunol, 191,117-34. Griffin DE, Ward BJ, Esolen LM (1994) Pathogenesis of measles virus infection: an hypothesis for altered immune responses. J infect Dis, 170(Suppl 1), S24-31 Gutierrez J, Issacson RS and Koppel BS (2010) Subacute sclerosing panencephalitis: an update. Developmental Medicine Child Neurology, 52, 901-907. Hara T, Yamashita S, Aiba H et al. (2000) Measles virus-specific T helper 1/T helper 2-cytokine production in subacute sclerosing panencephalitis. J Neuroviral. 6, 121-126. Hau EC, Jorio C, Sarangi F, et al. (2001) CDw 150(SLAM) is a receptor for a lymphotropic strain of measles virus and may account for the immunosuppressive properties of this virus. Virology,279, 9-21. Heffernan JM Keeling MJ. (2008) An in-host model of acute infection: Measles as a case study. Theoretical Population Biology, 73, 134-147. Hilleman MR. (1999) Combined measles, mumps and rubella vaccines. In: Ellis RW, editor. Vacinnes, development, clinical research and approval. Human Press.197-211. Horikami SM, Moyer SA. (1995) Structure, transcription and replication of measles virus. Curr Top Microbiol Immunol, 191, 35-50. Hunt (2008) Microbiology and immunology on-line: Measles (Rubeola) and mumps virus. University of South Carolina. Available at http://pathmicro.med.sc.edu/mhunt/mump-meas.htm (Access 28 February 2011) Karp CL, Wysocka M, Wahl LM et al. (1996) Mechanism of suppression of cell-mediated immunity by measles virus. Science,273, 228-231. Kehren JCMJ, Trescol-Biemont MC, Valentin AEH, et al. (2001) Mechanism of measles virus-induced suppression of inflammatory immune responses. Immunity, 14, 69-79. Kemper C, Chan AC, Green JM et al. (2003) Activation of human CD4+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype. Nature,421, 388-392. Koppel BS, Poon TP, Khandji A et al. (1996) Subacute sclerosing panencephalitis and acquire immunodeficiency syndrome: role of electroencephalography and magnetic resonance imaging. J Neuroimaging. 6,122-125. Lenoard VHJ et al. (2008) Measles virus blind to its epithelial cell receptor remains virulent in rhesus monkeys but cannot across the airway epithelium and is not shed. J Clin Invest, 118(7), 2386-2389. Makhortova NR, Askovich P, Patterson CE et al. (2007) Neurokinin-1 enables measles vorus trans-synaptic spread in neurons. Virology. 362, 235-244. Manchester M Rall GF. (2001) Model systems: Transgenic mouse models for measles pathogenesis. Trends in Microbiology, 9(1), 19-23. Marittila J, Hinkkanen A, Ziegler T, et al. (2001) Cell membrane-associated measles virus compoents inhibit antigen processing. Virology, 279, 422-428. Moss WJ Griffin DE (2006) Global measles elimination, Nature Reviews Microbiology, 2(12), 900-908. Available at nature.com/nrmicro/journal/v4/n12/box/nrmicro1550_BX1.html (Accessed 28 February 2011) Moss WJ, Ota MO, Griffin DE. (2004) Measles: immune suppression and immune responses. The international Journal of Biochemistry Cell biology, 36, 1380-1385. Moss WJ, Ryon JJ, Monze M et al. (2002) Differential regulation of interleukin (IL)-4, IL-5, and IL-10 during measles in Zambian children. Journal of Infectious Diseases, 186, 879-887. Naniche D, Yeh A, Eto D, et al (2000) Evasion of host defenses by measles virus: wild-type measles virus infection interferes with induction of Alpha/Beta interferon production. Journal of Virology, 74(16), 7478-7484. Niewiesk S, Ohnimus H, Schnorr JJ et al. (1999) Measels virus-induced immunosuppression in cotton rats is associated with cell cycle retardation in uninfected lymphocytes. Journal of General Virology, 80, 2023-2029. Ohtake S, Martin RA, Yee L et al. (2009) Heat-stable measles vaccine produced by spray drying. Vaccine, 28, 1275-1284. Oldstone MB, Lewicki H, Thomas D et al. (2004) Measles virus infection in a transgenic model: virus-induced immunosuppression and central nervous system disease. Cell, 98, 629-640. Patterson JB, Thomas D, Lewicki H et al. (2000) V and C proteins of measles virus function as virulence factors in vivo. Virology,287, 80-89. Sato H, Kobune F, Ami Y et al. (2008) Immune responses against measles virus in cynomolgus monkeys. Comparative Immunology, Microbiology Infection Diseases, 31, 25-35. Schneider-Schaulies S, Bieback K, Avota E et al. (2002) Regulation of gene expression in lymphocytes and antigen-presenting cells by measles virus: consequence for immunomodulation. 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How to Survive Failing a Class in College

How to Survive Failing a Class in College Oh my, now you’ve done it. You failed a class in college and what you once knew as a normal human life is about to descend into the seventh layer of†¦just kidding. Listen, it happens. Countless freshmen and sophomores lose sight, or let things slip. Sometimes upperclassmen take on more than they can handle. In this post we’ll look at a step-by-step process you can use to effectively deal with a big fat F. Step 1: Evaluate Overall GPA Fin-Aid Impact The moment you know you’re going to fail, or you happen to find out, the first thing you need to do is see how it will influence your overall GPA (big eye opener for most folks), and how it will impact financial aid. It could have a big impact on students with scholarships and things. Or who are getting funding from private sources with certain expectations. Whatever the case is, the first step to damage control is knowing the extent of the damage. Is this a course you absolutely must have for your major or are there other alternatives that may be better suited to you? How is this going to change your schedule for next quarter/semester? Does this mean that summer school is in your future? Maybe so. That’s not such a bad thing, but it could put a crimp in any road trip plans. Step 2: Evaluate Why You Think You Freaking Failed! Be honest and upfront with yourself. In the halls it sounds like a prison yard – everyone’s innocent! There’s a massive conspiracy going on, or the professor is being a hard ass with unreasonable expectations. Come on. Did you study as much as you should have or did you slack off and play video games with roomies instead? When you did poorly on the first couple tests, or struggled along why didn’t you join any study groups? What’s going on with you? Is this behavior causing you to come close to failing other classes? Come to terms, honestly, with the real cause for your failing and then do this next thing†¦ Step 3: Schedule Appointment with Professor If the class is one you have to take, then schedule an appointment with the professor. And, guess what, the reason your meeting with them is to apologize. That’s right! It’s your fault, not theirs. You’re going in there to say you’re sorry and you recognize the issue at hand. You’re ready and more than willing to correct things. Then, after you’ve genuinely humbled yourself, ask the professor for any advice they could give you to do better next time. DO NOT ask for a change in grade, insinuating they were somehow wrong or unfair to you. DO NOT walk in there and start playing the world’s smallest violin. They’ve heard it all, and at the end of the day your problems aren’t theirs. Most of the time this isn’t what they’ll expect. When they see how sorry and re-committed you are, they’ll tend to give you a little extra attention. Show professors you care, that you’re actually much better than this. Step 4: Make a New Plan Now, it’s time to fashion a new approach. One that will put you at the head of the class rather than the other end that you’re currently occupying. Bounce back like Rocky Balboa would! There’s no lack of support for students that are having trouble. Study groups are everywhere, along with tutors and fellow students that would appreciate the opportunity to practice what they know by teaching you on the side. If you don’t have a set studying schedule in general, now’s the time genius. Start devoting some time to online research as well. These days with access to the internet and the on-campus library system, there’s no excuse. Do you need to re-prioritize things? Is work playing a role here? You know the goal: turning that F into an A and bumping up the GPA. Set objectives, meet them and learn your lesson quickly. Avoiding problems is easier than solving them. So, find out how to avoid failing a college class even if you dont like it! Step 5: Don’t Hide It Don’t try and hide the failed class from family or friends. Be upfront with people. When they see that you’ve learned your lesson and are making changes to better yourself, you’ll get tons of extra support that you just didn’t know was there before because you weren’t trying. Study harder and in visible places where fellow majors will see you. Start hanging out with the other â€Å"studiers† and the students that are taking their education seriously. Step 6: Ace It! No worries, it happens. Do what you have to do to be more than you seem to be. You can and will ace these simple college level tests when you commit. The adult world is just around the corner where failures can be absolutely devastating.