Research on Malaria in Moyale District Essay Example for Free

Research on Malaria in Moyale District Essay The term `Malaria originates from Medieval Italian Mala aria which mean â€Å"bad air†; and the disease was formerly called Ague or Marsh fever due to its association with swamps and marshland, (Watkins, 2001). Scientific studies on Malaria made their first significant advance in 1880, when Charles Louis Alphonse Laveran a French army doctor working in the military hospital of Constantine in Algeria observed malaria plasmodium parasites inside the red blood cell of people suffering from Malaria. Documentation of report on discovery of origin of Malaria, one of the deadliest diseases of humanity shows that Chimpanzees, native to equatorial Africa have been identified as the original source of the parasite that likely moved from them to humans via mosquitoes. Wolfe, (2009) identified several parasites from Chimpanzee that show Malarial jumped from animal to human. Malaria is transmitted by Anopheline mosquitoes the number and type of which determine the extent of transmission in a given area. The plasmodium falciparum accounts for the majority of infections and is most lethal. Transmission is affected by climate and geography and often coincides with the rainy season. In WHO/UNICEF, (2005) report malaria is one of the most devastating global public health problems with more than one million deaths and approximately 300-500 million cases of malaria annually. WHO, (2010) report, Malaria is by far the world’s worse tropical parasitic disease, and kills more people than any other communicable disease. Several studies observed that malaria kills more than 3,000 children daily and is the single most important factor for mortality among children under the age of five. Additionally, an estimated 25 million pregnant women are at risk of malaria. Malaria is endemic in a total of 101 countries and territories 45 countries in WHO’s African region, 21 in WHO’s American region, 4 in WHO’s European region, 14 in WHO’s Eastern Mediterrarian Region, 8 In WHO’s South – East Asia region, and 9 in WHO’s Western Pacific region, (report from global health council on impact of infectious diseases. ) WHO, (2007) report has shown that malaria has reached epidemic proportions in many regions of the world and continues to spread unchecked. In many regions of developing countries malaria exacts an enormous toll in lives, medical costs, and in days of labor lost. According to Roll-Back Malaria (RBM), over 40 per cent of the World’s children live in malaria-endemic countries and 107 countries and territories are at risk of malaria transmission. Malaria causes 24 percent of under-five deaths in Equatorial Guinea (UNICEF 2008). Malaria is preventable, if adequate resources are invested in prevention. About 98 percent of Equatorial Guineans live in areas with endemic risk of malaria but only one percent of children under five sleeps under insecticide-treated nets. This is far fewer than in other Countries with similar malaria risk. This suggests inadequate efforts to prevent malaria that would contribute to the realization of the right to health of both children and adults. Children under the age of five, pregnant women, and people living with HIV and AIDS are at highest risk for developing clinical malaria. More than 80 per cent of these cases occur in sub-Saharan Africa. WHO/RBM, (2004). Malaria is a primary cause of poverty, putting additional burdens on health systems and costing Africa an estimated 12 billion USDs in lost production every year. The spread of the disease is fuelled by several factors: climate change, increasing population mobility, more frequent international transport, emergence of multi drug-resistant strains, and military and economic deterioration. Abuja summit in Nigeria in the year 2000, 44 African leaders reaffirmed their commitment to roll back malaria and set interim target for Africa. They challenged other world leaders to join them in recognizing the importance of tackling malaria as a disease of poverty. Following the Abuja summit, Africa Malaria Day was declared as a day to celebrate on malaria and a subsequent UN resolution declared 2001-2010. Roll Back Malaria, especially in Africa, giving prominence to Malaria in United Nations Millennium Development Goals. The Africa Malaria report, released in the year 2003/Nairobi/Geneva/New York by the World Health Organization (WHO 2005), and the United Nations Children’s Fund (UNICEF), said the death toll from malaria remains outrageously high-with a child dying in every 30 seconds. The report gives an African situation for the struggle against the diseases and highlights the urgent need to make effective anti-malarial treatment available to most at risk. â€Å"The roll back Malaria initiatives has made considerable progress since it was launched in 1998, but we need to increase to combat a devastating disease which is holding back the development of many African countries,† states Dr Gro Harlem Brundtland, Director-General of WHO. Nationally Malaria has been a serious public health problem in most Districts of Kenya and the leading cause of morbidity and mortality in Kenya. With more than 70% of the Kenya’s population living in areas where malaria is transmitted, Malaria is responsible for approximately 30% of out-patient visits (requiring more than eight million out-patient treatments each year), and 19% of all hospital admissions. At least 14,000 children are hospitalized annually for malaria, and there are an estimated 34,000 deaths among children under-five each year. Annually, an estimated six thousand pregnant women suffer from malaria-associated anemia, and four thousand babies are born with low birth weight as a result of maternal anemia, report from government health facility in 2007. Economically, it is estimated that 170 million working days are lost each year because of malaria illness. Culture and poor access to health facilities lead to increase in cases of malaria. The main thing peculiar with children under 5 years is that many cannot sleep under net due to incapability of their parent especially in rural areas, because of the few wages they hardly get from their casual work. Most children again play outside in the grasses or near drainage where mosquito’s breeds thus are exposed to mosquito bites. In local situation Malaria is the highest causes death of many people in the region of Moyale and districts of North Eastern province bordering Moyale district from east. Malaria claims the life of 1,500 in the year 1998 and out of that 45 death in Wajir district (Daily Nation, Thursday, February 1998). Sololo Mission Hospital reported the admission of 67 people. Out of 67people, 25 children of less than five years were reported cases of malaria (SMH/1999). 1. 2 problem articulation/ statement: Malaria is World’s most important parasite infectious disease. Over 2 billion people are at risk between 300 and 500 million episodes and over 1 million deaths annually, WHO, (2005). Over 90% of malaria burden are in sub-Saharan Africa. Malaria is one of the planets deadliest diseases and one of the leading causes of sickness and death in the developing world. Documentation also show that Malaria affect child cognitive, physical development and leads to poor school attendance. Malaria also leads to malnutrition and anemic condition in children. More so it also affects adult’s ability to make a living and care for their families. At country level malaria affects trade, tourism and foreign direct investment and there is significant correlation between malaria and poverty. An average GDP in malaria’s countries is five times lower than in non-malaria’s countries 1. 3 Objectives of the study To establish factors that lead to high prevalence of Malaria in children under five years in Obbu Division, Moyale District. 1. 4 Specific objectives: 1. To determine socio-demographic factors contributing to Malaria prevalence among the under five children in Obbu division. 2. To establish the level of knowledge on Malaria, among caregivers of children under five in Obbu Division. . 5 Research questions 1. What are the main factors contributing to high prevalence of Malaria among the under five children in Obbu division? 2. What is the knowledge level of care givers of children under five years about the risk factors of late treatment and prevention of Malaria? 3. To what extent the level of knowledge on Malari a, among caregivers of children under five in Obbu Division? 1. 6. Hypothesis/assumption There were no factors that contribute to prevalence of malaria in children less than five years in Obbu Division of Solol District 1. 7 Justification of the study. Malaria outbreak in mid July 2012, number of cases diagnosed were 82, and 8 out of 10 reported death were children under five (Malaria/SMH/ 20012/3). The prevalence was precipitated by illiteracy, migration lifestyle of pastoralists’ community and uncontrolled border intermingling and refugees from neighboring countries like Ethiopia and Somali as revealed by the study of Diseases Outbreak Management Unit-DOMU (2002). Socio demographic factors and knowledge about the diseases control and prevention attracted a lot of concern that call for research in these factors. Obbu division has few documentation of the study, so this will be helpful to academia as it will be used as document of references for a researcher in the same area of study. The government or other stakeholders will benefit from the findings and may take intervention measures for instance the Ministry of public health to educate people on the better prevention methods. The findings of the study will be used by people of the study area to plan for the prevention of the malaria, since it is preventable at every household. 1. 8 Scope of the study To investigate main factors contributing to high prevalence of Malaria among children less than five years of age in Obbu division of Moyale district. . 1. 9 Limitations 1. Data collection during interview was difficult due to migration of the population but the settlement around the centre of each four location was targeted. 2. Cost of getting trained research assistant was challenging. 3. The study was limited to factors contributing to prevalence of malaria in children less than five years of age. 2. 0 CHAPTER TWO: LITERATURE REVIEW 2. 1. 0 Origin of malaria. The history of malaria replete with a number of theories about its aetiology, the earliest theory was the Miasmatic. This theory postulated that swamp air contained chemicals which had been freed from rotting wood. This air was what was responsible for causing malaria (Ransford 1983). It was because of this theory that double storey buildings were preferred during the early days of the colonial period as it was believed that miasma did not rise above ground level (Ransford 1983) and that the miasma was thought to spread horizontally (King and King 1992). Ransford and Friedson claim that Africans were the ones who first recognized the link between mosquitoes and malaria (Ransford 1983; Friedson 1996) and in the West it was only known later through the pioneering works of Patrick Mason, Ronald Ross, Grassi and others around the 1890s. 2. 1. 1 Prevalence of Malaria. There are 300-500 million clinical cases of Malaria each year resulting in 1. 5 to 2. 7 million deaths (WHO, 2005). Global viral forecasting initiative and standard university, made the discovery published in the Aug. 2009 proceedings of the National academy of sciences Wolfe, (2009). Malaria in most countries of Western Pacific and Regional Organizations has significantly declined in the period 1992 to 2000. There is widespread consensus that the change to Artemisinin Based Combination (ACT) in Vietnam was a significant factor in the 98% drop in malaria mortality between 1992 and 2002. The geographical area affected by malaria has shrunk considerably over the past 50 years, but control is becoming more difficult and gains are being eroded. Increased risk of the disease is linked with changes in land use linked to activities like road building, mining, logging and Agricultural and irrigation projects, particularly in â€Å"frontier† areas like the rain forests. Other causes of its spread include global climatic change, disintegration of health services, armed conflicts and mass movements of refugees. According to citation from the August 97 issue of the American magazine the Atlantic Monthly entitled â€Å"Resurgence of a Deadly Disease† by Ellen Rippel Shell.

GFP Practical Report

GFP Practical Report GFP is very useful as a reporter protein. After its discovery in 1962 its practical applications were put into use 30 years later by adding the coding DNA of GFP before the stop codon of other proteins. This allows for an easily detectable marker of the proteins presence without needing additional cofactors or causing any harm to the organism. The spectral characteristics of GFP can be changed by making mutations to the protein. In this investigation a Y66W mutation was made to wildtype GFP in order to produce a shorter excitation and emission wavelength. The mutation was made using QuikChange site directed mutagenesis. The protein was then cloned into BL21(DE3) pLysS for expression. The cells were then lysed and applied to a Ni-NTA column. This fractionated the lysate in order to analyse these fractions using SDS-PAGE, fluorescence and Bradford assays. It was found that the Y66W mutation was successfully added but due to another mutation in the stop codon additional amino acids were added to the C terminus of the protein. It was also found that purification was partially successful as GFP was eluted in the correct fraction. This is supported by the Bradford and fluorescence assays. The green fluorescent protein (GFP) is a 238 amino acid protein with a molecular mass of 26,870 Da. It was first isolated from the jellyfish species Aequorea Victoria by Osamu Shimomura in 1962 (1). GFP is expressed in small photoorgans that are situated in the umbrella of the jellyfish. Douglas Prasher first realised the potential of GFP as a reporter protein (2). As proteins are smaller than the resolving power of electron microscopes, Prasher thought the GFP gene could be added into the gene for haemoglobin before the stop codon. This would allow the protein of interest to maintain all of its functions but would have the GFP protein at its C terminal end. This means that detection of GFP fluorescence would also indicate the presence of haemoglobin. Furthermore, GFP does not require additional cofactors or substrates to fluoresce. This means that it works extremely well as a non-invasive method of detection of protein expression. GFP is also non-toxic so it is able to be used in vi vo without causing damage or harm to the organism. Crystallisation studies (3) have shown that GFP has a barrel structure with the chromophore buried in the centre. This chromophore is comprised of 3 amino acids (Ser 65-Tyr 66-Gly 67) that undergo a series of spontaneous cyclisation reactions to create the active chromophore. Wild type GFP has a major excitation peak at 395 nm and a minor one at 475 nm with an emission peak at 509 nm. In vivo GFP is coupled to the protein aequorin which induces a blue glow when it interacts with Ca2+ ions and breaks down luciferin. This light is able to excite GFP and cause fluorescence. In vitro this is not the case, however GFP fluorescence can be easily induced by irradiating GFP with UV light. As with all proteins, GFP can be mutated. By mutating key residues, such as residues in the chromophore, it is possible to change the characteristics of GFPs fluorescence. The first of many mutations was the S65T mutation (4). This mutation improved the characteristics of the protein including increased photostability, fluorescence and a shift of the major excitation peak. This investigation is based on the engineering of GFP to create a mutant of GFP with a shorter excitation and emission wavelength by inducing the Y66W mutation. The aims of this investigation were as follows. To carry out site directed mutagenesis of GFPuv to clone into pET28c and transform the products into XL-1 super competent cells. Extraction of the plasmid after incubation overnight to check the purity and concentration of DNA. Preparation and transformation of BL21(DE3) cells. Lyse these cells and fractionate the lysate to purify his tagged GFP using a Ni-NTA column. Finally, detection of purified GFP by SDS- PAGE, Bradford assay and fluorescence. The workflow of the investigation can be found in figure 1 in appendix 1. A more detailed protocol can be found in the BIOC2302 semester 2 practical manual on pages 6-15 with rationale for all experiments. In site directed mutagenesis I 31 ÃŽ ¼l of water was added to the PCR reaction to give a total reaction volume of 50 ÃŽ ¼l. In site directed mutagenesis II a supplied culture of cells was used in the experiment rather than cells from the transformation colonies in site directed mutagenesis I. His tagged GFP was used instead of the mutant in the protein purification experiment in order for easier administration as the process is the same. Site directed mutagenesis I Before the wet lab work began it was first necessary to design primers for QuikChange to induce the Y66W mutation into the wild type GFP. These can be seen as figure 2 in appendix 2. These were created using the QuikChange primer design tool on the Agilent website. The site directed mutagenesis was carried out using the primers supplied to induce the correct mutation. The products of this were cloned into the pET28c plasmid and the XL-1 super competent cells. The cells were plated as per the BIOC2302 practical manual and left to incubate overnight. Site directed mutagenesis II Upon checking the plates in the next session it was found that no transformed colonies had grown so a new culture was supplied. The undigested plasmid control grew approximately 50 colonies The culture of BL21(DE3)pLysS cells was set up and the OD600 were recorded. They can be seen in table 1 in appendix 3. Within 50 minutes the culture had reached an OD600 of 0.483 meaning the cells were at the correct density for lysis. The cells were prepared as per the BIOC2302 practical manual and the recombinant plasmid was extracted. The concentration measured was 121.7 ng/ÃŽ ¼l and the A260/A280 was 1.86 using nanodrop. Therefore, the ethanol precipitation was not carried out. To prepare for sequencing 4.11 ÃŽ ¼l of this solution was diluted, with 5.98 ÃŽ ¼l EB buffer, to the correct concentration. This was then sent to be sequenced, the results of which can be seen in appendix 4. The primer has been highlighted in green and is surrounded by a box with the mutated codon in red. A deletion also occurred in the stop codon of the mutant as highlighted by the second box with deleted bases highlighted in blue. Protein purification The plates were inspected in the next session. It was found that the 200 ÃŽ ¼l transformation plate grew 3 colonies and the 50 ÃŽ ¼l transformation plate grew none. Transformation efficiency can be calculated for the 200 ÃŽ ¼l plate as 37 transformants/ÃŽ ¼g of DNA. The cells were weighed and found to be 0.539 g so 2 ml BugbusterTM used. After lysis and fractionation the SDS-PAGE samples of each fraction were prepared and loaded onto the gel. The Bradford assay was carried out while the gel ran.   The BSA standards were calculated and the contents of each standard well can be seen in table 2 in appendix 3. The fractions were then diluted into their wells and the contents can be seen in table 3 in appendix 3. The plate was filled according to the map in figure 2 in appendix 5. The plate was ran and the absorbances for the BSA standards were taken from the plate readout and inputted into table 4 in appendix 5. From here a calibration graph was set up using GraphPad Prism and can be seen as graph 1 in appendix 6. This graph shows that the data points for the standards do not fall near the line of best fit. The absorbance results from the plate readout for all of the fractions were imputed into table 5 in appendix 7. The equation of the line from graph 1 was then used to calculate the concentration of protein in each of the fractions. All of these values were also inputted into table 5. With the Bradford assay complete the SDS-PAGE gel was disassembled, stained and a picture was taken. A map of the gel can be seen as figure 3 in appendix 7 and the picture of the gel can be seen as figure 4 in appendix 8. By looking at the picture it can be seen that in lanes 2, 3, 4 and 9 there are dark bands spanning the entire lane. In 5, 6 and 8 there is faint banding across the well. In well 7 there is a distinct small band in between the 25 kDa and 37 kDa molecular markers. Lane 8 shows no bands at all. Finally the fluorescence assay was carried out as per the map of the microtiter plate in figure 5 in appendix 7. The results from the plate readout were inputted into table 5. From here a graph comparing the log of protein concentration compared to fluorescence of each fraction was plotted and can be found as graph 2 in appendix 6. This shows elution 1 with the highest fluorescence and the unbound x10 had the lowest. However, when comparing protein concentration the unbound fraction had the highest and wash 2 had none. Percentage fluorescence was also calculated and inputted into table 6 in appendix 9. The first aim of this experiment was to transform the site directed mutagenesis products into XL-1 super competent cells. The correct primers were used in order to induce the Y66W mutation into the parental DNA. However, no colonies that were meant to take up the mutated plasmid grew but the undigested control grew around 50 colonies. This means the cells did not take up the plasmid because otherwise they would have grown on the plate. This could be due to a mistake made in making the PCR reaction mixture or the DNA may have become damaged at some point in the experiment. Additionally, the suppliers of the XL-1 super competent cells advice to avoid large changes in temperature. This was unavoidable in this experiment and may have contributed to the cells not taking up the plasmid. In the future more care should be taken while plating and preparing the cells. Also preparation of any reaction mixtures should be checked very closely in order to ensure the correct reactants are added in the correct amounts. In site directed mutagenesis II the cell culture was lysed when the OD600 was 0.483. That is because E.coli cells are most likely to be made competent when they enter early log phase. This corresponds with an OD600 of 0.4-0.5. The DNA concentration extracted in this experiment was found to be 121.7 ng/ÃŽ ¼l and an A260/A280 of 1.86. This means that the DNA is good quality as the desirable range for A260/A280 is 1.7-2.0 and the concentration was much higher that what was required. However, in future experiments to test for reliability multiple results should be taken. Furthermore, the data could have been confirmed by using the spectrophotometric method alongside using nanodrop. The sequencing results in appendix 4 confirmed the successful incorporation of the Y66W mutation into GFP, creating the CFP mutant. However, the second mutation at the stop codon deleted 2 bases including the first base of the stop codon. This means that when the protein is expressed the ribosome will not stop and instead will continue to add amino acids onto the C terminus of the mutant until it reaches a new stop codon. There 144 bases between the original stop codon and the next in frame stop codon meaning 48 additional amino acids will be added to the C terminus. This codon can be seen highlighted in purple below the original stop codon. These additional amino acids could affect the folding or could increase the likelihood of aggregation of the mutant protein. In the protein purification experiment the 200 ÃŽ ¼l transformation plate grew 3 colonies and the 50 ÃŽ ¼l transformation plate grew none. The transformation efficiency on the 200 ÃŽ ¼l plate was 37 transformants/ÃŽ ¼g of DNA. The reason why this is so low could be due to a number of factors such as the plating technique or the cells may not have been left to chill on ice for the optimum amount of time. However, the negative control did not grow any colonies, confirming that all of the bacteria on the transformation plate were transformed. Again, more steps should be taken if this was to be carried out again to ensure that proper plating and prepping protocol is followed. The Bradford assay shows that in wash 2 there was no protein in the well. This means that any protein found in elutions 1 and 2 should all be His tagged GFP that bound the Ni-NTA column. This can be confirmed by the fluorescence results as the elution 1 fraction contained the majority of the total fluorescence with 44.13% of the total. However, all other fractions also produce some fluorescence. This could be due to GFP contamination in the other fractions. This could have occurred due to the resin being saturated, preventing further binding to the column. It could also be due to aggregation of the protein obscuring the His tag and preventing binding. Furthermore, the plots on the calibration graph do not fall on the line of best fit. This means that the equation of the line is not accurate and protein concentrations calculated using it are also inaccurate. Therefore, there could be more protein in each fraction than was calculated. This could account for the fluorescence in the wash and unbound fractions. The Bradford assay is quite limiting. This is due to the fact the assay only measures protein concentration rather than GFP concentration. This means that it is unsure whether the protein concentration measured in elution 1 and 2 is all GFP or it is contaminant protein. The same can be said for the other fractions, its unsure whether the protein concentration measured has been contaminated by GFP. In the future this assay should be carried out again to try and reduce contamination. The calibration graph should also be repeated until all of the data points fall on the line of best fit. Otherwise none of the calculated protein concentrations are accurate. Finally, the SDS-PAGE results shows banding in wash 1, 2 and elution 1 and 2. This suggests that there is contaminating protein in all of these fractions. Elution 1 shows a clear band at approximately the 26-27 kDa mark as it is present just above the 25 kDa marker and is well below the 37 kDa marker. This suggest the band in elution 1 is GFP as it is the appropriate size and is in the expected fraction. Another source of error could be due to the amount of pressure applied to the pipette. This will vary from person to person and will affect the volume of the solution being pipetted. As such small volumes were being used and there was a lot of solutions to be pipetted it is very possible a mistake was made. This mistake would have a big effect on the concentration and therefore could have a big effect on the absorbance values. These errors can be avoided in future by using the appropriate pipette for the volumes being used. Further reduction in errors can come from correct technique and by doing replicates and averaging values. There could be some error in the microtiter itself. There may have been markings or scratches on the plate that werent seen at the time. This could affect how the light passed through the reader and therefore affect the absorbance values. In conclusion, the aims of this investigation were to induce the Y66W mutation into wild type GFP using QuikChange site directed mutagenesis. Furthermore, the protein was to be expressed in competent BL21(DE3) pLysS cells. Finally wildtype GFP was to be purified using a Ni-NTA column and the fractions analysed with SDS-PAGE, fluorescence and Bradford assays. The investigation successfully introduced the Y66W mutation into wildtype GFP. However, the stop codon was also mutated adding an extra 48 amino acids on the C terminal of the protein.   A band indicating the presence of GFP was found at the 26.9 kDa mark in elution 1, indicating it was bound to the column and was eluted. However, all factions were contaminated with other protein. References      Ã‚   1. Shimomura, O., Johnson, F., and Saiga, Y. Extraction, purification and properties of aequorin, a bioluminescent protein from the luminous. s.l. : J. Cell. Comp. Physiol. 59:223-39, 1962. 2. Prasher, D., Eckenrode, V., Ward, W., Prendergast, F., and Cormier, M. Primary structure of the Aequorea Victoria green-fluorescent protein. s.l. : Gene 111 (2)229-33, 1992. 3. Ormo, M., Cubitt, A., Kallio, K., Gross, L., Tsien, R., and Remington. S. Crystal structure of the Aequorea Victoria green fluorescent protein. s.l. : Science 273:1392-5, 1996. 4. Heim R, Cubitt AB, Tsien RY. Improved green fluroescence. s.l. : Nature. 373 (6516): 663-4., 1995.

Analysis of Death of Ivan Ilych Essay -- essays research papers

Letting Pain Be   Ã‚  Ã‚  Ã‚  Ã‚  To many individuals the word â€Å"progress† has a positive meaning behind it. It suggests improvement, something humans have been obsessed with since the dawn of society. However, if closely examined, progress can also have a negative connotation as well. While bringing improvement, progress can simultaneously spark conformity, dependency, and the obsession of perfection within the individuals caught in its midst. It is this aspect of progress within modern society that negatively affects Ivan Ilych, Leo Tolstoy’s main character in The Death of Ivan Ilych. Ivan’s attempt to conform to modern society’s view of perfection takes away his life long before he dies. Furthermore, his fear of death and reactions towards it reflects modern society’s inability to cope with the ever present reminder that humans still suffer and die, despite all attempts to make life painless, perfect, and immortal.   Ã‚  Ã‚  Ã‚  Ã‚  Although we as a society have advanced and made people’s lives easier, our mental suffering is as present as ever, due to our incessant need to have everything perfect. We seem to forget that the fascination of living comes from the imperfect and the unexpected. In her essay â€Å"On the Fear of Death† Elisabeth Kubler-Ross suggests that the modern age, while increasing life span and ease of life, has at the same time given way to a â€Å"rising number of emotional problems,† amongst the living (Ross 407). She also suggests that because of modern society’s progress, there has been an increased anxiety towards death. While Ross is writing for twentieth century society her ideas apply to the nineteenth century as well, when Tolstoy wrote The Death of Ivan Ilych.   Ã‚  Ã‚  Ã‚  Ã‚  Ivan Ilych is living during the industrial revolution, a time of technological advancement, that mainly advances the upper class, which he is apart of. Ivan’s number one priority in life is to be comfortable and to do the correct thing at all times. Every decision he makes, including who he chooses to marry, is with the intent that it does not damage his â€Å"easy, agreeable, and always decorous character of his life,† (Tolstoy 213). Ivan is convinced that the best way to have an easy and agreeable life is to be wealthy, marry a woman from his own class, and live in a house full of modern conveniences and luxury. Ironically, it... ...roduction of Twentieth-Century Literary Criticism, Vol. 44 it is stated that â€Å"Ivan Ilych’s passage from life to death also entails a passage from falseness to truth†¦Ã¢â‚¬  (326). One could also look at this in a different light. From a physical perspective Ivan does go from life to death, from perfection to imperfection, but from a spiritual perspective it is actually the opposite. It takes the death of Ivan’s physical self to finally see what is important, his spirituality, his ‘divine spark.’ This, he finally realizes, is what true perfection is. Hence, Ivan is able to see past the falseness of conformity in the end and no longer fear death.   Ã‚  Ã‚  Ã‚  Ã‚  In his last moments of life, Ivan sees light instead of death. His final audible words are â€Å"What joy!† despite the pain he feels. This epiphany that he has happens in a single moment and in a sense makes him finally come alive. Thus, right before his final breath Ivan is able to say to himself â€Å"Death is finished, it is no more!† Death no longer has a hold on him because the quest of perfection no longer does. Ivan has finally decided, after a lifetime of denying it, to â€Å"let the pain be.†Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   Analysis of Death of Ivan Ilych Essay -- essays research papers Letting Pain Be   Ã‚  Ã‚  Ã‚  Ã‚  To many individuals the word â€Å"progress† has a positive meaning behind it. It suggests improvement, something humans have been obsessed with since the dawn of society. However, if closely examined, progress can also have a negative connotation as well. While bringing improvement, progress can simultaneously spark conformity, dependency, and the obsession of perfection within the individuals caught in its midst. It is this aspect of progress within modern society that negatively affects Ivan Ilych, Leo Tolstoy’s main character in The Death of Ivan Ilych. Ivan’s attempt to conform to modern society’s view of perfection takes away his life long before he dies. Furthermore, his fear of death and reactions towards it reflects modern society’s inability to cope with the ever present reminder that humans still suffer and die, despite all attempts to make life painless, perfect, and immortal.   Ã‚  Ã‚  Ã‚  Ã‚  Although we as a society have advanced and made people’s lives easier, our mental suffering is as present as ever, due to our incessant need to have everything perfect. We seem to forget that the fascination of living comes from the imperfect and the unexpected. In her essay â€Å"On the Fear of Death† Elisabeth Kubler-Ross suggests that the modern age, while increasing life span and ease of life, has at the same time given way to a â€Å"rising number of emotional problems,† amongst the living (Ross 407). She also suggests that because of modern society’s progress, there has been an increased anxiety towards death. While Ross is writing for twentieth century society her ideas apply to the nineteenth century as well, when Tolstoy wrote The Death of Ivan Ilych.   Ã‚  Ã‚  Ã‚  Ã‚  Ivan Ilych is living during the industrial revolution, a time of technological advancement, that mainly advances the upper class, which he is apart of. Ivan’s number one priority in life is to be comfortable and to do the correct thing at all times. Every decision he makes, including who he chooses to marry, is with the intent that it does not damage his â€Å"easy, agreeable, and always decorous character of his life,† (Tolstoy 213). Ivan is convinced that the best way to have an easy and agreeable life is to be wealthy, marry a woman from his own class, and live in a house full of modern conveniences and luxury. Ironically, it... ...roduction of Twentieth-Century Literary Criticism, Vol. 44 it is stated that â€Å"Ivan Ilych’s passage from life to death also entails a passage from falseness to truth†¦Ã¢â‚¬  (326). One could also look at this in a different light. From a physical perspective Ivan does go from life to death, from perfection to imperfection, but from a spiritual perspective it is actually the opposite. It takes the death of Ivan’s physical self to finally see what is important, his spirituality, his ‘divine spark.’ This, he finally realizes, is what true perfection is. Hence, Ivan is able to see past the falseness of conformity in the end and no longer fear death.   Ã‚  Ã‚  Ã‚  Ã‚  In his last moments of life, Ivan sees light instead of death. His final audible words are â€Å"What joy!† despite the pain he feels. This epiphany that he has happens in a single moment and in a sense makes him finally come alive. Thus, right before his final breath Ivan is able to say to himself â€Å"Death is finished, it is no more!† Death no longer has a hold on him because the quest of perfection no longer does. Ivan has finally decided, after a lifetime of denying it, to â€Å"let the pain be.†Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  

Symbolism of Albrecht Durer Essays -- Master Engravings Art Essays

Symbolism of Albrecht Durer Albrecht Durer completed the â€Å"Master Engravings† in the years 1513 and 1514. With these three engravings (Knight, Death, and Devil, St. Jerome in His Study, and Melencolia I) he reached the high point of his artistic expression and concentration. each print represents a different philosophical perspective on the â€Å"worlds† respectively of action, spirit, and intellect. Although Durer himself evidently did not think of the three as a set, He sometimes sold or gave St. Jerome and Melencolia I as a pair. In the engraving, Knight, Death, and Devil, it appears that the hero (the Knight) is gaining a moral victory over death. The Knight has often been interpreted as Erasmus’s sturdy Christian soldier who scoffs at death and the devil as he goes about God’s work in his journey through life. The conception of the ‘Christian soldier’ embodies and ideal of manly virtue which the traditional instincts of the Germanic race, German mysticism and Northern versions of Renaissance ideals all contributed to form. The Horse is represented in full profile as to show off it’s perfect proportions; it is forcefully modeled so as to give its perfect anatomy and it moves with regulated step of the riding school so as to give demonstration of perfect rhythm. The fact that a beautiful setter is running by the side of the horse completes the picture of the Christian man as known to the Late Middle Ages – the man who armed with faith and accompanied by religious zeal, symbolized by the faithful hound goes on his way along the narrow path of earthly life menaced by Death and the Devil. From the gloom of this â€Å"rough and dreary scenery there emerge Death and the Devil. Death wears a regal crown and is mounted on... ...giving them away together and that collectors looked at and discussed them side by side. No less than six copies were disposed of as pairs while only one copy of the Melancolia I was given singly and no impression of the Knight, Death and Devil changed hands together with either of the two other prints. In the years 1513 and 1514, Albrecht Durer completed what is now known together as the â€Å"Master Engravings,† Knight, Death, and Devil; St. Jerome in His Study; and Melencolia I. In general each print represents a different philosophical perspective on the â€Å"worlds respectively, of action, spirit and intellect. Bibliography Panofsky, Edwin. The Life and Art of Albrecht Durer. 4th ed. Princeton, New Jersey: Princeton University Press, 1955. Waetzoldt, Willhelm. Durer and His Times. translated by R.H. Boothroyd. London: Phaidon Press Ltd, 1950.

The Big Day :: Personal Narrative Writing

The Big Day â€Å"Heekin quit fucking staring at the clouds you might be playing this weekend,† screamed Coach Bernardi. All week I waited, sweating every night just wondering if Saturday would be the day I would start my first college football game. Every night I thought what I would do if I was to start, was I ready for this? I would be a little chihuahua amongst a pack of wolves on the field. But all week I had trained to the point that all the sweat in my shirt could have been rung out to make a full cup of water. My Saturday morning started just as every other football players did 10:00a.m wake up, then a short walk over to the dome for walkthroughs. Then to The Place for my usual breakfast the hungry man special: three eggs, two pieces of bacon, two patties of sausage, a portion of hash browns that was the size of my hand stretched out, and my choice of three pancakes or French toast. After that huge meal I couldn’t resist just going back to the dorms and finding a great resting place in my bed. For some reason every person in the damn dorms insisted in walking into my room and waking me up so I was not the most cheerful person when the alarm clock went off three hours later. â€Å"Trevor get you ass out of bed your late for team meal, said Bobby. No I can’t be I set my alarm for 2p.m. Yea but you have hit the snooze button five times so that means its about 2:20 right now and meal started five minutes ago.† That was a great way to get this all started walking late into team meal I could just imagine what the coaches were going to say to me when I got there. As I walk in to the dining hall I find Coach Bernardi sitting in a chair. â€Å"Damn Heekin where the hell have you been I thought you were going to be a no show! Were you afraid that you might have to play today?

Synthesis of Aspirin

Abstract: The purpose of this lab is to synthesise acetylsalicylic acid (aspirin) by creating a reaction between acetic anhydride and salicylic acid. This was be accomplished through the use of recrystallization. Acetic anhydride and salicylic acid are mixed together, and then acidified by the addition of a few drops of concentrated sulfuric acid, which catalyzed the reaction. The percent yield is calculated to determine the effectiveness of the reaction in preparing the desired product (aspirin).The limiting reactant of the equation was salicylic acid. After the limiting reactant was determined, the theoretical yield of aspirin was calculated at approximately 1.97g. The actual yield was only around 0.67g, producing a percent yield of 34.3%. These results show that the methods used were only partially successful at achieving the goal of the experiment (synthesising aspirin). The findings showed that acetylsalicylic acid can be produced through a reaction between salicylic acid and ac etic anhydride, but that a much lower yield will be produced. A higher yield could surely be achieved if several sources of error were to be eliminated.Introduction: Acetylsalicylic acid is commonly used to alleviate minor aches and pains (Wikipedia, Aspirin, 2013). The active metabolite ingredient in acetylsalicylic acid (aspirin) is salicylic acid (Wikipedia, Salicylic acid, 2013), which was first discovered by Edward Stone in 1763 (Wikipedia, Aspirin, 2013).Salicylic acid is toxic in large quantities but in small doses can be useful for food preservatives and as an antiseptic. Other than being used in the production of aspirin, acetic anhydride is used to convert cellulose to cellulose acetate, a key component in photographic film and other coated materials (Wikipedia, Acetic anhydride, 2013). Sulfuric acid has many applications, such as pigments, explosives, lubricants, batteries, antifreeze, and detergents. In the synthesis of aspirin, sulfuric acid is also used as a catalyst t o speed up the reaction (Wikipedia, Sulfuric acid, 2013).Limiting reactants are important in chemical reactions because a reaction cannot proceed without all of the reactants. That is to say, a reaction can  only occur until one reactant is used up (Kirk, 2013). Percent yields are related to limiting reactants because the formula to solve for percent yield includes theoretical and actual yield. The theoretical yield is the amount of a product formed when the limiting reactant in completely consumed, and is the maximum amount that can be produced from the amount of reactants used in the reaction. The theoretical yield is rarely obtained because of sources of error, side reactions, or other complications. The percent yield is the actual yield of a product given as a percentage of the theoretical yield (Kirk, 2013).Purpose:How can one prepare aspirin through a reaction between salicylic acid and acetic anhydride?Apparatus:(2) 250 mL beaker 10 mL graduated cylinder Filter paper Funnel support Hot plate 25 mL graduated cylinder 50 mL Erlenmeyer flask Eyedropper pipette Funnel 100 mL beaker Wash bottleMaterials:Boiling chips (calcium carbonate) Acetic anhydride 18M sulfuric acid Ethanol Salicylic acid Distilled water IceMethod: 1. Prepared a water bath by half-filling a 250 mL beaker with water and heating it on a hot plate to until it was near boiling. Placed a few boiling chips in the beaker to prevent bumping if the water began to boil. 2. Weighed out 1.5g of salicylic acid on a piece of filter paper. Recorded the weight on the data sheet. Transferred the salicylic acid to a 50 mL Erlenmeyer flask. 3. Measured out 5.0 mL of acetic anhydride in a graduated cylinder from the fume hood. Recorded the volume of acetic anhydride used on the data sheet. Poured the acetic anhydride into the 50 mL Erlenmeyer flask containing the salicylic acid.4. Took the Erlenmeyer flask to the fume hood and added 5 drops of concentrated sulfuric acid to the mixture. 5. Mixed the solut ion and placed the Erlenmeyer flask in the water bath for about 10 minutes, making sure the Erlenmeyer flask did not tip in the water bath. 6. After the 10 minutes elapsed, added 2 mL of distilled water with an eyedropper carefully to avoid splatter. Waited 6 minutes, during which time an ice water mixture was prepared in another 250 mL beaker. 7. After the 6 minutes elapsed, 10 mL of distilled water was added to the Erlenmeyer flask and placed in the ice water, avoiding getting any of the ice water in the Erlenmeyer flask. A precipitate formed as the solution cooled. Used the â€Å"scratching† method, in which the bottom of the Erlenmeyer flask is scraped, to speed up the process of precipitate formation.8. Prepared a piece of filter paper in a filter funnel and filtered off the precipitate from the Erlenmeyer flask solution. After the liquid drained through the filter paper, washed the filtrate with two 10 mL portions of cold distilled water. When all the water had drained through, the filter paper was removed, and the solid (impure aspirin) was scraped into a dry 100 mL beaker using a clean scoopula.Recrystallization9. Measured out 5 mL of ethanol from the fume hood in a graduated cylinder, and added it to the 100 mL beaker containing the solid aspirin. Swirled the beaker to dissolve as much of the solid as possible, then placed the beaker on the hot plate until the solid completely dissolved. 10. After the solid  dissolved, added about 15 mL of distilled water. Prepared another ice water mixture in the 250 mL beaker and placed the 100 mL beaker in the ice water. Waited about 10 minutes. 11. Weighed a piece of filter paper and recorded it on the data sheet. Prepared the filter paper in a funnel and filtered off the precipitate. Rinsed the dirty apparatus thoroughly with lots of water. After all of the water was filtered through, left the filter paper to dry until the next class. 12. Weighed the piece of filter paper with the aspirin on it. Recorded the weight on the data table. Discarded the aspirin.Results: Overall Findings: When the salicylic acid and acetic anhydride were mixed, a white, powdery solution formed. When the sulfuric acid was added, a clear solution formed that produced heat. After heating, then cooling and scratching the solution, a white precipitate formed. The moisture in the precipitate was filtered overnight and what was left over was the desired product, aspirin.Qualitative Data: The boiling chips (calcium carbonate) were white, opaque crystals. The acetic anhydride was a clear solution with a vinegar-like odour. The salicylic acid was a find, white solid powder. The ethanol was a clear solution with an odour similar to strong alcohol. The sulfuric acid was a clear solution with a strong odour when heated. The aspirin (acetylsalicylic acid) was a white, solid powder.When the acetic anhydride and salicylic acid were mixed, they produced a white, powdery solution. When the sulfuric acid was added to this s olution, it turned clear and was warm. Upon heating the solution and adding water, puffs of smoke were produced. When the solution cooled and the â€Å"scratching† method was used, a white precipitate formed.Quantitative Data: Density (Table #1) Substance Density Acetic anhydride 1.08 m/LVolume (Table #2) Substance Volume Acetic anhydride 5.0 mLMolar weight (Table #3) Substance Molar weight Salicylic acid 138.12 g/mol Acetic anhydride 102.09 g/mol Acetylsalicylic acid 180.16 g/mol Weight (Table #4) Substance Weight Salicylic acid 1.51 g Acetic anhydride 5.4 g Empty filter paper 1.27 g Filter paper and aspirin 1.946 g Aspirin 0.676 gPercent Yield (Table #5) Substance Percent Yield Aspirin 34.3%Analysis: Determine whether the limiting reactant is the salicylic acid or the acetic anhydride. First, convert both masses to moles. 1 mole is equal to the molar mass of a substance; therefore, the grams of acetic anhydride and grams of salicylic acid must be divided by their molar mass es respectively.Molar mass of acetic anhydride = 4(12.01) + 6(1.008) + 3(16) = 102.088g Molar mass of salicylic acid = 7(12.01) + 6(1.008) + 3(16) = 138.118 g Acetic anhydride: 5.4g C4H6O3 x 1 mole C4H6O3 l= 0.052895541 moles C4H6O3 102.088g C4H6O3Salicylic acid:1.51g C7H6O3 x 1 mole C7H6O3 = 0.01093268 moles C7H6O3 138.118 g C7H6O3Since both acetic anhydride and salicylic acid have a coefficient of 1, the smaller number is the limiting reactant. Therefore, salicylic acid is the limiting reactant of the reaction. Next, calculate the theoretical yield of aspirin by converting the mass of the limiting reactant to grams of aspirin. 1.51g C7H6O3 x 1 mole C7H6O3 x 1 mole C9H8O4 x 180.154 g C9H8O4138.118 g C7H6O3 1 mol C7H6O31 mol C9H8O4 = 1.969566168g AspirinUsing the theoretical yield and the actual yield (from the data table), calculate the percent yield.Percent yield = Actual yield x 100 = l 0.676g l x 100 = 34.3% Theoretical yield1.969566168gDiscussion: Sources of error that were pos sibly present in the synthesis of aspirin lab are an improperly calibrated balance, an inaccurate hot plate, contamination  of the substances, age of the substances, or contamination of the glassware. Inaccurate calibrations of the hot plate or balance could have shown higher or lower quantitative data which would have affected the results by producing either a higher or lower percent yield. A contamination of the substances used or the glassware could have caused the substances to react differently with each other, again causing the percent yield to change depending on how the contamination affected the substances by producing a higher or lower percent yield.Another source of error could have been due to the transport of the aspirin from the Erlenmeyer flask after cooling to the funnel to be filtered. Some of the aspirin may have been lost or left behind and that would have showed a lower percent yield. The accuracy of this lab could be improved with more precise equipment, allow ing the experimenter to be more confident in the accuracy of the measurements obtained. While the aspirin was left overnight to allow time for the moisture to be filtered out, the air could have been a contaminant.A way to get rid of the source of error would be to keep the samples in a more isolated area where there is a smaller chance of contamination. Aspirin has many real-life applications. It is a pain reliever and a non-steroidal anti-inflammatory (NSAID). It has become very common as an antiplatelet to prevent blood clot formation and is used to prevent heart attacks and strokes. It has been present for over one hundred years and is one of the most widely used medications in the world. Conclusion:The main objective of the synthesis of aspirin lab was so produce aspirin (acetylsalicylic acid) through the reaction of salicylic acid and acetic anhydride. The methods used included recrystallization and scratching to produce a precipitate, which was then filtered to remove any exc ess moisture. The results displayed a percent yield of 34.3%, from a theoretical yield of about 1.97g of aspirin and an actual yield of approximately 0.68g of aspirin. Upon completion of the lab, analysis, and calculations, it is evident that the synthesis of aspirin is possible using these methods but that the yield will be relatively low.

Ansoff Matrix Essay

1 What are the iv increase appendage strategies according to the Ansoff hyaloplasm? Critically evaluate each of them with an curb example of each.Answer1(1) carrefour strategies for cultivation a characterful way of looking at growth opportunities is offered by the Ansoff Matrix as it is a practical framework for view about how growth gutter be achieved by means of result strategy. It comprises four ecumenic approaches to cut-rate gross revenue growth food mart acumen/e labor partyation, product using, market teaching and diversification. foodstuff sharpness and expansion are strategies relating to increment exiting products in real markets. commercialize discernment depends on getning competitors guests or buying competitors (thereby increasing market get by). Defense of increase penetration may be through discouraging competitive entry. Market expansion may be through converting non-users to users or increasing usage rate. Although market share may not increase, sales growth is achieved through increasing market size.Product increase is a strategy for ontogenesis recentborn products for subsisting markets. It has three variants extending active product lines (brand extensions) to give current customers great choice product re forward-lookingal (updates of octogenarian products) and innovation (developing fundamentally different products). Market development is a strategy for winning existing products and marketing them in raw(a) markets. This may be through the advance of young uses of existing products to new customers, or the marketing of existing products to new market segments (e.g. overseas markets). Diversification (entry into new markets) is a strategy for developing new products for new markets. It is the about risky of the four growth strategies but in like manner potentially the most rewarding. (2) For example market penetration (Cadbury Schweppes did by increasing economic consumption by 87 percent over a four-year period) market expansion (Kelloggs has targeted lapsed breakfast cereal users who rediscover the pleasure of eat cornflakes when feeding their children) product development (the development of the compact disc is an example) market development (Andy Thornton Ltd., an interior design business, successfully increase sales by entranceway Scandinavia and Germany, twain geographic segments that provided new expansion opportunities for its services.) diversification (Sonys bowel movement into 8 mm camc rigs)Answer2Ansoff Matrix ( can deal with new product)In order to increase sales volume, Ansoff matrix provides a framework, by corporate trust portray product and new product, present market and new market into 2*2 matrixes, which are market penetration or expansion, product development, market development and diversification.1. Existing product + existing market. The strategies for this matrix are market penetration or expansion. For penetration, the most basic way is to wi n competitors customers. This may be achieved by more effective use of promotion (compared with competitors) or distribution, or by cutting prices. Increasing promotional expenditure is other method of winning competitors customers, as Cadbury did by increasing expenditure by 87 per cent over a four-year period. Another way to win competitors customer is to buy competitors. The biggest advantage of this method is to magnetize customers immediately. Moreover, buying other rivals can excessively gain their limited resources and advanced skills and expertise.However, it besides has its disadvantages, such as high monetary value of capital and risk. In renderition, in order to protect gained penetration, a company has to discourage new competitors to enter into market. Barriers can be created by cost advantages. For example, low labor cost. Highly differentiated products and high displacement costs as well as displaying aggressive tendencies to retaliate play a role in repelling new entrants. As for expansion, there are ii methods to boost sales. One is to convert non-user to user, another is to increase usage rate. For example, carnation entered the powdery drinking chocolate whitening market with coffee mate, a key success actor was its ability to persuade hitherto non-user of powdery whiteners to switch from milk.2. sensitive product + existing market. The strategy for this category is product development. It can be achieved by three ways. The inaugural way is innovation. Both extend existing product lines for giving customers more choices and add new feature to trigger the commerce up can increase sale volume. The second way is product switch, which involves the replacement of previous(a) brands/models with new one. This is common in car industry and oft involves an upgrading of the old model with a new replacement. The last-place oneis replacement of an old product with a fundamentally different one, often found on technology change. The deve lopment of CD is an example.3 Existing product + new market. The strategy is market development, which fee-tail promotions of existing product to a new market, or existing product to a new segment. For instance, nylon is marketed as a replacement of silk, but expanded into shirt, carpet and so on. For new segment, Andy Thornton Ltd. Successfully increased sales by entering Scandinavia and Germany, two geographic segments that provided new expansion opportunities for its services.4 New product + new market. The strategy for it is entering into new markets (diversification). This is the most risky option, particularly when the entry strategy is not based on the core competences. However, it can also be the most rewarding, as exemplified by Hondas move from motorcycles to cars and Sonys move into 8mm camcorders.