Friday, September 6, 2019
Letter of motivation Essay Example for Free
Letter of motivation Essay Letter of motivation I am senior student of bachelor of computer engineering at Sepahan institute of higher education and I want to continue my study in telecommunications engineering at the Politecnico di Milano in Italy. here are my reasons for this choice. I always tried to do my best to follow and understand the evolving and growing line of technology which is going as fast as it can, so I chose Computer Engineering for my bachelor degree and every class was a great opportunity for me to learn something new and helpful but for my master degree I wanted to go deeper in the field of omputer networks and telecommunications which is my passion and my goal is to learn more and more and to put my learnings and knowledge finally in the field. ne of my favorite company that I want to be part of is Cisco which is the best network company out there. And my reasons for choosing Italy are that this will be a great and life changing opportunity for me to visit another countries and get familiar with other cultures and traditions and the important part is that Italy is a great developed and technological country which provides me with such a professional environment or me to grow my skills and be an expert in my field. The important part of studying abroad is to choose the best university in a country. so I did a lot of research about university rankings and the programs they offer and even asked a lot of the students who chose polimi for their destination. And with all that in mind and some other factors such as the faculty I chose polimi to continue my study in master. With all that and my knowledge of my self and my education and skill background I know I can be a great candidate for admission. and I hope I could get everything possible to learn from this program.
Thursday, September 5, 2019
Issues in American Electoral System
Issues in American Electoral System John Palenschat WORST CASE SCENARIO RESEARCH AND REFLECTION PAPER Like many other Americans, the election of Donald Trump was one of the worst things I could imagine happening. Even now, I am puzzled as to why Donald Trump was elected because a majority of voters view him unfavorably (Pew, 2017). So just how did he get elected? The point of a democratic election is to represent the will of voters in choosing an executive. With so many dissatisfied with the results of the election, one must wonder if our current electoral system is fulfilling its stated purpose. Might there be something wrong with the way elections are held now? [G1][G2] I did some research and have come to several conclusions: namely, that our current system of First Past the Post consistently leads to elections for candidates that are generally unfavored by the majority of the population (Pew, 2016). I believe that the United States should, as an incremental reform, generally adopt ranked choice voting: in order to reduce vote splitting, voter disenfranchisement, and to reduce the negativity of campaigning. Right now, most elections in the United States utilize First Past the Post voting, which is a system of elections in which an individual voter has only one vote and is allowed to vote for only one candidate (Aceproject, 2017). This system has a big flaw. People may vote for a candidate that they may not necessarily prefer in order that they do not split the vote in favor of an opponent. In the 2000 Presidential election, Republican George W. Bush beat Democrat Al Gore by less than 600 votes in the decisive Florida election. Green Party candidate Ralph Nader received over 100,00 votes in Florida. [G3]While he may not have spoiled the election, surveys indicate that people who voted for Nader probably would have voted for Gore had they known how tight the race would be (Jones, 2004). This event has had serious consequences for the American people. For example, a Gore administration might not have invaded Iraq in 2003, which destabilized the region and cost US taxpayers over $2 Trillion dollars (Trotta, 2013). Modern voters are cognizant of the results of that election and have adjusted their votes accordingly. As a result, voters now do not necessarily vote for their first choice. There has to be a better way. As I looked for an alternative voting method to First Past the Post, I discovered a system called Ranked Choice voting (RCV). RCV is a system of elections in which electors rank the candidates in the order of their choice, by marking a 1 for their favorite, 2 for their second choice, 3 for their third choice and so on (FairVote Instant Runoff). Although there are other ways (perhaps even better!) of doing RCV, for the purposes of this paper, I will be specifically discussing the form known as Instant-Runoff voting as it appears to be the most feasible to implement in our current political situation. [G4][G5] In this system, if no candidate has a clear majority of first votes, the trailing candidate may be dropped and the first votes for the dropped candidate are eliminated. Then, the second choices of the voters who voted first for the dropped candidate are distributed to the remaining candidates. This process is repeated until a candidate has a clear majority of the vote.[G6] The main advantage of Ranked Choice Voting is that the eventual candidate chosen better represents the consensus of voters. As candidates are unlikely to earn the majority of votes in the first round of counting, candidates may moderate their rhetoric in an attempt to earn second place votes (Aceproject, 2017); The candidates may tamp down on their own campaigns negative ads in order to not alienate potential voters, and they would want to appeal to the greatest possible base. Since voting for a third party candidate in this system is less risky, a wider variety of interests would likely be represented. As an example, in the recent election, a person could safely cast their first vote for Jill Stein and their second for Sanders and so on without spoiling their vote and splitting the ticket for a more popular candidate that they might agree less with, such as Clinton. As voters would not be forced to vote for the lesser of two evils, one might expect to see a proliferation of more diverse third parties that better represent [G7]the constituents desires. I believe that if Ranked Choice Voting is adopted broadly across the United States, voters will feel more satisfied with the results of the election[8] At first, I though that RCV was just an academic exercise, thought up by some Poli-Sci grad student working on their thesis[G9], but I was surprised to learn that Ranked Choice Voting has already been put to effective use worldwide and has proven to be a reliable system for several decades now[10]. For example, it is used in such diverse races as parliamentary elections in Australia (Paul, Owen, 2013), presidential elections in Ireland (Citizens Information, 2016), and in municipal elections in Minneapolis and Saint Paul (City of Minneapolis). [G11] Recently, the State of Maine voted to adopt an Instant Runoff system for congressional, senatorial, and gubernatorial elections (Grabar, 2016). According to a study funded by Fairvote, an electoral reform advocacy group, citizens in cities that have adopted RCV report that campaigns are less negative, that the system is easily understandable, and that they believe that it should be adopted more widely (Tolbert, et al). As people realize that the current form of voting isnt the only choice available, I believe that voters will increasingly demand RCV from election committees.[G12] However, there are several legitimate issues with Ranked Choice Voting that need to be addressed; Jason McDaniels of San Francisco State University believes that increasing the complexity of voting is much more cognitively demanding than merely choosing a preference For some, this may seem like a small change, but for others, it could make the already daunting task of being an informed voter even more challenging. Decades of research show us that when voting is made more complex, it tends to lead to lower participation and more unequal outcomes. (McDaniels, 2016). However, studies taking place in Californian cities that have adopted RCV paint a different picture. Nearly 90% of those polled reported that they had an easy time understanding how their ballots worked (Tolbert, et al). Perhaps, pre-election day, a city or state could wage a concentrated, multimedia campaign to educate voters on the new system. A multifaceted approach utilizing TV news spots, radio jingles, and mailed remi nder cards could be particularly effective. Another possible issue with RCV is that confused voters may simply list their preference by order in which the candidates appear on the ballot, as has been the case in Australia. This problem could perhaps be solved by holding a random drawing each election to determine in which order the candidates are listed on the ballot (AEC, 2016). In conclusion, I believe that seriously examining the institutions of our society and critically deconstructing their use and origin will help to build a more perfect union. It is important to recognize that structural systems have a large impact on our daily life and to realize that they are not unchangeable. Due to the effects of the recent election, I am very cognizant of how our electoral system alienates the very people that it was created to represent. Rather than giving into resignation, I have researched the issue and have come up with at least a very general course of action that could be taken to avoid another divisive election. I hope that I have interested you in the topic of electoral reform and encourage you to research the topic yourself and come to your own conclusions.[13] An informed and active citizenship is the best guarantee for the continuation of the republican ideal. Work Cited FairVote (No publication date). Ranked Choice Voting / Instant Runoff. FairVote. http://www.fairvote.org/rcv#rcvbenefits. Accessed 19 February. 2017 Minneapolis Elections and Voter services (No publication date). Frequently Asked Questions about Ranked-Choice Voting. The city of Minneapolis.[G14] http://vote.minneapolismn.gov/rcv/what-is-rcv. Accessed 19 February. 2017 [G15] Paul, Owen (2013). How does Australias voting system work?. The Guardian. https://www.theguardian.com/world/2013/aug/14/how-does-australia-s-voting-system-work. Accessed 19 February 2017 McDaniels, Jason. (2016). What Ive found researching ranked-choice voting: It makes voting harder, lowers participation. Bangor Daily News. http://bangordailynews.com/2016/08/20/opinion/contributors/what-ive-found-researching-ranked-choice-voting-it-makes-voting-harder-lowers-participation/. Accessed 19 February. 2017 Aceproject. (No publication date) Advantages and disadvantages of first past the post. ACE Electoral Knowledge Network. http://aceproject.org/ace-en/topics/es/esd/esd01/esd01a/esd01a01. Accessed 20 February. 2017 Pew Research Center. (2017). Early public attitudes about Donald Trump. People-Press.org. http://www.people-press.org/2017/02/16/1-early-public-attitudes-about-donald-trump/ Accessed 22 February 2017. Pew Research Center. (2016). Voters evaluation of the campaigns. People-Press.org. http://www.people-press.org/2016/11/21/voters-evaluations-of-the-campaign/ Accessed 22 February 2017. Citizens information. (2016). Proportional Representation. The [G16]Republic of Ireland. http://www.citizensinformation.ie/en/government_in_ireland/elections_and_referenda/voting/proportional_representation.html. Accessed 22 February 2017. Grabar, Henry. (2016). Maine Just Voted for a Better Way to Vote. Slate.com. http://www.slate.com/articles/business/moneybox/2016/11/maine_just_passed_ranked_choice_voting_bravo.html. Accessed 22 February 2017. Tolbert, Caroline, et al. (No publication date). Ranked Choice Voting in Practice. Fairvote https://fairvote.app.box.com/v/APSA-Civility-Brief-2015. Accessed 22 February 2017 Trotta, Daniel. (2013). Iraq War cost US more than $2 trillion: study. Reuters.com http://www.reuters.com/article/us-iraq-war-anniversary-idUSBRE92D0PG20130314. Accessed 22 February 2017. AEC. (2016). Positions on the ballot paper, draw for the Senate and draw for the House of Representatives. Australian Elections Commission[G17]. http://www.aec.gov.au/Voting/ballot-draw.htm. Accessed 23 February 2017. Jones, Jeffrey. (2004). The Nader Factor. Gallup.com. http://www.gallup.com/poll/10798/nader-factor.aspx. Accessed 22 February 2017 [G1]Deleted:, [G2]Deleted:u [G3]Inserted: , [G4]Deleted:u [G5]Deleted:. [G6]Inserted: s [G7]Inserted: , [8]This is a strong point in favor. Think of all the recent turmoil after the election. If everyone was content with the outcome of the election (even if they didnt get their first pick), that would be a great motivation to change the voting system. You could probably expound more on this point, or why you believe it to be true. [G9]Inserted: , [10]This is another strong point. The best predictor for success is past success. Nice! [G11]Deleted:, [G12]Inserted: n [13]Your two most important paragraphs are the first, and the last. In the first, you tell your audience what youre going to say, and in the last, you tell your audience what youve said. The last sentence will likely stay with your reader. After you recap your essay in the last paragraph, leave them with a final deep thought or conclusive statement that sums up your argument and/or point. Or maybe something theatrically doomsday-ish. Perhaps, The election of Trump is a direct consequence of our current voting system; If we dont take a good, hard look at the way we currently push people into power, the consequences could get even worst. A bit much perhaps, but its your final punch to convince the reader that this is something they need to act on. [G14]Inserted: The c [G15]Deleted:C [G16]Inserted: The [G17]Inserted: s
Wednesday, September 4, 2019
Causes, Symptoms and Treatments of Anaemia
Causes, Symptoms and Treatments of Anaemia 1. Introduction Anaemia is a syndrome characterised by a lack of healthy red blood cells or haemoglobin deficiency in the red blood cells, resulting in inadequate oxygen supply to the tissues. The condition can be temporary, long-term or chronic, and of mild to severe intensity. There are many forms and causes of anaemia. Normal blood consists of three types of blood cells: white blood cells (leucocytes), platelets and red blood cells (erythrocytes). The first generation of erythrocyte precursors in the developing foetus are produced in the yolk sac. They are carried to the developing liver by the blood where they form mature red blood cells that are required to meet the metabolic needs of the foetus. Until the 18th week of gestation, erythrocytes are produced only by liver after which the production shifts to the spleen and the bone marrow. The life of a red blood cell is about 127 days or 4 months (Shemin and Rittenberg, 1946; Kohgo et al., 2008). The main causes of anaemia are blood loss, product ion of too few red blood cells by the bone marrow or a rapid destruction of cells.           Haemoglobin, a protein, present in the red blood cells is involved in the transport of oxygen from the lungs to all the other organs and tissues of the body. Iron is an important constituent of the haemoglobin protein structure which is intimately involved in the transport of oxygen. Anaemia is generally defined as a lower than normal haemoglobin concentration. The normal blood haemoglobin concentration is dependent on age and sex, and, according to the World Health Organisation (WHO) Expert Committee Report, anaemia results when the blood concentration of haemoglobin falls below 130 g/L in men or 120 g/L in non-pregnant women (WHO, 1968). However, the reference range of haemoglobin concentration in blood could vary depending on the ethnicity, age, sex, environmental conditions and food habits of the population analysed. According to Beutler and Warren (2006), more reasonable benchmarks for anaemia are 137 g/L for white men aged between 20 and 60 years and 132 g/L for older men. The value for women of all ages would be 122 g/L. Also, the lower limit of normal of haemoglobin concentrations of African Americans are appreciably lower than that of Caucasians (Beutler and Warren, 2006).           Besides the well recognised iron deficiency anaemia, several inherited anaemias are also known. These are mostly haemoglobinopathies. Adult haemoglobin is a tetrameric haeme-protein. Abnormalities of beta-chain or alpha-chain produce the various medically significant haemoglobinopathies. The variations in amino acid composition induced genetically impart marked differences in the oxygen carrying properties of haemoglobin. Mutations in the haemoglobin genes cause disorders that are qualitative abnormalities in the synthesis of haemoglobin (e.g., sickle cell disease) and some that are quantitative abnormalities that pertain to the rate of haemoglobin synthesis (e.g., the thalassemias) (Weatherall., 1969). In SCD, the missense mutation in the ÃŽ ²-globin gene causes the disorder. The mutation causing sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid 6. The substitution converts a glutamic acid codon (GAG) to a valine codon (GTG). The form of haemoglobin in persons with sickle cell anemia is referred to as HbS. Also, the valine for glutamic acid replacement causes the haemoglobin tetramers to aggregate into arrays upon deoxygenation in the tissues. This aggregation leads to deformation of the red blood cell making it relatively inflexible and restrict its movement in the capillary beds. Repeated cycles of oxygenation and deoxygenation lead to irreversible sickling and clogging of the fine capillaries. Incessant clogging of the capillary beds damages the kidneys, heart and lungs while the constant destruction of the sickled red blood cells triggers chronic anaemia and episodes of hyperbilirubinaemia.           Fanconi anaemia (FA) is an autosomal recessive condition, and the most common type of inherited bone marrow failure syndrome. The clinical features of FA are haematological with aplastic anaemia, myelodysplastic syndrome (MDS), and acute myeloid leukaemia (AML) being increasingly present in homozygotes (Tischkowitz and Hodgson, 2003). Cooleys anaemia is yet another disorder caused by a defect in haemoglobin synthesis.           Autoimmune haemolytic anaemia is a syndrome in which individuals produce antibodies directed against one of their own erythrocyte membrane antigens. The condition results in diminished haemoglobin concentrations on account of shortened red blood cell lifespan (Sokol et al., 1992).           Megaloblastic anaemia is a blood disorder in which anaemia occurs with erythrocytes which are larger in size than normal. The disorder is usually associated with a deficiency of vitamin B12 or folic acid . It can also be caused by alcohol abuse, drugs that impact DNA such as anti-cancer drugs, leukaemia, and certain inherited disorders among others (Dugdale, 2008).           Malaria causes increased deformability of vivax-infected red blood cells (Anstey et al., 2009). Malarial anaemia occurs due to lysis of parasite-infected and non-parasitised erythroblasts as also by the effect of parasite products on erythropoiesis (Ru et al., 2009).           Large amounts of iron are needed for haemoglobin synthesis by erythroblasts in the bone marrow. Transferrin receptor 1 (TfR1) expressed highly in erythroblasts plays an important role in extracellular iron uptake (Kohgo et al., 2008). Inside the erythroblasts, iron transported into the mitochondria gets incorporated into the haeme ring in a multistep pathway. Genetic abnormalities in this pathway cause the phenotype of ringed sideroblastic anemias (Fleming, 2002). The sideroblastic anemias are a heterogeneous group of acquired and inherited bone marrow disorders, characterised by mitochondrial iron overload in developing red blood cells. These conditions are diagnosed by the presence of pathologic iron deposits in erythroblast mitochondria (Bottomley, 2006).  2. Classification of anaemia Anaemia can be generally classified based on the morphology of the red blood cells, the pathogenic spectra or clinical presentation (Chulilla et al., 2009). The morphological classification is based on mean corpuscular volume (MCV) and comprises of microcytic, macrocytic and normocytic anaemia.      (a) Microcytic anaemia refers to the presence of RBCs smaller than normal volume, the reduced MCV ( 15 would probably indicate IDA (Chulilla et al., 2009).           In macrocytic anaemia, erythrocytes are larger (MCV > 98 fL) than their normal volume (MCV = 82-98 fL). Vitamin B12 deficiency leads to delayed DNA synthesis in rapidly growing hematopoietic cells, and can result in macrocytic anemia. Drugs that interfere with nucleic acid metabolism, such as.hydroxyurea increases MCV (> 110 fL) while alcohol induces a moderate macrocytosis (100-110 fL). In the initial stage, most anaemias are normocytic. The causes of normocytic anaemia are nutritional deficiency, renal failure and haemolytic anemia (Tefferi, 2003). The most common normocytic anaemia in adults is anaemia of chronic disease (ACD) (Krantz, 1994). Common childhood normocytic anaemias are, besides iron deficiency anaemia, those due to acute bleeding, sickle cell anemia, red blood cell membrane disorders and current or recent infections especially in the very young (Bessman et al., 1983). Homozygous sickle cell disease is the most common cause of h aemolytic normocytic anemias in children (Weatherall DJ, 1997a).           In practice, the morphological classification is quicker and therefore, more useful as a diagnostic tool. Besides, MCV is also closely linked to mean corpuscular haemoglobin (MCH), which denotes mean haemoglobin per erythrocyte expressed in picograms (Chulilla et al., 2009). Thus, MCV and MCH decrease simultaneously in microcytic, hypochromic anemia and increase together in macrocytic, hyperchromic anemia.           Pathogenic classification of anaemia is based on the production pattern of RBC: whether anaemia is due to inadequate production or loss of erythrocytes caused by bleeding or haemolysis. This approach is useful in those cases where MCV is normal. Pathogenic classification is also essential for proper recognition of the mechanisms involved in the genesis of anaemia. Based on the pathogenic mechanisms, anaemia is further divided into two types namely, (i) hypo-regenerative in which the bone marrow production of erythrocytes is decreased because of impaired function, decreased number of precursor cells, reduced bone marrow infiltration, or lack of nutrients; and (ii) regenerative: when bone marrow upregulates the production of erythrocytes in response to the low erythrocyte mass (Chulilla et al., 2009). This is typified by increased generation of erythropoietin in response to lowered haemoglobin concentration, and also reflects a loss of erythrocyt es, due to bleeding or haemolysis. The reticulocyte count is typically higher.           Sickle cell disease is characterised by sickled red cells. The first report of SCD was published a century ago noting the presence of peculiar elongated cells in blood by James Herrick, an American physician (1910). Pauling et al. (1949) described it as a molecular disease. The molecular nature of sickle haemoglobin (Hb S) in which valine is substituted for glutamic acid at the sixth amino acid position in the beta globin gene reduces the solubility of Hb, causing red cells to sickle (Fig. 1). Sickling of cells occurs at first reversibly, then finally as a state of permanent distortion, when cells containing HbS and inadequate amounts of other haemoglobins including foetal haemoglobin, which retards sickling, become deoxygenated (Bunn, 1997). The abnormal red cells break down, leading to anaemia, and clog blood vessels with aggregates, leading to recurrent episodes of severe pain and multiorgan ischaemic damage (Creary et al., 2007). The high levels of inflammatory cytokines in SCD may promote retention of iron by macrophage/reticuloendothelial cells and/or renal cells. SCD care commonly depends on transfusion that results in iron overload (Walter et al., 2009). 3. Pathogenesis of anaemia Anaemia is a symptom , or a syndrome, and not a disease (Chulilla et al., 2009). Several types of anaemia have been recognised, the pathogenesis of each being unique. Iron deficiency anaemia (IDA) is the most common type of anaemia due to nutritional causes encountered worldwide (Killip et al., 2008). Iron is one of the essential micronutrients required for normal erythropoietic function While the causes of iron deficiency vary significantly depending on chronological age and gender, IDA can reduce work capacity in adults (Haas Brownlie, 2001) and affect motor and mental development in children (Halterman et al., 2001). The metabolism of iron is uniquely controlled by absorption rather than excretion (Siah et al., 2006). Iron absorption typically occurring in the duodenum accounts for only 5 to 10 per cent of the amount ingested in homoeostatis. The value decreases further under conditions of iron overload, and increases up to fivefold under conditions of iron depletion (Killip et al., 2008). Iron is ingested as haem iron (10%) present in meat, and as non-haem ionic form iron (90%) found in plant and dairy products. In the absence of a regulated excretion of iron through the liver or kidneys, the only way iron is lost from the body is through bleeding and sloughing of cells. Thus, men and non-menstruating women lose about 1 mg of iron per day while menstruating women could normally lose up to 1.025 mg of iron per day (Killip et al., 2008). The requirements for erythropoiesis which are typically 20-30 mg/day are dependent on the internal turnover of iron (Munoz et al., 2009) For example, the amount of iron required for daily production of 300 billion RBCs (20-30 mg) is provided mostly by recycling iron by macrophages (Andrews, 1999).           Iron deficiency occurs when the metabolic demand for iron exceeds the amount available for absorption through consumption. Deficiency of nutritional intake of iron is important, while abnormal iron absorption due to hereditary or acquired iron-refractory iron deficiency anemia (IRIDA) is another important cause of unexplained iron deficiency. However, IDA is commonly attributed to blood loss e.g., physiological losses in women of reproductive age. It might also represent occult bleeding from the gastrointestinal (GI) tract generally indicative of malignancy (Hershko and Skikne, 2009).           Iron absorption and loss play an important role in the pathogenesis and management of IDA. Human iron disorders are necessarily disorders of iron balance or iron distribution. Iron homeostasis involves accurate control of intestinal iron absorption, efficient utilisation of iron for erythropoiesis, proper recycling of iron from senescent erythrocytes, and regulated storage of iron by hepatocytes and macrophages (Andrews, 2008). Iron deficiency is largely acquired, resulting from blood loss (e.g., from intestinal parasitosis), from inadequate dietary iron intake, or both. Infections, for example, with H pylori, can lead to profound iron deficiency anemia without significant bleeding. Genetic defects can cause iron deficiency anaemia. Mutations in the genes encoding DMT1 (SLC11A2) and glutaredoxin 5 (GLRX5) lead to autosomal recessive hypochromic, microcytic anaemia (Mims et al., 2005). Transferrin is a protein that keeps iron nonreactive in the circulation, and delivers iron to cells possessing specific transferrin receptors such as TFR1 which is found in largest amounts on erythroid precursors. Mutations in the TF gene leading to deficiency of serum transferrin causes disruption in the transfer of iron to erythroid precursors thereby producing an enormous increase in intestinal iron absorption and consequent tissue iron deposition (Beutler et al., 2000). Quigley et al. (2004) found a haem exporter, FLVCR, which appears to be necessary for normal erythroid development. Inactivation of FLVCR gene after birth in mice led to severe macrocytic anaemia, indicating haem export to be important for normal erythropoiesis.           The anaemia of chronic disease (ACD) found in patients with chronic infectious, inflammatory, and neoplastic disorders is the second most frequently encountered anaemia after iron-deficiency anaemia. It is most often a normochromic, normocytic anaemia that is primarily caused by an inadequate production of red cells, with low reticulocyte production (Krantz, 1994). The pathogenesis of ACD is unequivocally linked to increased production of the cytokines including tumour necrosis factor, interleukin-1, and the interferons that mediate the immune or inflammatory response. The various processes leading to the development of ACD such as reduced life span of red cells, diminished erythropoietin effect on anaemia, insufficient erythroid colony formation in response to erythropoietin, and impaired bioavailability of reticuloendothelial iron stores appear to be caused by inflammatory cytokines (Means, 1996;2003). Although iron metabolism is characterist ically impaired in ACD, it may not play a key role in the pathogenesis of ACD (Spivak, 2002). Neither is the lack of available iron central to the pathogenesis of the syndrome, according to Spivak (2002), who found reduced iron absorption and decreased erythroblast transferrin-receptor expression to be the result of impaired erythropoietin production and inhibition of its activity by cytokines. However, reduced erythropoietin activity, mostly from reduced production, plays a pivotal role in the pathogenesis of ACD observed in systemic autoimmune diseases (Bertero and Caligaris-Cappio, 1997). Indeed, iron metabolism as well as nitric oxide (NO), which contributes to the regulation of iron cellular metabolism are involved in the pathogenesis of ACD in systemic autoimmune disorders. Inflammatory mediators, particularly the cytokines, are important factors involved in the pathogenesis of the anaemia of chronic disease, as seen in rheumatoid arthritis anaemia (Baer et al., 1990), the cyt okines causing impairment of erythroid progenitor growth and haemoglobin production in developing erythrocytes.           Anaemia is also commonly found in cases of congestive heart failure (CHF), again caused by excessive cytokine production leading to reduced erythropoietin secretion, interference with erythropoietin activity in the bone marrow and reduced iron supply to the bone marrow (Silverberg et al., 2004). However, in the presence of chronic kidney insufficiency, abnormal erythropoietin production in the kidney plays a role in the pathogenesis of anaemia in CHF.           The myelodysplastic syndromes (MDS) are common haematological malignancies affecting mostly the elderly as age-related telomere shortening enhances genomic instability (Rosenfeld and List, 2000). Radiation, smoking and exposure to toxic compounds e.g., pesticides, organic chemicals and heavy metals, are factors promoting the onset of MDS via damage caused to progenitor cells, and, thereby, inducing immune suppression of progenitor cell growth and maturation. TNF- and other pro-apoptotic cytokines could play a central role in the impaired haematopoiesis of MDS (Rosenfeld and List, 2000). Premature intramedullary cell death brought about by excessive apoptosis is another important pathogenetic mechanism in MDS (Aul et al., 1998).           Sickle cell disease (SCD) arising from a point mutation in the ÃŽ ²-globin gene and leading to the expression of haemoglobin S (HbS) is the most common monogenetic disorder worldwide. Chronic intravascular haemolysis and anaemia are some important characteristics of SCD. Intravascular haemolysis causes endothelial dysfunction marked by reduced nitric oxide (NO) bioavailability and NO resistance, leading to acute vasoconstriction and, subsequently, pulmonary hypertension (Gladwin and Kato, 2005).  However, a feature that differentiates SCD from other chronic haemolytic syndromes is the persistent and intense inflammatory condition present in SCD. The primary pathogenetic event in SCD is the intracellular polymerisation or gelation of deoxygenated HbS leading to rigidity in erythrocytes (Wun, 2001). The deformation of erythrocytes containing HbS is dependent on the concentration of haemoglobin in the deoxy conformation (Rodgers et al., 1985). It has been demonstrated that sickle monocytes are activated which, in turn, activate endothelial cells and cause vascular inflammation. The vaso-occlusive processes in SCD involve inflammatory and adhesion molecules such as the cell adhesion molecules (CAM family), which play a role in the firm adhesion of reticulocytes and leukocytes to endothelial cells, and the selectins, which play a role in leukocyte and platelet rolling on the vascular wall (Connes et al., 2008). Thus, inflammation, leucocyte adhesion to vascular endothelium, and subsequent endothelial injury are other crucial factors contributing to the pathogenesis of SCD (Jison et al., 2004). 4. Current therapies for clinical management of sickle cell diseaseincludingacritical appraisal of transfusion Between 1973 and 2003, the average life expectancy of a patient with SCD increased dramatically from a mere 14 years to 50 years thanks to the development of comprehensive care models and painstaking research efforts in both basic sciences especially molecular and genetic studies, and clinical aspects of SCD (Claster and Vichinsky, 2003). The clinical manifestations of SCD are highly variable. Both the phenotypic expression and intensity of the syndrome are vastly different among patients and also vary longitudinally within the same patient (Ballas, 1998). New pathophysiological insights available have enabled treatments to be developed for the recognised haematologic and nonhaematologic abnormalities in SCD (Claster and Vichinsky, 2003). The main goals of SCD treatment are symptom alleviation, crises avoidance and effective management of disease complications. The strategy adopted is primarily palliative in nature, and consists of supportive, symptomatic and preventative approaches to therapy. Symptomatic management includes pain mitigation, management of vasoocclusive crisis, improving chronic haemolytic anaemia, treatment of organ failure associated with the disease, and detection and treatment of pulmonary hypertension (Distenfeld and Woermann, 2009). The preventative strategies include use of prophylactic antibiotics (e.g., penicillin) in children, prophylactic blood transfusion for prevention of stroke in patients especially young children who are at a very high risk of stroke, and treatment with hydroxyurea of patients experiencing frequent acute painful episodes (Ballas, 2002). Currently, curative therapy for sickle cell anaemia is only available through bone marrow and stem cell transplantation. Hematopoietic cell transplantation using stem cells from a matched sibling donor has yielded excellent results in paediatric patients (Krishnamurti, 2007). Curative gene therapy is still at the exploratory stage (Ballas, 2002). Current and potential therapies The potential treatment strategies basically target cellular dehydration, sickle haemoglobin concentrations, endothelial dysfunction, and abnormal coagulation regulation (Claster and Vichinsky, 2003). HbS concentrations are essentially tackled through transfusions while approaches to reduce HbS polymerisation which is the main mechanism for the development of vaso-occlusion include (a) increasing foetal haemoglobin (HbF) concentration using hydroxyurea (Fig. 2), butyrate, or erythropoietin, and (b) preventing sickle cell dehydration using Clotrimazole (Fig. 3) or Mg2+pidolate. Hydroxyurea therapy increases the production of HbF in patients with sickle cell anaemia, and, thereby, inhibits the polymerisation of HbS and alleviates both the haemolytic and vaso-occlusive manifestations of the disease (Goldberg et al., 1990). Recombinant erythropoietin also increases the number of reticulocytes with HbF. Additionally, it has been observed that administration of intravenous recombinant eryt hropoietin with iron supplementation alternating with hydroxyurea enhances HbF levels more than hydroxyurea alone (Rodgers et al., 1993). As SCD is essentially characterized by an abnormal state of endothelial cell activation that is, a state of inflammation, a pharmacologic approach to inhibit endothelial cell activation has proved clinically beneficial (Hebbel and Vercellotti, 1997). Thus, administration of sulfasalazine which is a powerful inhibitor of activation of nuclear factor (NF)-B, the transcription factor promoting expression of genes for a number of pro-adhesive and procoagulant molecules on endothelium to humans has been found to provide transcriptional regulation of SCD at the endothelium level (Solovey et al., 2001). Red blood cell transfusion : a critical appraisal A key therapy that is applied regularly in the clinical management of patients with SCD is packed red blood cell transfusion. RBC transfusion improves the oxygen-carrying capacity which is achieved by enhancing the haemoglobin levels, causes dilution of HbS concentration thereby, reducing blood viscosity and boosting oxygen saturation. Furthermore, RBC transfusion is helpful in suppressing endogenous production of sickle RBCs by augmenting tissue oxygenation ( Josephson et al., 2007). There are two major types of RBC transfusion therapy: intermittent and chronic which are further classified as prophylactic or therapeutic. Intermittent transfusions are generally therapeutic in nature and administered to control acute manifestations of SCD whereas chronic transfusions are performed as general preventative measures to check complications of SCD. RBC transfusion given as a single dose is termed as simple transfusion. Exchange transfusion involves administration of a larger volume of RBCs replacing the patients RBCs that are simultaneously removed. Details of the various types of RBC transfusion and the major clinical indications for the same in SCD patients are listed in Table 1.      SCD (Source: Josephson et al., 2007) Indications for Intermittent transfusions Indications for intermittent transfusions include acute manifestations of SCD, as indicated in Table 1, that require redressal through therapeutic transfusions. However, under certain circumstances intermittent transfusions could be prophylactic such as for instance, when SCD patients are transfused before specific surgeries viz., those related to pregnancy complications or renal failure (Table 1).           Acute Chest Syndrome (ACS) describes a manifestation of SCD in which, due to sickling, infectious and noninfectious pulmonary events are complicated, resulting in a more severe clinical course. The diagnosis is the presence of a new infiltrate on chest radiography that is accompanied by acute respiratory symptoms. ACD accounts for nearly 25% of all deaths from SCD (Vichinsky, 2002). Repeated episodes of ACS are associated with an increased risk of chronic lung disease and pulmonary hypertension (Castro, 1996). The severe pulmonary events occurring in SCD may be precipitated by any trigger of hypoxia (Vichinsky, 2002). Transfusions are very efficacious and provide immediate benefit by reversing hypoxia in ACS. Transfusion of leucocyte-poor packed red cells matched for Rh, C, E, and Kell antigens can curtail antibody formation to below 1% (Vichinsky, 2002). Simple transfusions suffice for less severe cases; however, exchange transfusion is recomm ended to minimise the risk of increased viscosity. Also, chronic transfusion appears promising for prevention of recurrence in selected patients (Styles and Vichinsky, 1994). In a multicentre ACS trial, prophylactic transfusion was found to almost completely eliminate the risk of pulmonary complications (Vichinsky, 2002).           Acute Symptomatic Anaemia arises in SCD as a result of blood loss, increased RBC destruction, suppression of erythropoiesis etc. and is effectively treated with intermittent transfusion of RBCs to relieve symptoms of cardiac and respiratory distress (Josephson et al., 2007).           Aplastic Anaemia is commonly caused in SCD on account of infection of haematopoietic precursors in the bone marrow by Parvovirus B19 leading to a steep fall in RBCs. According to Josephson et al. (2007), therapeutic intermittent transfusion of RBCs is again the recommended first-line of treatment to improve total haemoglobin count and prevent cardiac decompensation. However, in those patients who are prone to fluid overload on account of cardiac or renal dysfunction an alternative transfusion strategy is to remove the whole blood and replace it with packed cells while avoiding the addition of excess volume (Josephson et al., 2007).           Acute Stroke is a high risk especially in paediatric SCD cases because of elevated cerebral flow. Enormous decline in stroke rate have occurred in children receiving intermittent simple transfusion (Adams et al., 1998). However, the identification of the stroke type would be necessary in all SCD patients in order to determine the appropriate treatment approach since the occurrence of infarctive strokes is higher in children as opposed to a higher incidence of haemorrhagic strokes in adults (Adams, 2003). Indications for Chronic Transfusions Prophylactic chronic RBC transfusion every 3 to 4 weeks to maintain HbS levels lower than 30% is crucial for preventing first as well as recurrent strokes in children (Johnson et al., 2007). The transfusions could either be chronic simple transfusion or prophylactic chronic RBC exchange transfusion. Prophylactic chronic transfusions are recommended for patients with chronic renal failure so as to avoid severe symptomatic anaemia and for those patients with SCD undergoing pregnancy with complications. However, prophylactic transfusion is not indicated for SCD patients with normal pregnancy (Tuck et al., 1987). Controversial and indeterminate indications for intermittent or chronic transfusion According to Hankins et al. (2005), chronic transfusion therapy is helpful in reducing the incidence of strokes in children but not the severity of strokes. In the case of acute priapism, improvement in patients has been observed after exchange or simple transfusion (Rifikind et al., 1979). Yet, due to the ASPEN syndrome, transfusion currently is only a second-line therapy in the management of priapism ( Miller et al., 1995).           RBC transfusion is a vital component in the management of symptoms and complications of SCD. It has drastically reduced the morbidity and mortality of SCD. Yet, immune-related effects such as FNHTRs and alloimmunisation to HLAs, and nonimmune-related effects e.g., iron overload and transfusion-transmitted infections are serious adverse effects of the transfusion therapy that need to be attended to in SCD patients receiving transfusion (Johnson et al., 2007). Chronic transfusions could result in an inexorable accumulation of tissue iron that could become fatal if not treated (Cohen, 1987). Excess iron damages the liver, endocrine organs, and heart and may be fatal by adolescence (Engle, 1964). 5. Critical review of thalassemias : (i) Molecular pathogenesis The large number of inherited haemoglobin disorders known today include (a) those related to anomalies in the haemoglobin structure e.g., sickle cell disease, and (b) the thalassemias whose hallmark is globin-chain deficiency of one or other of the globin chains of adult haemoglobin in erythroid cells. ÃŽ ²-Thalassaemias These are a set of genetic disorders inherited as simple codominant traits affecting haemoglobin synthesis. Depending on the haemoglobin chain affected, 2 types of thalassemia are recognised: ÃŽ ±-thalassaemia and ÃŽ ²-thalassaemia. Homozygous ÃŽ ²-thalassaemia is marked by a quantitative deficiency of the ÃŽ ²-globin chains in the erythroid cells. A complete absence of the ÃŽ ²-globin chains occurs in homozygous ÃŽ ²o-thalassaemia whereas in homozygous ÃŽ ²+-thalassaemia the ÃŽ ²-globin chains are present at less than 30% of normal. Accounting for nearly 90% of the cases, ÃŽ ²+-thalassaemia is the most commonly observed form of ÃŽ ²-thalassaemia. The condition is termed thalassaemia major when there is microcytic hypochromic anaemia with severe haemolysis, hepatosplenomegaly, skeletal deformities and iron overload. ÃŽ ²-thalassaemia homozygotes exhibit severe transfusion-dependent anaemia in the very first year of life. Homozygotic individuals having a relatively benign clinical phe notype and surviving with or without transfusion are described as thalassaemia intermedia (Weatherall, 1969). The thalassaemias, thus, encompass a wide gamut of clinical disability from intrauterine death to a mild anaemia with no overt symptoms (Weatherall, 1997b). The coexistence of Î ± -thalassaemia leading to reduction in the synthesis of ÃŽ ±-globin chains, and a genetic predisposition to produce high levels of HbF, could be important factors for the extensive p Causes, Symptoms and Treatments of Anaemia Causes, Symptoms and Treatments of Anaemia 1. Introduction Anaemia is a syndrome characterised by a lack of healthy red blood cells or haemoglobin deficiency in the red blood cells, resulting in inadequate oxygen supply to the tissues. The condition can be temporary, long-term or chronic, and of mild to severe intensity. There are many forms and causes of anaemia. Normal blood consists of three types of blood cells: white blood cells (leucocytes), platelets and red blood cells (erythrocytes). The first generation of erythrocyte precursors in the developing foetus are produced in the yolk sac. They are carried to the developing liver by the blood where they form mature red blood cells that are required to meet the metabolic needs of the foetus. Until the 18th week of gestation, erythrocytes are produced only by liver after which the production shifts to the spleen and the bone marrow. The life of a red blood cell is about 127 days or 4 months (Shemin and Rittenberg, 1946; Kohgo et al., 2008). The main causes of anaemia are blood loss, product ion of too few red blood cells by the bone marrow or a rapid destruction of cells.           Haemoglobin, a protein, present in the red blood cells is involved in the transport of oxygen from the lungs to all the other organs and tissues of the body. Iron is an important constituent of the haemoglobin protein structure which is intimately involved in the transport of oxygen. Anaemia is generally defined as a lower than normal haemoglobin concentration. The normal blood haemoglobin concentration is dependent on age and sex, and, according to the World Health Organisation (WHO) Expert Committee Report, anaemia results when the blood concentration of haemoglobin falls below 130 g/L in men or 120 g/L in non-pregnant women (WHO, 1968). However, the reference range of haemoglobin concentration in blood could vary depending on the ethnicity, age, sex, environmental conditions and food habits of the population analysed. According to Beutler and Warren (2006), more reasonable benchmarks for anaemia are 137 g/L for white men aged between 20 and 60 years and 132 g/L for older men. The value for women of all ages would be 122 g/L. Also, the lower limit of normal of haemoglobin concentrations of African Americans are appreciably lower than that of Caucasians (Beutler and Warren, 2006).           Besides the well recognised iron deficiency anaemia, several inherited anaemias are also known. These are mostly haemoglobinopathies. Adult haemoglobin is a tetrameric haeme-protein. Abnormalities of beta-chain or alpha-chain produce the various medically significant haemoglobinopathies. The variations in amino acid composition induced genetically impart marked differences in the oxygen carrying properties of haemoglobin. Mutations in the haemoglobin genes cause disorders that are qualitative abnormalities in the synthesis of haemoglobin (e.g., sickle cell disease) and some that are quantitative abnormalities that pertain to the rate of haemoglobin synthesis (e.g., the thalassemias) (Weatherall., 1969). In SCD, the missense mutation in the ÃŽ ²-globin gene causes the disorder. The mutation causing sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid 6. The substitution converts a glutamic acid codon (GAG) to a valine codon (GTG). The form of haemoglobin in persons with sickle cell anemia is referred to as HbS. Also, the valine for glutamic acid replacement causes the haemoglobin tetramers to aggregate into arrays upon deoxygenation in the tissues. This aggregation leads to deformation of the red blood cell making it relatively inflexible and restrict its movement in the capillary beds. Repeated cycles of oxygenation and deoxygenation lead to irreversible sickling and clogging of the fine capillaries. Incessant clogging of the capillary beds damages the kidneys, heart and lungs while the constant destruction of the sickled red blood cells triggers chronic anaemia and episodes of hyperbilirubinaemia.           Fanconi anaemia (FA) is an autosomal recessive condition, and the most common type of inherited bone marrow failure syndrome. The clinical features of FA are haematological with aplastic anaemia, myelodysplastic syndrome (MDS), and acute myeloid leukaemia (AML) being increasingly present in homozygotes (Tischkowitz and Hodgson, 2003). Cooleys anaemia is yet another disorder caused by a defect in haemoglobin synthesis.           Autoimmune haemolytic anaemia is a syndrome in which individuals produce antibodies directed against one of their own erythrocyte membrane antigens. The condition results in diminished haemoglobin concentrations on account of shortened red blood cell lifespan (Sokol et al., 1992).           Megaloblastic anaemia is a blood disorder in which anaemia occurs with erythrocytes which are larger in size than normal. The disorder is usually associated with a deficiency of vitamin B12 or folic acid . It can also be caused by alcohol abuse, drugs that impact DNA such as anti-cancer drugs, leukaemia, and certain inherited disorders among others (Dugdale, 2008).           Malaria causes increased deformability of vivax-infected red blood cells (Anstey et al., 2009). Malarial anaemia occurs due to lysis of parasite-infected and non-parasitised erythroblasts as also by the effect of parasite products on erythropoiesis (Ru et al., 2009).           Large amounts of iron are needed for haemoglobin synthesis by erythroblasts in the bone marrow. Transferrin receptor 1 (TfR1) expressed highly in erythroblasts plays an important role in extracellular iron uptake (Kohgo et al., 2008). Inside the erythroblasts, iron transported into the mitochondria gets incorporated into the haeme ring in a multistep pathway. Genetic abnormalities in this pathway cause the phenotype of ringed sideroblastic anemias (Fleming, 2002). The sideroblastic anemias are a heterogeneous group of acquired and inherited bone marrow disorders, characterised by mitochondrial iron overload in developing red blood cells. These conditions are diagnosed by the presence of pathologic iron deposits in erythroblast mitochondria (Bottomley, 2006).  2. Classification of anaemia Anaemia can be generally classified based on the morphology of the red blood cells, the pathogenic spectra or clinical presentation (Chulilla et al., 2009). The morphological classification is based on mean corpuscular volume (MCV) and comprises of microcytic, macrocytic and normocytic anaemia.      (a) Microcytic anaemia refers to the presence of RBCs smaller than normal volume, the reduced MCV ( 15 would probably indicate IDA (Chulilla et al., 2009).           In macrocytic anaemia, erythrocytes are larger (MCV > 98 fL) than their normal volume (MCV = 82-98 fL). Vitamin B12 deficiency leads to delayed DNA synthesis in rapidly growing hematopoietic cells, and can result in macrocytic anemia. Drugs that interfere with nucleic acid metabolism, such as.hydroxyurea increases MCV (> 110 fL) while alcohol induces a moderate macrocytosis (100-110 fL). In the initial stage, most anaemias are normocytic. The causes of normocytic anaemia are nutritional deficiency, renal failure and haemolytic anemia (Tefferi, 2003). The most common normocytic anaemia in adults is anaemia of chronic disease (ACD) (Krantz, 1994). Common childhood normocytic anaemias are, besides iron deficiency anaemia, those due to acute bleeding, sickle cell anemia, red blood cell membrane disorders and current or recent infections especially in the very young (Bessman et al., 1983). Homozygous sickle cell disease is the most common cause of h aemolytic normocytic anemias in children (Weatherall DJ, 1997a).           In practice, the morphological classification is quicker and therefore, more useful as a diagnostic tool. Besides, MCV is also closely linked to mean corpuscular haemoglobin (MCH), which denotes mean haemoglobin per erythrocyte expressed in picograms (Chulilla et al., 2009). Thus, MCV and MCH decrease simultaneously in microcytic, hypochromic anemia and increase together in macrocytic, hyperchromic anemia.           Pathogenic classification of anaemia is based on the production pattern of RBC: whether anaemia is due to inadequate production or loss of erythrocytes caused by bleeding or haemolysis. This approach is useful in those cases where MCV is normal. Pathogenic classification is also essential for proper recognition of the mechanisms involved in the genesis of anaemia. Based on the pathogenic mechanisms, anaemia is further divided into two types namely, (i) hypo-regenerative in which the bone marrow production of erythrocytes is decreased because of impaired function, decreased number of precursor cells, reduced bone marrow infiltration, or lack of nutrients; and (ii) regenerative: when bone marrow upregulates the production of erythrocytes in response to the low erythrocyte mass (Chulilla et al., 2009). This is typified by increased generation of erythropoietin in response to lowered haemoglobin concentration, and also reflects a loss of erythrocyt es, due to bleeding or haemolysis. The reticulocyte count is typically higher.           Sickle cell disease is characterised by sickled red cells. The first report of SCD was published a century ago noting the presence of peculiar elongated cells in blood by James Herrick, an American physician (1910). Pauling et al. (1949) described it as a molecular disease. The molecular nature of sickle haemoglobin (Hb S) in which valine is substituted for glutamic acid at the sixth amino acid position in the beta globin gene reduces the solubility of Hb, causing red cells to sickle (Fig. 1). Sickling of cells occurs at first reversibly, then finally as a state of permanent distortion, when cells containing HbS and inadequate amounts of other haemoglobins including foetal haemoglobin, which retards sickling, become deoxygenated (Bunn, 1997). The abnormal red cells break down, leading to anaemia, and clog blood vessels with aggregates, leading to recurrent episodes of severe pain and multiorgan ischaemic damage (Creary et al., 2007). The high levels of inflammatory cytokines in SCD may promote retention of iron by macrophage/reticuloendothelial cells and/or renal cells. SCD care commonly depends on transfusion that results in iron overload (Walter et al., 2009). 3. Pathogenesis of anaemia Anaemia is a symptom , or a syndrome, and not a disease (Chulilla et al., 2009). Several types of anaemia have been recognised, the pathogenesis of each being unique. Iron deficiency anaemia (IDA) is the most common type of anaemia due to nutritional causes encountered worldwide (Killip et al., 2008). Iron is one of the essential micronutrients required for normal erythropoietic function While the causes of iron deficiency vary significantly depending on chronological age and gender, IDA can reduce work capacity in adults (Haas Brownlie, 2001) and affect motor and mental development in children (Halterman et al., 2001). The metabolism of iron is uniquely controlled by absorption rather than excretion (Siah et al., 2006). Iron absorption typically occurring in the duodenum accounts for only 5 to 10 per cent of the amount ingested in homoeostatis. The value decreases further under conditions of iron overload, and increases up to fivefold under conditions of iron depletion (Killip et al., 2008). Iron is ingested as haem iron (10%) present in meat, and as non-haem ionic form iron (90%) found in plant and dairy products. In the absence of a regulated excretion of iron through the liver or kidneys, the only way iron is lost from the body is through bleeding and sloughing of cells. Thus, men and non-menstruating women lose about 1 mg of iron per day while menstruating women could normally lose up to 1.025 mg of iron per day (Killip et al., 2008). The requirements for erythropoiesis which are typically 20-30 mg/day are dependent on the internal turnover of iron (Munoz et al., 2009) For example, the amount of iron required for daily production of 300 billion RBCs (20-30 mg) is provided mostly by recycling iron by macrophages (Andrews, 1999).           Iron deficiency occurs when the metabolic demand for iron exceeds the amount available for absorption through consumption. Deficiency of nutritional intake of iron is important, while abnormal iron absorption due to hereditary or acquired iron-refractory iron deficiency anemia (IRIDA) is another important cause of unexplained iron deficiency. However, IDA is commonly attributed to blood loss e.g., physiological losses in women of reproductive age. It might also represent occult bleeding from the gastrointestinal (GI) tract generally indicative of malignancy (Hershko and Skikne, 2009).           Iron absorption and loss play an important role in the pathogenesis and management of IDA. Human iron disorders are necessarily disorders of iron balance or iron distribution. Iron homeostasis involves accurate control of intestinal iron absorption, efficient utilisation of iron for erythropoiesis, proper recycling of iron from senescent erythrocytes, and regulated storage of iron by hepatocytes and macrophages (Andrews, 2008). Iron deficiency is largely acquired, resulting from blood loss (e.g., from intestinal parasitosis), from inadequate dietary iron intake, or both. Infections, for example, with H pylori, can lead to profound iron deficiency anemia without significant bleeding. Genetic defects can cause iron deficiency anaemia. Mutations in the genes encoding DMT1 (SLC11A2) and glutaredoxin 5 (GLRX5) lead to autosomal recessive hypochromic, microcytic anaemia (Mims et al., 2005). Transferrin is a protein that keeps iron nonreactive in the circulation, and delivers iron to cells possessing specific transferrin receptors such as TFR1 which is found in largest amounts on erythroid precursors. Mutations in the TF gene leading to deficiency of serum transferrin causes disruption in the transfer of iron to erythroid precursors thereby producing an enormous increase in intestinal iron absorption and consequent tissue iron deposition (Beutler et al., 2000). Quigley et al. (2004) found a haem exporter, FLVCR, which appears to be necessary for normal erythroid development. Inactivation of FLVCR gene after birth in mice led to severe macrocytic anaemia, indicating haem export to be important for normal erythropoiesis.           The anaemia of chronic disease (ACD) found in patients with chronic infectious, inflammatory, and neoplastic disorders is the second most frequently encountered anaemia after iron-deficiency anaemia. It is most often a normochromic, normocytic anaemia that is primarily caused by an inadequate production of red cells, with low reticulocyte production (Krantz, 1994). The pathogenesis of ACD is unequivocally linked to increased production of the cytokines including tumour necrosis factor, interleukin-1, and the interferons that mediate the immune or inflammatory response. The various processes leading to the development of ACD such as reduced life span of red cells, diminished erythropoietin effect on anaemia, insufficient erythroid colony formation in response to erythropoietin, and impaired bioavailability of reticuloendothelial iron stores appear to be caused by inflammatory cytokines (Means, 1996;2003). Although iron metabolism is characterist ically impaired in ACD, it may not play a key role in the pathogenesis of ACD (Spivak, 2002). Neither is the lack of available iron central to the pathogenesis of the syndrome, according to Spivak (2002), who found reduced iron absorption and decreased erythroblast transferrin-receptor expression to be the result of impaired erythropoietin production and inhibition of its activity by cytokines. However, reduced erythropoietin activity, mostly from reduced production, plays a pivotal role in the pathogenesis of ACD observed in systemic autoimmune diseases (Bertero and Caligaris-Cappio, 1997). Indeed, iron metabolism as well as nitric oxide (NO), which contributes to the regulation of iron cellular metabolism are involved in the pathogenesis of ACD in systemic autoimmune disorders. Inflammatory mediators, particularly the cytokines, are important factors involved in the pathogenesis of the anaemia of chronic disease, as seen in rheumatoid arthritis anaemia (Baer et al., 1990), the cyt okines causing impairment of erythroid progenitor growth and haemoglobin production in developing erythrocytes.           Anaemia is also commonly found in cases of congestive heart failure (CHF), again caused by excessive cytokine production leading to reduced erythropoietin secretion, interference with erythropoietin activity in the bone marrow and reduced iron supply to the bone marrow (Silverberg et al., 2004). However, in the presence of chronic kidney insufficiency, abnormal erythropoietin production in the kidney plays a role in the pathogenesis of anaemia in CHF.           The myelodysplastic syndromes (MDS) are common haematological malignancies affecting mostly the elderly as age-related telomere shortening enhances genomic instability (Rosenfeld and List, 2000). Radiation, smoking and exposure to toxic compounds e.g., pesticides, organic chemicals and heavy metals, are factors promoting the onset of MDS via damage caused to progenitor cells, and, thereby, inducing immune suppression of progenitor cell growth and maturation. TNF- and other pro-apoptotic cytokines could play a central role in the impaired haematopoiesis of MDS (Rosenfeld and List, 2000). Premature intramedullary cell death brought about by excessive apoptosis is another important pathogenetic mechanism in MDS (Aul et al., 1998).           Sickle cell disease (SCD) arising from a point mutation in the ÃŽ ²-globin gene and leading to the expression of haemoglobin S (HbS) is the most common monogenetic disorder worldwide. Chronic intravascular haemolysis and anaemia are some important characteristics of SCD. Intravascular haemolysis causes endothelial dysfunction marked by reduced nitric oxide (NO) bioavailability and NO resistance, leading to acute vasoconstriction and, subsequently, pulmonary hypertension (Gladwin and Kato, 2005).  However, a feature that differentiates SCD from other chronic haemolytic syndromes is the persistent and intense inflammatory condition present in SCD. The primary pathogenetic event in SCD is the intracellular polymerisation or gelation of deoxygenated HbS leading to rigidity in erythrocytes (Wun, 2001). The deformation of erythrocytes containing HbS is dependent on the concentration of haemoglobin in the deoxy conformation (Rodgers et al., 1985). It has been demonstrated that sickle monocytes are activated which, in turn, activate endothelial cells and cause vascular inflammation. The vaso-occlusive processes in SCD involve inflammatory and adhesion molecules such as the cell adhesion molecules (CAM family), which play a role in the firm adhesion of reticulocytes and leukocytes to endothelial cells, and the selectins, which play a role in leukocyte and platelet rolling on the vascular wall (Connes et al., 2008). Thus, inflammation, leucocyte adhesion to vascular endothelium, and subsequent endothelial injury are other crucial factors contributing to the pathogenesis of SCD (Jison et al., 2004). 4. Current therapies for clinical management of sickle cell diseaseincludingacritical appraisal of transfusion Between 1973 and 2003, the average life expectancy of a patient with SCD increased dramatically from a mere 14 years to 50 years thanks to the development of comprehensive care models and painstaking research efforts in both basic sciences especially molecular and genetic studies, and clinical aspects of SCD (Claster and Vichinsky, 2003). The clinical manifestations of SCD are highly variable. Both the phenotypic expression and intensity of the syndrome are vastly different among patients and also vary longitudinally within the same patient (Ballas, 1998). New pathophysiological insights available have enabled treatments to be developed for the recognised haematologic and nonhaematologic abnormalities in SCD (Claster and Vichinsky, 2003). The main goals of SCD treatment are symptom alleviation, crises avoidance and effective management of disease complications. The strategy adopted is primarily palliative in nature, and consists of supportive, symptomatic and preventative approaches to therapy. Symptomatic management includes pain mitigation, management of vasoocclusive crisis, improving chronic haemolytic anaemia, treatment of organ failure associated with the disease, and detection and treatment of pulmonary hypertension (Distenfeld and Woermann, 2009). The preventative strategies include use of prophylactic antibiotics (e.g., penicillin) in children, prophylactic blood transfusion for prevention of stroke in patients especially young children who are at a very high risk of stroke, and treatment with hydroxyurea of patients experiencing frequent acute painful episodes (Ballas, 2002). Currently, curative therapy for sickle cell anaemia is only available through bone marrow and stem cell transplantation. Hematopoietic cell transplantation using stem cells from a matched sibling donor has yielded excellent results in paediatric patients (Krishnamurti, 2007). Curative gene therapy is still at the exploratory stage (Ballas, 2002). Current and potential therapies The potential treatment strategies basically target cellular dehydration, sickle haemoglobin concentrations, endothelial dysfunction, and abnormal coagulation regulation (Claster and Vichinsky, 2003). HbS concentrations are essentially tackled through transfusions while approaches to reduce HbS polymerisation which is the main mechanism for the development of vaso-occlusion include (a) increasing foetal haemoglobin (HbF) concentration using hydroxyurea (Fig. 2), butyrate, or erythropoietin, and (b) preventing sickle cell dehydration using Clotrimazole (Fig. 3) or Mg2+pidolate. Hydroxyurea therapy increases the production of HbF in patients with sickle cell anaemia, and, thereby, inhibits the polymerisation of HbS and alleviates both the haemolytic and vaso-occlusive manifestations of the disease (Goldberg et al., 1990). Recombinant erythropoietin also increases the number of reticulocytes with HbF. Additionally, it has been observed that administration of intravenous recombinant eryt hropoietin with iron supplementation alternating with hydroxyurea enhances HbF levels more than hydroxyurea alone (Rodgers et al., 1993). As SCD is essentially characterized by an abnormal state of endothelial cell activation that is, a state of inflammation, a pharmacologic approach to inhibit endothelial cell activation has proved clinically beneficial (Hebbel and Vercellotti, 1997). Thus, administration of sulfasalazine which is a powerful inhibitor of activation of nuclear factor (NF)-B, the transcription factor promoting expression of genes for a number of pro-adhesive and procoagulant molecules on endothelium to humans has been found to provide transcriptional regulation of SCD at the endothelium level (Solovey et al., 2001). Red blood cell transfusion : a critical appraisal A key therapy that is applied regularly in the clinical management of patients with SCD is packed red blood cell transfusion. RBC transfusion improves the oxygen-carrying capacity which is achieved by enhancing the haemoglobin levels, causes dilution of HbS concentration thereby, reducing blood viscosity and boosting oxygen saturation. Furthermore, RBC transfusion is helpful in suppressing endogenous production of sickle RBCs by augmenting tissue oxygenation ( Josephson et al., 2007). There are two major types of RBC transfusion therapy: intermittent and chronic which are further classified as prophylactic or therapeutic. Intermittent transfusions are generally therapeutic in nature and administered to control acute manifestations of SCD whereas chronic transfusions are performed as general preventative measures to check complications of SCD. RBC transfusion given as a single dose is termed as simple transfusion. Exchange transfusion involves administration of a larger volume of RBCs replacing the patients RBCs that are simultaneously removed. Details of the various types of RBC transfusion and the major clinical indications for the same in SCD patients are listed in Table 1.      SCD (Source: Josephson et al., 2007) Indications for Intermittent transfusions Indications for intermittent transfusions include acute manifestations of SCD, as indicated in Table 1, that require redressal through therapeutic transfusions. However, under certain circumstances intermittent transfusions could be prophylactic such as for instance, when SCD patients are transfused before specific surgeries viz., those related to pregnancy complications or renal failure (Table 1).           Acute Chest Syndrome (ACS) describes a manifestation of SCD in which, due to sickling, infectious and noninfectious pulmonary events are complicated, resulting in a more severe clinical course. The diagnosis is the presence of a new infiltrate on chest radiography that is accompanied by acute respiratory symptoms. ACD accounts for nearly 25% of all deaths from SCD (Vichinsky, 2002). Repeated episodes of ACS are associated with an increased risk of chronic lung disease and pulmonary hypertension (Castro, 1996). The severe pulmonary events occurring in SCD may be precipitated by any trigger of hypoxia (Vichinsky, 2002). Transfusions are very efficacious and provide immediate benefit by reversing hypoxia in ACS. Transfusion of leucocyte-poor packed red cells matched for Rh, C, E, and Kell antigens can curtail antibody formation to below 1% (Vichinsky, 2002). Simple transfusions suffice for less severe cases; however, exchange transfusion is recomm ended to minimise the risk of increased viscosity. Also, chronic transfusion appears promising for prevention of recurrence in selected patients (Styles and Vichinsky, 1994). In a multicentre ACS trial, prophylactic transfusion was found to almost completely eliminate the risk of pulmonary complications (Vichinsky, 2002).           Acute Symptomatic Anaemia arises in SCD as a result of blood loss, increased RBC destruction, suppression of erythropoiesis etc. and is effectively treated with intermittent transfusion of RBCs to relieve symptoms of cardiac and respiratory distress (Josephson et al., 2007).           Aplastic Anaemia is commonly caused in SCD on account of infection of haematopoietic precursors in the bone marrow by Parvovirus B19 leading to a steep fall in RBCs. According to Josephson et al. (2007), therapeutic intermittent transfusion of RBCs is again the recommended first-line of treatment to improve total haemoglobin count and prevent cardiac decompensation. However, in those patients who are prone to fluid overload on account of cardiac or renal dysfunction an alternative transfusion strategy is to remove the whole blood and replace it with packed cells while avoiding the addition of excess volume (Josephson et al., 2007).           Acute Stroke is a high risk especially in paediatric SCD cases because of elevated cerebral flow. Enormous decline in stroke rate have occurred in children receiving intermittent simple transfusion (Adams et al., 1998). However, the identification of the stroke type would be necessary in all SCD patients in order to determine the appropriate treatment approach since the occurrence of infarctive strokes is higher in children as opposed to a higher incidence of haemorrhagic strokes in adults (Adams, 2003). Indications for Chronic Transfusions Prophylactic chronic RBC transfusion every 3 to 4 weeks to maintain HbS levels lower than 30% is crucial for preventing first as well as recurrent strokes in children (Johnson et al., 2007). The transfusions could either be chronic simple transfusion or prophylactic chronic RBC exchange transfusion. Prophylactic chronic transfusions are recommended for patients with chronic renal failure so as to avoid severe symptomatic anaemia and for those patients with SCD undergoing pregnancy with complications. However, prophylactic transfusion is not indicated for SCD patients with normal pregnancy (Tuck et al., 1987). Controversial and indeterminate indications for intermittent or chronic transfusion According to Hankins et al. (2005), chronic transfusion therapy is helpful in reducing the incidence of strokes in children but not the severity of strokes. In the case of acute priapism, improvement in patients has been observed after exchange or simple transfusion (Rifikind et al., 1979). Yet, due to the ASPEN syndrome, transfusion currently is only a second-line therapy in the management of priapism ( Miller et al., 1995).           RBC transfusion is a vital component in the management of symptoms and complications of SCD. It has drastically reduced the morbidity and mortality of SCD. Yet, immune-related effects such as FNHTRs and alloimmunisation to HLAs, and nonimmune-related effects e.g., iron overload and transfusion-transmitted infections are serious adverse effects of the transfusion therapy that need to be attended to in SCD patients receiving transfusion (Johnson et al., 2007). Chronic transfusions could result in an inexorable accumulation of tissue iron that could become fatal if not treated (Cohen, 1987). Excess iron damages the liver, endocrine organs, and heart and may be fatal by adolescence (Engle, 1964). 5. Critical review of thalassemias : (i) Molecular pathogenesis The large number of inherited haemoglobin disorders known today include (a) those related to anomalies in the haemoglobin structure e.g., sickle cell disease, and (b) the thalassemias whose hallmark is globin-chain deficiency of one or other of the globin chains of adult haemoglobin in erythroid cells. ÃŽ ²-Thalassaemias These are a set of genetic disorders inherited as simple codominant traits affecting haemoglobin synthesis. Depending on the haemoglobin chain affected, 2 types of thalassemia are recognised: ÃŽ ±-thalassaemia and ÃŽ ²-thalassaemia. Homozygous ÃŽ ²-thalassaemia is marked by a quantitative deficiency of the ÃŽ ²-globin chains in the erythroid cells. A complete absence of the ÃŽ ²-globin chains occurs in homozygous ÃŽ ²o-thalassaemia whereas in homozygous ÃŽ ²+-thalassaemia the ÃŽ ²-globin chains are present at less than 30% of normal. Accounting for nearly 90% of the cases, ÃŽ ²+-thalassaemia is the most commonly observed form of ÃŽ ²-thalassaemia. The condition is termed thalassaemia major when there is microcytic hypochromic anaemia with severe haemolysis, hepatosplenomegaly, skeletal deformities and iron overload. ÃŽ ²-thalassaemia homozygotes exhibit severe transfusion-dependent anaemia in the very first year of life. Homozygotic individuals having a relatively benign clinical phe notype and surviving with or without transfusion are described as thalassaemia intermedia (Weatherall, 1969). The thalassaemias, thus, encompass a wide gamut of clinical disability from intrauterine death to a mild anaemia with no overt symptoms (Weatherall, 1997b). The coexistence of Î ± -thalassaemia leading to reduction in the synthesis of ÃŽ ±-globin chains, and a genetic predisposition to produce high levels of HbF, could be important factors for the extensive p
To Kill a Mockingbird by Harper Lee - The Influences Parents Have On Th
Throughout our lives we're influenced by many. It can have an effect on the way we view issues within societal boundaries. One of the major influences children have in their lives comes from their parents. The parents of a child can have both a positive and a negative influence on their lives. In the novel "To Kill A Mockingbird", there are two excellent examples of how parents can be a major influence on their children. Atticus Finch, father of Jem and Scout Finch, plays the loving, kind and knowledgeable father. He is an example of how parents can have a positive influence on their children. Bob Ewell, father of Mayella Ewell, plays the drunken, abusive, and neglectful father. He is an example of how a parent can be a negative influence on their children's lives. Both fathers are very influential on the psychological development of their children. Parents can influence how their children behave, feel, and act towards the outside world. If a child is brought up with hatred and anger, they can learn to view the world in a very negative way, by being critical and prejudice towards other people. However if a child is brought up with caring and nourishment, they can learn to see the world from all different angles. Atticus Finch raises his children with love and care, and teaches them to consider all angles of a situation before you judge someone; "You never really understand a person until you consider things from his point of view"... "Until you clim...
Tuesday, September 3, 2019
The Pediatric Sector Essay -- Health, Pharmaceutical, HIPAA
The Pediatric sector is one of the major economic contributors for health care industry (Slonim, LaFleur, Ahmed, & Joseph, 2003). The major cause of pediatric deaths is due to lack of interoperability among pediatric clinics. Medical errors are very common in pediatric departments. According to study by Kozer, Berkovitch, and Koren (2006) most of the drugs for children under age 12 are off-labeled and there is no standard dosing available. â€Å"Off-label use is a practice of prescribing pharmaceuticals for an unapproved indication†(Stanford, 2008). Some medications are adjusted according to body weight and nature of children. It is also very difficult to find medical reactions in children compared to older people. Some drugs referred by physicians needs to be diluted and doses needs to be calculated before they are given to children (Kozer, Berkovitch, & Koren, 2006). Calculation errors can end up in overdose of medicines, which can result in deaths (Kozer, Berkovitch, & Kor en). There are many reasons for the medical errors in health care industry. In year 2000, a study by IOM reported that there is economic loss from medical errors due to which health care industry was in a crisis (Kohn, 2000). It was found that even with the advancement of technological innovations health care is not utilizing technologies like electronic format of records. According to law set by US congress, President Bush declared that â€Å"every American should have an electronic medical record within 2014.†(Pear, 2007). The goal was to use technological innovation like Electronic health record system (EHR) across the country for all health care departments (Bush, 2004). With change in presidency the goal became more as a requirement. President Obama started intr... ...nt challenge faced by health care sector is the resistance to adopt newer technologies (Gupta & Murtaza, 2009). This is more common with major clinics and hospitals as they have to change the clinical workflows. Even if there are many benefits in using new technologies there are major challenges faced by the physicians, nurses and staff in redoing their workflow (Ilie, Slyke, Parikh, & Courtney, 2009). This study will be focusing on the pediatric departments with in the city of Chicago and analyzes the perceptions of using newer technologies in the work. Even if there are mandatory laws from government to move towards the EHR systems, the health care can push back with the challenges they will face when moving to a new technology. The study should also provide useful insights on how health care officials perceive the challenge of computerizing medical information.
Monday, September 2, 2019
Looming Economic Crisis in United States
On January 21st and 22nd 2008, world financial markets crashed amidst the fears of American economy slowly are gradually moving toward recession. The emerging markets world over corrected almost 20 to 30 percent while the developed financial markets of Europe and American corrected over 10-15 percent. At present the DOW is 20 percent below its July top a signal that financial markets are entering a bear phase. (Landler & Timmons 2008) The paper will try to shed light on what is looming large on American economy, what are the policy or market failures which are taking the economy into recession, How the present Bush plan of stimulus will impact the scenario in future and will it be good enough to bring the economy back on track. Main contributors to the slowdown of the economy American economy is hit by numerous factors at the same time – growth slowdown, increasing unemployment numbers, falling retail sales, increasing trade deficit, weakness of dollars, emergence of Euro, housing crisis and failure of financial markets. (Landler & Timmons 2008) Housing Market – The housing market has been slowing down for an year now and most presidential candidates are suggesting ways on how American economy can come out this mess. The slowdown in the housing market is due to high default rate on mortgages especially sub-prime mortgages. During the credit expansion time post first Bush tax cuts banks and financial institutions lowered their vigilance on credit rating and in quest to expand market end up giving housing mortgages to shady borrowers. Another reason why this happened was – money was easy to come and housing market was on uptrend so in case of failure of installment and foreclosure the banks and financial institutes were able to get the money back through increased price of the houses. But after the slowing down of housing markets real estate rates have fallen 5-10 percent in last year only and according to UBS it is expected go down by 15-20 percent more in coming year. Increasing National Debt – the present national debt is around 9 trillion dollars which accounts for almost 65 percent of the Gross Domestic Product. Such high level of national debt increases the interests on payments significantly and reduces the elbow space of the government in tinkering with the fiscal policy. In the past America able to finance its debt by weakening the dollar but now with emergence of Euro it has become increasing difficult to export the national debt to foreign institutions and countries which in past are happy to maintain huge dollar reserves. (Kjeldsen, 2002) Increasing Trade Deficit – The profitability of American companies have grown over the past half a decade but the trade deficit hasn’t come down. The main reason for it is off-shoring and outsourcing. American companies are making the most of low cost manufacturing and services in countries like China and India to boost their bottomline. Low level of saving rates – In response to the main reason for credit card default rate one women respondent on CNBC summed up the saving rate of Americans – â€Å"we all like to buy things, we all love to travel and we don’t want to wait for it†. This culture of plastic money spending today paying later has brought down saving rates to alarming levels and it can significantly hamper the investment in the economy. Increasing inequality among Americans – the last tax cuts provided immense benefits to the rich Americans and increased the income gap between the rich nation and poor nation. Hurricane Katrina exposed the underbelly of this growing inequality in the country and it will take years of corrective actions. Financial Markets crash – America is financial market sensitive country by that it means that the wealth effect among American can be reflected by the state of the financial markets as more than 80 percent of the population invest in the financial markets. This has let the consumer sentiments down which is resulting in lowering retail sales and subsequently lowering employment generation. (Landler & Timmons 2008) President Bush Stimulus Plan President Bush has passed the stimulus plan of 168 billion into law, the stimulus plan will ensure money in the hand of real consumers in short time which will help in keeping the economy afloat by not letting the demand go drastically down. In the long run along with the tax cuts and stimulus plan the economy will able to get new investments which can bolster production and employment opportunities. The stimulus package will start providing tax cuts after May and before that it provide a one time rebate of 600 dollars for the individual and 1200 for couple and an additional 300 dollar each for a child in the family.  (MSNBC, 2008) The stimulus plan may be a step in right direction but the challenges the economy is facing are fundamental one. With high oil prices and fears of inflation the tax cuts may end up fuelling the inflation in the economy resulting in more import of cheap products from countries like China which is maintaining fixed exchange rates. Conclusion At present the economy is looking down the barrel and there is a very slim chance that it will escape recession and more importantly a growth slowing down in next 2-3 years. America is fast graying and productivity going down with increasing health costs, the times seems to be certainly tough in future. The one ray of hope is creating of jobs by investing in new technologies which America is historically good at. References Kjeldsen-Kragh, Soeren. (2002) International Economics. Copenhagen, , DNK: Copenhagen Business School Press, 2002. Mark Landler and Heather Timmons (2008) Stocks Plunge Worldwide on Fears of a U.S. Recession. Retrieved on 17th Feb from http://www.nytimes.com/2008/01/21/business/22stox-web.html?_r=1&hp&oref=slogin MSNBC (2008) Bush signs stimulus package into law. Retrieved on 17th Feb from http://www.msnbc.msn.com/id/23143814 http://www.trb.org/publications/millennium/00138.pdf Â
Sunday, September 1, 2019
Grief and Rosaldo’s Rage Essay
She had not suffered much. Her death came and went quickly. Michelle was dead, gone forever at the blink of an eye. As her husband looked over her body at the bottom of a 65 foot sheer precipice, many ideas and emotions fluttered in his mind. Renato Rosaldo describes his experience at the site of the fatal accident, overlooking the body of his lifeless wife, Michelle Rosaldo: â€Å"I felt like in a nightmare, the whole world around me expanding and contracting, visually and viscerally heaving (476).†Although at the time of the tragedy and many months after, Renato Rosaldo found himself in an almost delusional state of grief, the calamity helped Rosaldo reach a state of enlightenment with his study of the Ilongot tribe. Michelle and Renato Rosaldo had studied the Ilongot tribe in the northern part of the Philippines as anthropologists. Renato Rosaldo’s past attempts at understand the Ilongot’s reason for head hunting, â€Å"rage, born of grief,†had failed using his method of hermeneutics. The conclusions Rosaldo drew from this explanation were, at best, educated guesses. Trying to be objective to his study of the Ilongot tribe, Rosaldo could not understand the driving factor behind killing a fellow human as a way of dealing with the loss of someone close to you. What he later started to understand was that the ritual was something that could not easily and readily be described. It was not until the time of his wife’s death that he could comprehend the force of anger possible in bereavement. The force was so strong within him that drawing parallels with the ways Rosaldo’s own culture had molded him into dealing with bereavement started to overlap with the Ilongot way. This emotional force became the key in helping Rosaldo unlock the mystery of this rage via bereavement, and unfortunately, it could only come at the price of Michelle Rosaldo. Renato Rosaldo’s explanation of why the Ilongot used head hunting as a way of dealing with bereavement is compelling due to his understanding of emotional force through his own personal experience. After the loss of his brother, then four years later, the loss of his colleague, friend, and wife Michelle Rosaldo, Rosaldo experienced bereavement and the emotional force that accompanies it first hand. Spending months grieving, Rosaldo’s insights on the topic of head hunting had changed dramatically. Shortly after his wife’s death, an excerpt from his journal concurs with the change of perception of the Ilongot people. My journal went on to reflect more broadly on death, rage, and headhunting by speaking of my ‘wish for the Ilongot solution; they are much more in touch with reality than Christians. So, I need a place to carry my anger – and can we say a solution of the imagination is better than theirs? And can we condemn them when we napalm villages? Is our rationale so much sounder than theirs (478)? Rosaldo’s experience with personal bereavement left him with a sense of what despair and rage could conjure up in the human being. Wishing for the Ilongot solution himself, Rosaldo finally realized that the Ilongot were not as different as he had originally thought. The emotional force Rosaldo had felt has the same core as the force that pushed the older tribesman into a headhunting raid. Rosaldo’s comparison of his solution of the imagination and the ritualistic headhunting had rage as the common seed. Rosaldo’s initial attempts to find what drives the older Ilongot men to headhunt using traditional ethnographic methods failed. Renato and Michelle Rosaldo played a tape of a headhunting celebration five years prior, evoking great emotion from the crowd of Ilongot because the celebrator on the tape had already been deceased and headhunting was now forbidden. â€Å"The song pulls at us, drags our hearts, it makes us think of our dead uncle†¦Leave off now, isn’t that enough? Even I, a woman, cannot stand the way it feels inside my heart†¦At the time I could only feel apprehensive and diffusely sense the force of the emotions experienced†¦(473-474).†Rosaldo’s emotional detachment from the man speaking on the tape recorder prevents him with identifying with the Ilongot tribesmen. This lack of emotional connection is understandable, as Rosaldo himself was obviously not as close to the man practicing the ceremony as his family. This understanding of the rage and sorrow that the Ilongot members had felt during the listening is a crucial element of how the dynamic between bereavement and sorrow function. Rosaldo understood that his analysis could easily be brought under fire due to the tying in of personal experiences during his ethnography of the Ilongot culture. Rosaldo concurs that there is potential for risk by saying, â€Å"Introducing myself into this account requires a certain hesitation both because of the discipline’s taboo and because of its increasingly frequent violation by essays laced with trendy amalgams of continental philosophy and autobiographical snippets (475).†The possibility for an anthropologist who brings personal experience into an analysis of a foreign culture to become too self absorbed is always possible. Rosaldo avoids this frequent ethnographic infringement by separating self righteousness from applying personal experiences for comparison in anthropology. Rosaldo claims that his and all interpretations are provisional, stating that â€Å"they are made by positioned subjects who are prepared to know certain things and not others (476),†which presents that he only began to fathom the force of what the Ilongot’s had been describing as the anger held because of bereavement. Although some would argue that the risks with mixing emotion during anthropological study are too great, total objectivity can not always provide a complete analysis. Although being objective and getting the factual aspects of rituals and cultural symbols provides great insight of a culture and its formal procedures, it does not necessarily give the ethnographer the true experience of the event; let it be bereavement or something else. The true meaning behind many events and cultural symbols that are looked at objectively are really quite open to interpretation. Who is to say that what the ethnographer interprets as being one thing, in turn, does not represent something totally different for the subject actually being studied? Although it is not true for all cases, bereavement and the emotional forces that are its byproduct can only be successfully analyzed and interpreted when the observer’s experience overlaps or parallels that of the subject’s. Rosaldo later found his own experience overlapping that of the Ilongot’s. After suffering through not only the loss of his young brother’s life, but the loss of his wife’s, Renato Rosaldo’s view of headhunting had drastically changed. Although Rosaldo had spent fourteen years attempting to conclude the actual drive behind the Ilongot murderous ritual using current anthropological methodology, in one swift moment, he had felt the drive within himself. This emotional force had left him seeking for the Ilongot solution. Realizing that this rage within him had pieced together the ethnographic puzzle of the Ilongot headhunting, Rosaldo masterfully avoided becoming too self absorbed while giving his account of the Ilongot ritualistic beheading. Rosaldo posed the question, â€Å"Do people always in fact describe most thickly what matters most to them (470)?†After review of Rosaldo’s essay, one will most likely conclude that the answer is no. Works Cited Rosaldo, Renato. â€Å"Grief and a Headhunter’s Rage.†Literacies. Ed. Terence Brunk Suzanne Diamond Priscilla Perkins Ken Smith New York, W. W. Norton & Company, 1997. 469-487
Subscribe to:
Posts (Atom)