Cambodian Genocide free essay sample

Cambodia, a southeastern Asian nation, has persevered through numerous accomplishments in history and has regularly been vanquished yet never has it considered such to be demolition as grievous as in the year 1970. With a populace of about 7 million individuals at that point, practically all Cambodians before annihilation rehearsed Buddhism. The nation was ruled by France for almost 100 years lastly picked up autonomy in 1953. Cambodia at that point turned into a protected government when Prince Sihanouk occurred as ruler. After much battling to keep his property autonomous from different nations, Sihanouk was dismissed in a military overthrow including Prime Minister General Lon Nol. This caused the Vietnamese socialists that lived halfway in Cambodia to frame a defiant gathering called the Khmer Rouge. Intrusions appeared to be endless for the nation, as Sihanouk couldn't recover his capacity as lord. Strain between Lon Nol’s government and Khmer Rouge had ascended to an untouched high until Khmer Rouge increased total intensity of the nation in 1975 and the official name was even changed to Democratic Kampucha. We will compose a custom paper test on Cambodian Genocide or on the other hand any comparative theme explicitly for you Don't WasteYour Time Recruit WRITER Just 13.90/page What we realize today as called Cambodia turned into an unfriendly and hazardous spot to live, as it was fundamentally war justification for the Vietnamese war. Ousted by Khmer Rouge pioneer Pol Pot, Cambodians had to follow a sorted out radical program to reenact Maoist socialism. All laws and rights recently appreciated by the nation were prematurely ended and Pol Pot’s plan was to obliterate conventional Cambodian culture. Individuals whose families had lived in Cambodia for incalculable ages were unexpectedly constrained without prior warning escape their homes. The Khmer Rouge savagely killed any individual on the spot in the event that they would not leave their homes or even took too long to even think about leaving. The individuals who didn’t obey orders were shot. Infants, wiped out youngsters, the older and debilitated individuals were likewise gone for not having the option to leave soon enough. All foundations were closed down. Industrial facilities, emergency clinics, schools, sanctuaries and colleges did not exist anymore, nor did religion, music or individual connections. All individuals who had earnedâ professional titles, for example, specialists, educators, designers, legal advisors and innumerable others were searched out by Khmer Rouge and killed nearby their more distant families. Individuals who were kept in the nation had to work in labor camps and were scarcely kept alive. Endless became sick and later kicked the bucket from poor day to day environments since they were not rewarded or thought about. All minorities including Chinese, Vietnamese and Thai were killed. Half of the Muslim populace was cleared out, alongside approximately 8,000 Christians. All through the 1980’s endeavors were made by outside nations to wreck the Khmer Rouge and revive Cambodian culture. At long last in 1991 Cambodia achieved a harmony bargain to implement truce and in the end Sihanouk was recovered the King, after two years. Reproduction was difficult since the entirety of the individuals who were prepared in building, law, medication and pioneers were slaughtered. Likewise the economy was annihilated because of Pol Pot and his attitude toward remote guide. A harmony keeping power was made to manage any issues including displaced people. Today Cambodia is by and by an established government and is constrained by a senate and various different lawmakers. A progressed and sorted out government unmistakably exists and terrains that were once places of dread have now been made into remembrances committed to the numerous Cambodians who were killed. In spite of the fact that the mental scars that were brought about by horrendous slaughter will never stop, a more prominent feeling of patriotism has been made and the populace that is comprised of for the most part individuals who haven’t encountered the destruction has achieved an extraordinary recuperation. I feel that the means that were taken by the individuals who freed Cambodia were effective in reclaiming their general public, taking into account how upsetting the massacre was. The destruction laws that were authorized for this situation appear to be for the most part for political reasons, yet there were exemptions of laws that just were not sensible. Laws that confined individuals from taking an interest in school, rehearsing their particular exchange and setting off to their place of religion or in any event, imploring, can be ordered as politically determined since the Khmer Rouge was resolved to make Cambodia indistinguishable from Maoist China. The thinking behind laws, for example, the restriction of individual connections, wearing eye glasses, music, radio sets, knowing an unknown dialect, giggling, crying and articulations of friendship are not political, but instead childish and clearly narrow minded. Since this particular annihilation is connected to the Vietnamese War that included mass passing in different nations too, it is possible that the close to districts that accomplished destruction too were very comparative. A record that is tantamount to the Cambodian slaughter is the destruction that happened in Rwanda. Other than the way that Rwanda likewise has an excellent subtropical atmosphere, the two nations endured frightful because of the wrongdoing of their own kin. The two nations persevered through a devastating slaughter that will everlastingly stay in their history and be returned to by the endless individuals who lost their families. Likewise, the economies of the nations were both seriously harmed, leaving today’s populace with a detriment as the economy and instruction frameworks advance at an extremely moderate pace. I have never experienced any kind of slaughter or awful disaster, particularly at this scale, yet can identify for the individuals who did or didn't endure this repulsiveness. Since I haven’t experienced anything like this I don’t have anything individual to share concerning annihilation. Despite the fact that by being an American in the 21st century, the fear based oppressor assaults known as 9/11 is a relatable catastrophe. A large number of individuals were harmed or killed that day due to the view the fear based oppressors had towards America. The measure of individuals who were slaughtered was not so much disastrous to our general public as on account of Cambodia and I don't know whether it can essentially be viewed as massacre however the goals of the fear based oppressors are comparable in a manner to those of Khmer Rogue. Khmer Rogue was narrow minded and controlling when they were not defended in doing as such, particularly considering the measure of blameless individuals who were killed. Pol Pot knew how we needed to run his form of Cambodia and couldn't have cared less that Khmer Rogue was dangerous towards Cambodian culture. I accept that when the Al-Qaeda fear based oppressors collided with the twin towers their goals were to disable our general public and offer the expression that they don't concur with the manner in which we run our nation. Despite what number of individuals are executed in endeavor to hurt a country’s society, the individuals who murder because of narrow mindedness don't have the right to exist. Over portion of the number of inhabitants in Cambodia was killed all through the couple of years that the Khmer Rogue was in power, therefor hurting their future potential on the planet. I imagine that the odds of war ever reaching a conclusion for individuals everywhere throughout the world are incredibly thin, yet in the event that war for narrow minded authority over individuals keeps on happening war will never end. Destruction spreads scorn that can't be pulverized.

Symbolism and Setting in The Great Gatsby Essay Example

Imagery and Setting in The Great Gatsby Essay The United States was a land loaded up with different open doors during the 1920s. World War I was finished and a huge number of individuals from everywhere throughout the globe were going to the United States competing for a fresh start. These individuals were completely charmed yet the possibility of The American Dream. The American Dream is the possibility that each United States resident ought to have an equivalent chance to make progress and flourishing through difficult work, assurance, and activity. It doesn't make a difference where you originated from, all you need is an enthusiasm to succeed. This thought assumed a job in The Great Gatsby through the characters, imagery, and settings in the story. The American Dream was a significant piece of the characters in the story. This thought significantly affected their decisions from how they lived to how they acted. The wealthiest characters were Daisy and Tom Buchanan, and Jay Gatsby. These three accepted they could do anything since they were in a class higher than every other person. They just thought about what was happening right now and never stressed over the results of their activities. They were extremely insatiable individuals and just thought about their assets. This goes with the conviction of the American Dream and that you can accomplish anything on the off chance that you set your attention to it. A case of this is the way Tom goes behind Daisy's back with Myrtle Wilson. He does this since he just observes Daisy one of his possessions. I initially met Tom Buchanan’s special lady. The way that he had one was demanded any place he was known. His colleagues disliked the way that he turned up in well known eateries with her and, leaving her at a table, walked about, visiting with whomsoever he knew (Fitzgerald, 27). Notwithstanding Tom and Myrtle being a piece of two diverse social classes he keeps on observing her behind Daisys back. He couldn't care less about his decisions right now however they will in the long run cause issues down the road for him in the butt. Consistently Gatsby tosses ludicrous gatherings to dazzle Daisy We will compose a custom article test on Symbolism and Setting in The Great Gatsby explicitly for you for just $16.38 $13.9/page Request now We will compose a custom article test on Symbolism and Setting in The Great Gatsby explicitly for you FOR ONLY $16.38 $13.9/page Recruit Writer We will compose a custom article test on Symbolism and Setting in The Great Gatsby explicitly for you FOR ONLY $16.38 $13.9/page Recruit Writer

Gist, Christopher

Gist, Christopher Gist, Christopher gist [key], c.1706â€"1759, American frontiersman, b. Maryland. Commissioned by the Ohio Company to explore their western lands. In 1750 he descended the Ohio River, explored E Kentucky, and crossed to Roanoke, N.C.; he thus penetrated the Kentucky region 18 years before the more celebrated Daniel Boone. The next season he more carefully traversed and mapped the Ohio watershed in western Virginia. He accompanied George Washington in 1753â€"54 on his historic trip to order the French out of the Ohio valley and on the journey twice saved Washington's life. On Gen. Edward Braddock's expedition (1755) against Fort Duquesne, Gist served as a guide. He died of smallpox in the Cherokee country, where he had gone to enlist the Native Americans' aid against the French. An expert woodsman and surveyor, he was highly regarded by his contemporaries. See his journals ed. by W. M. Darlington (1893). The Columbia Electronic Encyclopedia, 6th ed. Copyright © 2012, Columbia University Press. All rights reserved. See more Encyclopedia articles on: U.S. History: Biographies

The Criminal Case Of Dr. Richard Heartman, An Internal...

Health insurance fraud is what drives up health insurance premium costs, wastes taxpayer’s money, but can also endanger beneficiaries or leave them uninsurable. In 2015, Medicare Strike Force reported over $700 million in false billing by doctors, nurses, other licenses medical professionals, laboratories, and individuals (FBI.gov). This is a staggering figure that is only getting worse. In this fictitious federal case I will be describing the criminal offender, the crime that was committed, the charge handed down by law enforcement, and the judicial process from the beginning of the criminal case to the sentencing of Dr. Richard Heartman, an internal medicine physician. The Defendant Defendant Richard Heartman, a licensed internal†¦show more content†¦Charges The U.S. Attorney General, or prosecutor Amita Anders, provided the grand jury all the evidence and testimony from witnesses, who voted to indict Dr. Richard Heartman based on the strong evidence by the U.S. Attorney General, which was able to establish Dr. Heartman was found guilty beyond a reasonable doubt. On January 31, 2016, FBI agents arrive at his office at Heartless Rd, Heartotack, Illinois and place Dr. Heartman under arrest. He is read his Miranda rights and has been advised of the charges against him. Because he has been determined to be a flight risk, he will be detained in the county jail until his arraignment. Defendant Heartman, has been charged with 10 counts of wire fraud, for knowingly caused to be transmitted by means of wire communication in interstate commerce from the account of Medicare at Citibank in Indianapolis to the defendants account at JP Morgan Chase in Heartotack, Illinois, which represents the payments by Medicare on all claims submitted from 2005-2015 by all the individuals. This is a violation of Title 18, United States Code, Section 1343 (Cornell Law, 2016). Defendant Heartman also has been charged with 10 counts of U.S. Mail fraud, for knowingly caused to be delivered by United States mail, envelopes containing checks from commercial and private health insurance carriers, which represented the payments by the

Haemoglobinopathies - Free Essay Example

Sample details Pages: 25 Words: 7474 Downloads: 5 Date added: 2017/06/26 Category Statistics Essay Did you like this example? Abstract Haemoglobinopathies or inherited disorders of haemoglobin are the most common monogenic disorders in humans. Red cell transfusion is a well accepted therapy for clinical management of the most severe form of haemoglobinopathies namely, sickle cell disease (SCD) and ÃŽÂ ²-thalassaemia major. Patients affected by SCD need red blood cell transfusions on a regular basis to reduce morbidity and mortality. Don’t waste time! Our writers will create an original "Haemoglobinopathies" essay for you Create order The transfusions are administered intermittently to control or prevent a serious complication of SCD, and as a perioperative measure. Or, as a chronic procedure, transfusion strategy is applied to prevent the recurrence, or the first occurrence, of stroke which is a major crisis in SCD, and to manage pulmonary hypertension and other sources of morbidity and mortality. Exchange transfusions are used to reduce the sickle cell haemoglobin (HbS) levels during crisis. Several situations also exist wherein the indication for red cell transfusion is controversial, uncertain, or downright injudicious. Many side effects of transfusion have been identified and methods to overcome them have been developed. Iron overload (remedy: iron chelation), and alloimmunisation (remedy: phenotypical matching of transfused blood) are two notable examples. Association of haemoglobinopathies and neurologic sequelae after transfusion is also known. At the present time, bone marrow transplant is the only curati ve procedure available for both SCD and ÃŽÂ ²-thalassaemia major. Potential therapies involving stem cell transplantation and gene techniques are being vigorously researched. A detailed discussion of the current status of clinical management strategies as applied to inherited haemoglobin-related diseases in particular, sickle cell disease and the thalassaemias, is presented in this paper. 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 ÃŽÂ 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 ( 82 fL) reflecting decreased haemoglobin synthesis.   Thus, it is usually associated with hypochromic anaemia. Microcytic anaemia can result from defects either in iron acquisition or availability (Iolascon et al., 2009), or disorders of haeme metabolism or globin synthesis (Richardson, 2007). The differential diagnosis for microcytic anaemia includes iron deficiency anaemia (IDA), thalassaemia, ACD, and rarely sideroblastic anaemia (Chulilla et al., 2009). Microcytosis without anaemia is characteristic of thalassaemia trait. The red blood cell distribution width (RDW) obtained with haematological analysers provides the index of dispersion in the erythrocyte distribution curve and complements MCV values. RDW is helpful to differentiate between thalassaemia and IDA. RDW is normal in thalassemia; on the contrary, microcytic anemia with RDW 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 haematopoietic cells, and can result in macrocytic anaemia. 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 ACD (Krantz, 1994). Common childhood normocytic anaemias are, besides iron deficiency anaemia, those due to acute bleeding, sickle cell anaemia, 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 haemolytic 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 anaemia 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 erythrocytes, due to bleeding or haemolysis. The r eticulocyte 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 (HbS) in which valine is substituted for glutamic acid at the sixth amino acid position in the beta globin gene reduces the solubility of haemoglobin, 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 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 characteristically 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 cytokines causing impairment of erythroid p rogenitor 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).   SCD arising from a point mutation in the ÃŽÂ 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 a ctivated 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 disease including a critical 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). 4.1 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). 4.2 Red blood cell transfusion 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. 4.3 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. ACS 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 recommended 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). 4.4 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). 4.5 Controversial and indeterminate indications for transfusion Several situations also exist wherein the indication for red cell transfusion is controversial, uncertain, or downright injudicious in SCD management. Some examples are indicated in Table 1. 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 therapy 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 (Febrile Non-Haemolytic Transfusion Reaction i.e., fever resulting from a blood transfusion) and alloimmunisation to HLAs (Human Leucocyte Antigens),   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. 5.1 ÃŽÂ 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: ÃŽÂ ±-thalassaemia and ÃŽÂ ²-thalassaemia. Homozygous ÃŽÂ ²-thalassaemia is marked by a quantitative deficiency of the ÃŽÂ ²-globin chains in the erythroid cells. A complete absence of the ÃŽÂ ²-globin chains occurs in homozygous ÃŽÂ ²o-thalassaemia whereas in homozygous ÃŽÂ ²+-thalassaemia the ÃŽÂ ²-globin chains are present at less than 30% of normal. Accounting for nearly 90% of the cases, ÃŽÂ ²+-thalassaemia is the most commonly observed form of ÃŽÂ ²-thalassaemia. The condition is termed thalassaemia major when there is microcytic hypochromic anaemia with severe haemolysis, hepatosplenomegaly, skeletal deformities and iron overload. ÃŽÂ ²-thalassaemia homozygotes exhibit severe transfusion-dependent anaemia in the very first year of life. Homozygotic individ uals having a relatively benign clinical phenotype 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   ÃŽÂ ± -thalassaemia leading to reduction in the synthesis of ÃŽÂ ±-globin chains, and a genetic predisposition to produce high levels of HbF, could be important factors for the extensive phenotypic variability described above (Weatherall, 1996). The milder form of thalassaemia intermedia is the result of a lesser imbalance in globin chain synthesis probably the result of residual ÃŽÂ ² -globin chain synthesis due to mild mutation or due to reduced synthesis of ÃŽÂ ±-globin chains due to co-inheritance of ÃŽÂ ±-thalassaemia (Nadkarni et al., 2001). Persons having the heterozygous form of the disorder are usually asymptomatic but can be recognised by typical abnormalities of red cell morphology (shown in Fig.4) and indices (Spritz and Forget, 1983). Compared to the heterozygous form of ÃŽÂ ²-thalassaemia, a larger imbalance exists in the ÃŽÂ ±- to ÃŽÂ ²-globin chain synthesis in the homozygous ÃŽÂ ²-thalassemia or Cooley anaemia. The excess ÃŽÂ ±-globin chains are liable to precipitate, causing damage to the ÃŽÂ ²-thalassemic red cell membrane and affecting erythropoiesis. Important manifestations of homozygous ÃŽÂ ²-thalassemia are severe chronic microcytic haemolytic anaemia and hepatosplenomegaly due to extramedullary haematopoiesis (Spritz and Forget, 1983). As many as 175-200 molecular mutations affecting the ÃŽÂ ²-globin gene complex are involved in creating the ÃŽÂ ²-thalassaemia syndromes with the resultant altered synthetic ratios of ÃŽÂ ±- to ÃŽÂ ²-globin chains, precipitation of excess unbalanced ÃŽÂ ±-globin chains, and programmed cell death of erythroid precursors (Steinberg and Rodgers, 2001; Gambari, 2010). Hence, the pathogenetic basis of the clinical diversity of the ÃŽÂ ²-thalassaemia syndromes essentially rests with the striking heterogeneity of mutations in the ÃŽÂ ²-globin gene (Thein, 1993). The -158 (C ÃÆ'   T) substitution in the GÃŽÂ ³ gene has been found to be linked to the increase in HbF synthesis leading to less severe disease in thalassaemia intermedia (Gilman and Huisman, 1985; Ragusa et al., 1992). 5.2 Red blood cell transfusion and iron overload Regular RBC transfusions have proved to be efficacious in the treatment of ÃŽÂ ²-thalassemia by nullifying the complications of anaemia and compensatory bone marrow (BM) expansion. However, thalassaemias are also complicated by physiological iron overload which gets exacerbated by blood transfusion and causes various endocrine diseases, liver cirrhosis, cardiac failure and also death (Engle, 1964). Complemented with iron-chelating therapy (e.g., deferoxamine) for iron overload, the prognosis of thalassemia major has become dramatic (Olivieri and Brittenham, 1997).  Ãƒâ€šÃ‚   Recently, the mechanism of iron overload in the absence of transfusion in thalassaemia has been unraveled by Tanno et al. (2007) who observed that the overproduction of the protein GDF15 suppresses the production of the liver protein, hepcidin in thalassaemia patients which eventually leads to an increase in the uptake of dietary iron in the gut. This information could translate into new diagnostic and therapeutic tools in the future. 6. Critical review of thalassemias : (ii) Clinical management therapies ÃŽÂ ²-thalassaemia syndromes are the most common genetic diseases worldwide. Improvements in treatment strategies have resulted in good prognosis. Yet, disease- and treatment-related complications get exacerbated over time, increasing morbidity and curtailing life expectancy of the patients. Currently, the only curative treatment available for thalassaemia is stem cell transplantation (SCT) (Gaziev et al., 2008) which is a gold standard in treating the disease. Many challenges exist for transplantation therapy including graft versus host disease (GVHD), rejection of the donated stem cells, and infections while a major limitation for SCT is finding HLA-matched blood-related donors viz., siblings. Currently available high-resolution HLA-typing could minimise rejection and GVHD by matching major as well as minor HLA (Gaziev et al., 2008). The advanced techniques of HLA-typing can also identify unrelated but suitable voluntary donors. Intermittent red blood cell transfusion is the recommended mode of treatment for people who have moderate or severe thalassaemias. ÃŽÂ ²-thalassemia major, or Cooleys anaemia require regular blood transfusions. 6.1 Emerging Therapies Gene therapy for treatment of thalassaemia is still evolving. Research is focussed on finding a potential treatment of ÃŽÂ ² -thalassemia based on globin gene transfer. One of the aims of the genetic research is to trigger the production of HbF in adults to make up for the lack of healthy adult haemoglobin. The molecular mechanisms that initiate the change in gene expression during the switch from foetal (HbF) to adult (HbA) have been partially elucidated. Several chemical compounds able to reactivate HbF synthesis in vitro and in vivo in adult bone marrow have been identified (Testa, 2009). Induction of HbF to treat thalassaemia is a novel therapeutic strategy especially for those patients who are resistant to conventional therapy that is, regular blood transfusions and chelation therapy (Gambari, 2010). In view of the fact that gene therapy could be inaccessible to many because of biological/genetic as well as economic constraints (Gambari, 2010), chemical inducers are being extensively studied. Hydroxyurea has already been used as HbF inducer in both moderate and severe forms of ÃŽÂ ²-thalassaemia (Testa, 2009). Some of the potential inducers of HbF are histone deacetylase inhibitors, DNA-binding drugs and inhibitors of the mammalian target of rapamycin or mTOR pathway (Gambari and Fibach, 2007). Also, according to Gambari and Fibach (2007) chemical inducers need to be used with caution since many of those used so far were potentially cytotoxic. Accelerated apoptosis has been observed in the erythroid progenitors of patients with ÃŽÂ ²-thalassaemia major (Silva et al., 1996). The hormone erythropoietin (Epo), which is the principal regulator of red blood cell production, is known to interact with high-affinity receptors on the surface of erythroid progenitor cells and promote cell viability. Epo has been shown to repress apoptosis via Bcl-XL and Bcl-2 during proliferation and differentiation of erythroid progenitors (Silva et al., 1996). Hence, recombinant human erythropoietin (rHuEpo) could have potential application in the treatment of transfusion-dependent thalassaemia patients as it promotes the differentiation and proliferation of erythroid cells, and stimulates the production of HbF (Makis et al., 2001). 7. Conclusion Inherited haemoglobinopathies including sickle cell disease and thalassaemias result from genetic abnormalities in the synthesis of globin protein chains. Sickle cell disease (SCD) is caused by structural defects in the haemoglobin molecule while thalassaemias occur due to reduced or absent globin chain. Only bone marrow or haematopoietic stem cell transplantation can cure patients with either disease. Clinical management of SCD generally involves supportive therapy consisting of pain relief, fluids and antibiotics, and folic acid supplements. Red cell transfusion is currently a well accepted therapy for clinical management of inherited haemoglobinopathies including SCD and the thalassaemias. Intermittent red cell transfusion is administered to most patients, pre-surgery and in specific cases of severe complications. Persons with severe complications such as stroke, acute chest syndrome or frequent painful sickling crises are treated with hydroxyurea. The only cure available currently for ÃŽÂ ²-thalassaemia major is haematopoietic stem cell transplantation from a compatible donor. Most thalassaemia patients require regular transfusions of red cells and all patients need iron chelation therapy to overcome iron overload. References Adams, R., 2003. Haemoglobinopathies. Haematology (Am Soc Haematol Educ Program) pp.14-39. Adams, R., McKie, V., Brambilla D, et al., 1998. Stroke prevention trial in sickle cell Anaemia. Control Clin Trials 19, pp.110- 129. Andrews, N.C., 1999. Disorders of iron metabolism. N Engl J Med, 341, pp.1986-1995. Andrews, N.C., 2008. Forging a field: the golden age of iron biology. Blood, 112(2), pp.219-230. Anstey, N.M., Russel, B., Yeo, T.W., et al., 2009. The pathophysiology of vivax malaria. Trends Parasitol., 25(5), pp.220-227. Aul, C., Bowen, D.T. Yoshida, Y., 1998. Pathogenesis, etiology, and epidemiology of myelodysplastic syndromes. Haematologica, 83(1), pp. 71-86. Ballas, S.K., 1998. Sickle cell disease: clinical management. Baillieres Clinical   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Haematology, 11 (1), pp.185-214. Ballas, S.K., 2002. Sickle cell anaemia: progress in pathogenesis and treatment. Drugs, 62(8), pp.1143-1172. Bertero, M.T. Caligaris-Cappio, F., 1997. Anemia of chronic disorders in systemic autoimmune disease. Haematologica, 82(3), pp.375-81. Bessman, J.D., Gilmer, P.R. Gardner, F.H., 1983. Improved classification of anemias by MCV and RDW. Am J Clin Pathol 80, pp.322-326. Beutler, E., Gelbart, T., Lee, P., et al., 2000. Molecular characterisation of a case of Atransferrinemia. Blood, 96, pp.4071-4074. Beutler, E. Waalen, J., 2006. The definition of anemia: what is the lower limit of normal of the blood hemoglobin concentration?. Blood, 107(5), pp. 1747-1750. Bottomley, S.S., 2006. Congenital sideroblastic anemias. Curr Hematol Rep., 5(1), 41-49. Bunn H.F., 1997. Pathogenesis and treatment of sickle cell disease. N Engl Med.,337(11), pp.762-769. Castro, O., 1996. Systemic fat embolism and pulmonary hypertension in sickle cell Disease. Hematol Oncol Clin North Am. 10(6), pp.1289-1303. Centis, F., Tabellini, L., Lucarelli, G., et al., 2000. The importance of erythroid expansion in determining the extent of apoptosis in erythroid precursors in patients with beta- thalassaemia major. Blood, 96, pp.3624-3629. Chulilla, J.A.M., ColÃÆ' ¡s, M.S.R. MartÃÆ' ­n, M.G., 2009. Classification of anemia for Gastroenterologists. World J Gastroenterol. 15(37), pp.4627-4637. Claster, S. Vichinsky, E.P., 2003. Managing sickle cell disease. BMJ,327, pp.1151- 1155. Cohen, A.R., 1987. Management of iron overload in the paediatric patient. Haematol   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Oncol Clin North Am., pp. 521-544. Connes, P., Hue, O., Tripette, J., et al., 2008. Blood rheology abnormalities and vascular   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   cell adhesion mechanisms in sickle cell trait carriers during exercise. Clinical   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Hemorheology Microcirculation, 39(1-4), pp. 179-184. Creary, M., Williamson, D., Kulkarni, R., 2007. Sickle cell disease: current activities, public health implications, and future directions. J Womens Health, 16(5),575-582. Distenfeld, A. Woermann, U., 2009. Sickle Cell Anemia. Accessed 15 February 2010 https://emedicine.medscape.com/article/205926-overview. Dugdale, D.C., 2008. Megaloblastic anemia. Medline Plus, Accessed 28 Jan 2010  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   https://www.nlm.nih.gov/medlineplus/ency/article/000567.htm Engle, M.A., Erlandson, M. Smith, C.H., 1964. Late cardiac complications of chronic, severe, refractory anaemia with haemochromatosis. Circulation, 30, pp.698-705. Fleming, M.D., 2002. The genetics of inherited sideroblastic anemias. Semin Hematol.    39, pp.270-281. Gambari, R., 2010. Foetal haemoglobin inducers and thalassaemia: novel achievements. Blood Transfus. 8(1), pp. 5-7. Gambari, R. Fibach, E., 2007. Medicinal chemistry of foetal haemoglobin inducers for treatment of beta-thalassaemia. Curr Med Chem.14, pp.199-212. Gaziev J, Sodani P Lucarelli C, 2008, Haematopoietic stem cell transplantation in thalassaemia, Bone Marrow Transplantation, 42, S41. Gilman, J.G. Huisman, T.H.J., 1985. A sequence variation associated with elevated foetal GÃŽÂ ³globin production. Blood, 66, pp.783-787. Gladwin, M.T. Kato, G.J., 2005. Cardiopulmonary complications of sickle cell disease: role of nitric oxide and hemolytic anemia. Haematology (Am Soc Hematol Educ   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Program), pp. 51-57. Goldberg, M.A., Brugnara, C., Dover, G.J. et al., 1990. Treatment of sickle cell anaemia with hydroxyurea and erythropoietin. NEJM, 323(6), pp. 366-372. Haas JD Brownlie T, 2001, Iron deficiency and reduced work capacity: a critical review of the research to determine a causal relationship, J Nutr., 131(2 Suppl): 676S-690S. Halterman, J.S., Kaczorowski, J.M., Aligne, C.A. et al., 2001. Iron deficiency and cognitive achievement among school-aged children and adolescents in the United States. Pediatrics, 107, pp. 1381-1386.      Hankins J, Jeng M, Harris S, et al., 2005, Chronic transfusion therapy for children with sickle cell disease and recurrent acute chest syndrome, J Paediatr Haematol Oncol 27:158 161. Herrick JB, 1910, Peculiar elongated and sickle-shaped red corpuscles in a case of severe anemia, Arch Intern Med.6:517-521. Hershko C Skikne B, 2009, Pathogenesis and management of iron deficiency anaemia: Emerging role of Celiac disease, Helicobacter pylori, and autoimmune gastritis, Seminars in Hematology, 46 (4): 339-350.Iolascon A, De Falco L. Beaumont C, 2009, Molecular basis of inherited microcytic anemia due to defects in iron acquisition or heme synthesis, Haematologica 94(3): 395-408. Jison ML, Munson PJ, Barb JJ et al., 2004, Blood mononuclear cell gene expression profiles characterize the oxidant, hemolytic, and inflammatory stress of sickle cell disease, Blood, 104(1): 270-280.   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Killip S, Bennett JM Chambers MD, 2008, Iron deficiency anemia, American Family Physician, 75(5): 671-678. Kohgo Y, Ikuta K, Ohtake T. et al., 2008, Body iron metabolism and pathophysiology of iron overload, Int J Hematol. 88(1): 7-15. Krantz SB, 1994, Pathogenesis and treatment of the anemia of chronic disease, Am J   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Med Sci.,307(5): 353-359. the art, Expert Opinion on Biological Therapy, 7(2): 161-172. Josephson CD, Su LL, Hillyer KL, et al., 2007, Transfusion in the Patient With Sickle Cell Disease: A Critical Review of the Literature and Transfusion Guidelines, Transfusion Medicine Reviews, 21(2): 118-133. MakisAC, ChaliasosN, Hatzimichael EC et al., 2001, Recombinant human   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   erythropoietin therapy in a transfusion-dependent ÃŽÂ ²-thalassaemia major patient,   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Annals of Haematology, 80(8):492-495. Means RT Jr., 1996, Advancement in the anemia of chronic disease: A cytokine- mediated anemia, Stem Cells, 13(1): 32-37. Means RT Jr., 2003, Recent developments in the anemia of chronic disease, Current   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Hematology Reports, 2(2):116-121. Miller S, Rao S, Dunn K, et al., 1995, Priapism in children with sickle cell disease, J   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Urol, 154:844- 847. Mims MP, Guan Y, Pospisilova D, et al., 2005, Identification of a human mutation of DMT1 in a patient with microcytic anemia and iron overload, Blood,105:1337- 1342. MuÃÆ' ±oz M, Villar I GarcÃÆ' ­a-Erce JA, 2009, An update on iron physiology, World J Gastroenterol, 15(37): 4617-4626. Nadkarni A, Gorakshakar AC, Lu CY, et al., 2001, Molecular pathogenesis and clinical variability of ÃŽÂ ²-thalassaemia syndromes among Indians, American Journal of Haematology, 68:75-80. Olivieri NF Brittenham GM, 1997, Iron-chelating therapy and the treatment of   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   thalassaemia, Blood, 89(3): 739-761 Pauling L, Itano HA, Singer SJ, et al., 1949,   Sickle cell anemia: a molecular disease, Science, 110(2865):543-548. Quigley JG, Yang Z, Worthington MT, et al. 2004, Identification of a human heme exporter that is essential for erythropoiesis, Cell, 118:757-766. Ragusa A, Lambardo M, Beldjord C, et al., 1992, Genetic epidemiology of ÃŽÂ ²- thalassaemia in Sicily: do sequences 58 to the GÃŽÂ ³ gene and 58 to the ÃŽÂ ² gene interact to enhance HbF expression in ÃŽÂ ² -thalassemia?, Am J Hematol, 40:199-206. Richardson M, 2007, Microcytic anemia, Pediatrics in Review, 28:5-14. Rifikind S, Waisman J, Thompson R, et al., 1979, RBC exchange pheresis for priapism in sickle cell disease, JAMA, 242:2317 2318. Rodgers GP, Noguchi CT, Schechter AN, 1985, Irreversibly sickled erythrocytes in sickle cell anemia: A quantitative reappraisal, Am J Hematol., 20(1): 17-23. Rodgers GP, Dover GJ, Uyesaka N, et al., 1993, Augmention by erythropoietin of the fetal-hemoglobin response to hydroxyurea in sickle cell disease, NEJM, 328(2): 73- 80. Rosenfeld C List A, 2000, A hypothesis for the pathogenesis of myelodysplastic syndromes: implications for new therapies, Leukemia, 14(1): 2-8. Ru YX, Mao BY, Zhang FK et al., 2009, Invasion of erythroblasts by Plasmodium vivax: A new mechanism contributing to malarial anaemia, Ultrastruct. Pathol., 33(5):236-42.   Shemin, D. Rittenberg D, 1946, The life span of the human red blood cell, J Biol Chem, 166: 627-636. Siah CW, Ombiga J, Adams LA, et al., 2006, Normal iron metabolism and the pathophysiology of iron overload disorders, Clin Biochem Rev. 27:5-16. Silva M, Grillot D, Benito A, et al., 1996, Erythropoietin can promote erythroid progenitor survival by repressing apoptosis through Bcl-XL and Bcl-2. Blood, 88:1576-1582. Sokol RJ, Booker DJ Stamps R, 1992, The pathology of autoimmune haemolytic anaemia, J Clin Pathol., 45: 1047-1052. Spivak, JL, 2002, Iron and the anemia of chronic disease, Oncology, 16(9 Suppl 10):25- 33. Spritz RA Forget BG, 1983, The thalassemias: molecular mechanisms of human genetic disease, Am J Hum Genet., 35:333-361. Steinberg MH Rodgers GP, 2001, Pharmacologic modulation of foetal haemoglobin, Medicine, 80:328-344. Styles LA Vichinsky E, 1994, Effects of a long-term transfusion regimen on sickle cell- related illnesses, J Pediatr., 125:909-911. Tanno T, Bhanu NV, Oneal PA et al., 2007, High levels of GDF15 in thalassemia   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   suppress expression of the iron regulatory protein hepcidin, Nature   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Medicine, 13:1096 1101. Tefferi A, 2003, Anaemia in adults: a contemporary approach to diagnosis, Mayo Clin   Proc.78:1274-1280. Testa U, 2009, Fetal hemoglobin chemical inducers for treatment of   Haemoglobinopathies, Ann Hematol. 88:505-528. Thein SL, 1993, ÃŽÂ ²- Thalassaemia. In: Higgs DR Weatherall DA, editors, Baillieres clinical haematology: the hemoglobinopathis, Vol 6, Bailliere Tindall, London, p151-175. Tischkowitz MD Hodgson SV, 2003, Fanconi anaemia, J Med Genet 2003;40:1-10 doi:10.1136/jmg.40.1.1 Tuck S, James C, Brewster E, et al., 1987, Prophylactic blood transfusions in maternal sickle cell syndromes, Br J Obstet Gynaecol., 94:121 125. Walter PB, Harmatz P Vichinsky E, 2009, Iron metabolism and iron chelation in sickle cell disease, Acta Haematol., 122(2-3):174-183. Weatherall DJ, 1969, The genetics of the thalassaemias, British Medical Bulletin, 25(1): 24-29. Weatherall DJ, 1996, The molecular basis for phenotypic variability of the common thalassaemias, Mol Med Today 1:15-20.   Weatherall DJ, 1997a, ABC of clinical haematology. The hereditary anaemias, BMJ 314:492-496. Weatherall DJ, 1997b, Fortnightly review: the thalassaemias, BMJ, 314(7095):1675- 1678. WHO (1968), Nutritional anaemias. Report of a WHO scientific group. World Health Organ Tech Rep Ser. 1968;405:5-37. Wun T, 2001, The role of inflammation and leukocytes in the pathogenesis of sickle cell disease, Hematology, 5(5): 403-412.

The Validity of Knowledge Free Essays

Lia Thompson Mr. Faria HZT 4U1 Wednesday January 18, 2012 The Validity of Knowledge This paper will explain the validity of John Locke’s Theory of Knowledge. Epistemology has been the topic of discussion for many philosophers over the centuries. We will write a custom essay sample on The Validity of Knowledge or any similar topic only for you Order Now The study of knowledge is important because as humans, it is necessary to understand where the basis for our knowledge originates. Locke, like many philosophers believed that all knowledge about the world is derived from sensory perceptions. Empiricists such as Locke believe this â€Å"posteriori† view of knowledge. He explains in his theory that we are born with â€Å"blank slates† or Tabula Rasa, the term used in Locke’s theory in his writing, â€Å"An Essay Concerning Human Understanding† (Locke 163). Philosophical arguments are as varied as the philosophers who construct them. For each theory, there is an opposing view. Rationalists, such as Rene Descartes would argue against Locke and his empiricist view of knowledge, believing knowledge to be innate. Descartes believed that all humans are innately born with these truths without the aid of our senses as argued in his first, second and third Meditations (Descartes 3). Locke’s theory goes against not only Descartes views but Plato’s as well. But Despite the arguments against Locke’s empiricist view, he is most reasonable. I agree with John Locke’s theory of sensory perception because we would not be able to survive without our senses. John Locke was born on August 29, 1632 in a village in Somerset, England (John Locke-Biography). He wrote several major works that have made a big impact on today’s view of the world, but his major theory on knowledge was in his book, â€Å"An Essay Concerning Human Understanding†, where he outlined his views as well as argued against rationalist’s view on innate knowledge. He wrote his book based on his belief that true knowledge is gained through experience, â€Å"a posteriori† (Velasquez 330). â€Å"Locke holds that the mind is a tabula rasa or blank sheet until experience in the form of sensation and reflection provide the basic materials — simple ideas — out of which most of our more complex knowledge is constructed† (Uzgalis). Reflection and sensory experiences go hand in hand because in order for our senses to be used, we must experience the world around us. Once we have experienced, for example the sweet taste of an apple, from eating it, we are able to reflect on what our senses were able to establish about it and gain truths about what we experienced. â€Å"Reason is our intellect, our power to think and make judgments based on our sensory experience† (Locke 59). Locke does agree that we as humans have reason but our senses are paired up with reason, as we are to reason what our senses are experiencing. Locke created the theory of â€Å"Primary and Secondary Qualities† to explain his ideas about the differences between our perception of the world and what the world really is. Based on scientific research, humans are aware that not everything we perceive is the same as how other living creatures perceive it. Animals in comparison to humans may experience the same things as humans do, but the way they are perceived can be totally different. For example, it is scientifically proven that dogs cannot see in colour, so to them everything is in black and white. Dogs still use their sight, but are unable to see the same colour humans can. Primary Qualities are measurable qualities by size, weight, shape etc. and will stay the same regardless of our perception. Secondary Qualities are the hidden powers an object has that can produce in us a sensory experience such as the colour we see in the sky. (Velasquez 333) We can understand his theory on Primary and Secondary Qualities because scientists are able through research to study other living things and their perceptions of senses. Locke’s theories are a clear explanation to the many things we experience as human beings. Descartes was born on March 31st, 1596 in Touraine. After finishing school in 1612, it left him feeling unsettled and dissatisfied. He felt the need to travel, so he could discover new surroundings and he joined the army at the age of seventeen. He was in search of discovering more truth than he had found at school. Descartes lived in a time of great uncertainty as to what truth was, and what it wasn’t. There were new scientific discoveries being made which were unheard of at that time, as well as the new protestant branch of Christianity that went against the old traditional religious beliefs. With everything around Descartes changing, he began to doubt all his prior knowledge (Velasquez 320). Descartes began to search for true knowledge, which was the beginning of Descartes’ first meditation on Doubt. He questioned the idea that we may all be unaware of our state of mind; are we dreaming, or are we awake? Descartes concluded that there are no ways to tell whether or not we are awake or dreaming. So where did this idea come from? He went on to say that there must be something of a higher power deceiving him, an â€Å"evil genius† of deceiving nature creating this illusion for all to get caught up in. Descartes reasoned that, if this were the case, we couldn’t trust our senses at all because our senses are illusions. With this mindset, Descartes believed that the only basic truths are those that cannot be doubted. The undeniable truth he discovered was â€Å"I think, therefore I am† which he reasoned that even if he was being deceived about everything else, he could not be deceived that he was thinking he was deceived, therefore he exists† (Velasquez 321). In order for Descartes to rule out sensory perceptions, he would need to rely on another basis for our knowledge. Based on his inner reflection, he believed that knowledge is not learned, ideas are present i n the mind at birth. â€Å"We have a priori knowledge – we are born with knowledge and truths without the aid of sense perceptions†¦Ã¢â‚¬ (Velasquez 324). Descartes would argue against Locke’s sensory perceptions theory because to Descartes, our senses are invalid. In Descartes† second meditation, he uses an example of a piece of wax to prove our senses wrong. â€Å"Let us take, for example this piece of wax: it has been taken quite freshly from the hive, and it has not yet lost its sweetness of the honey which it contains; it still retains somewhat of the odor of the flowers from which it has been culled; its colour, its figure, its size are apparent; it is hard, cold, easily handled, and if you strike it with a finger, it will emit a sound† (Descartes 190-191). Here Descartes explains, in every respect all physical aspects of the wax that is experienced with our senses. â€Å"But notice that while I speak and approach the fire what remained of the taste is exhaled, the smell evaporated, the colour alters, the figure is destroyed, the size increases, it becomes liquid, it heats, scarcely one can handle it, and when one strikes it, no sound is emitted†¦What then did I know so distinctly of this piece of wax? It could certainly be nothing of all that the senses brought to my notice, since all hese things which fall under taste, smell, sight, touch, and hearing, are found to be changed, and yet the same wax remains†¦ it is mind alone which perceives†¦this piece of wax† (Descartes 190-191). Descartes explains that because the wax can transform, leaving us with different sense perceptions than before, it cannot be trusted as knowledge. Descartes was unable to grasp Locke’s concepts of sensory experiences and therefore rejects everything but the knowledge we are innately born with. Although Descartes gives an adequate theory, his views do not stand up to Locke and other philosopher’s criticisms. To Locke, Descartes’ whole argument on innate knowledge and the ideas behind his meditations are weak, not only invalid because of their opposing views on how humans attain knowledge, but invalid in regards to his reasoning behind his theories. There are many things to point out about Descartes, based on Locke’s ideas. Locke understood the ideas of innate knowledge, but disagreed because he believes we are too much a part of this world to doubt its existence. If innate knowledge were the only true way to have knowledge, people would not be having arguments of what is right and what is wrong. â€Å"[Descartes ideas of doubt are invalid] because there are none to which all mankind give a universal assent† (Uzgalis). Descartes’ explanation of existence of things states that because Descartes can think, and because thinking things exist, Descartes therefore exists. But this argument is invalid because this is the same as saying, â€Å"I am walking, hence I am the walking. The author, William Benton in the book, â€Å"Descartes/Spinoza† objected to Descartes’ second meditation on doubt by saying, â€Å"this is an assumption on Descartes part to say that which one understands is the same exercise of understanding†¦for the entity of understanding itself, is one thing and the essence is another† (Benton 135). This relates back to Descartes invalid argument because Descartes defense can be restated as a cla im that he is thought. One may think, but can never be the â€Å"entity† or the actual action of thinking. All of Descartes meditations on knowledge surround the main idea of innate knowledge and thought, â€Å"but whence comes our knowledge of this proposition, I think? †¦ we cannot think of leaping, apart from that which leaps, of knowing apart from a knower, of thinking without a thinker† (Benton 135). Descartes has no explanations of how we are able to come to thoughts on actions. Actions can relate to the idea of innate knowledge because they both are thought, but are unseen to the senses, at least until the thought or action is indeed physically done. â€Å"But for example, willing fearing and denying always go hand in hand with something physical as the subject of those thoughts, you cannot have the knowledge of what scares you without experiencing it in some way† (Hutchins 138). Locke also expresses his opinion not on emotions that derive from experiences but with the nature of this world. For I imagine any one will easily grant that it would be impertinent to suppose the ideas of colours innate in a creature to whom God hath given sight, and a power to receive them by the eyes from external objects: and no less unreasonable would it be to attribute several truths to the impressions of nature, and innate characters† (Uzgalis). If we know what the term â€Å"colour† means, that is some sort of knowledge, and so we are unable to identify colour unless we use our senses. We cannot believe we know the term colour, without actually experiencing it. Just as the author in the book â€Å"Descartes/Spinoza† explains that one is unable to know what an actual angel looks like, but from our experiences through visual senses, we are able to construct ideas of what one might look like based on our visual surroundings. (Hutchins 136) Now this goes against Descartes ideas of thought and innate knowledge because, â€Å"Notice that in order for Descartes to doubt his beliefs, he needs a language in which to express his doubt. But then, if Descartes were to doubt his beliefs about what words mean, then he could not formulate any doubts at all. He would be totally incapable to express his doubts. Thus the attempt to doubt anything would be necessarily self defeating† (Albert). Descartes’ arguments on doubt are self-defeating because Descartes does not believe anything exists but his mind, ruling out all language and terms used and formulated in this world. The example of wax used by Descartes to validate his view that sensory knowledge is the only knowledge, can be looked at differently to validate sensory experiences. From an empiricist’s point of view, one would indeed gain knowledge by putting the wax near the fire because in doing so, one would understand what happens to wax when it is being scorched. By using the senses to experience the wax in a different form, one is able to reflect and learn from the experiment. Descartes theories have many flaws, therefore making his arguments invalid. Although there are many other rationalists that oppose the views of empiricism, Plato was another great philosopher who developed the very foundations of innate knowledge based on Socrates dialogue with the slave boy. Socrates, being one of the significant founders of western philosophy, along with his student Plato was famous for imposing difficult thought-provoking inquiries to the fellow Athenian citizens. Although Socrates did not record any of his philosophical discussions or inquiries, his student Plato explains to us the works of Socrates. Plato, like Descartes believed that there was only one way to have knowledge. He believed knowledge was not acquired through the use of our senses, but merely obtained before we were born. Plato went farther than Descartes by believing that our souls must have lived in another universe before being born in this one. This other universe would have been perfect where we would have been able to experience perfect objects and were able to experience all that was perfect in the prior universe. The reason we would have innate knowledge would be because when we were born into this imperfect world, according to Plato, all the perfect concepts of the previous world would still be within our souls. â€Å"Most rationalist philosophers have rejected Plato’s claim that before we were born we existed in another perfect universe. But many rationalists have accepted Plato’s more basic insight: we do not acquire the basic truths of math and science by observing the world around us†(Velasquez 326). Although his beliefs about how we attained innate knowledge were not much accepted, he uses a dialogue between Socrates and Meno, the slave boy’s master to explain his beliefs on innate knowledge. â€Å"In Meno, Plato tells us how Socrates once made a slave boy â€Å"remember† his knowledge of geometry by showing him some imperfect figures drawn on the ground. Socrates shows the slave boy a square that is supposed to be two feet by two feet in size. Socrates asks the boy to draw a second square that is exactly twice the size of the first square†¦the boy initially realizes that his first answer is wrong. If you double the length of each side of the square, you will get a new square that is exactly four times as big as the first square. Yet the boy knows this without making exact measurements†¦ and even if the boy had measured the squares, they would probably not have turned out to be exactly the right sizes. So where did this boy’s knowledge come from? (Velasquez 324) In this summary of the dialogue, Plato argues that the boy’s knowledge of the Pythagorean theorem could not have come from observing the imperfect figures drawn on the ground. This proves that it must be knowledge that is already in our minds then, because Plato explains that the knowledge of mathematical theorems are not obtained through sensory experi ences. It is impossible to rely on our senses to give us knowledge of math because there is no physical experience to go hand in hand them. This belief is the total opposite of Locke’s views because Plato denies any thing that relies on the senses. In Plato’s dialogue involving the slave boy, there is some questionable material that can relate back to Locke’s beliefs of relying on our senses. Even though the slave boy was able to answer Socrates’ geometrical question, the dialogue stated that the boy hesitated and also made a mistake before arriving at the correct answer. â€Å"At first the boy says that if you double the length of each side of the first square, you will get a second square that is exactly twice the size of the first square†¦the boy quickly realizes that his first answer is wrong. (Velasquez 324) His knowledge was based on observation not innate knowledge. The boy was able to use his visual perception to determine the measurements of the squares. As Locke would say, â€Å"Reason is our intellect, our power to think and make judgments based on our sensory experience† (Locke 59). It merely takes reason and reflection to first observe the dimensions of square and then come to a re alization about how to double the square. Although he was answering a question, Socrates used an example of an imperfect square and then asked him to solve the question. The answer was discovered through trial and error. It was clearly not based on innate knowledge but visual senses. I agree with Locke’s theory because it is the most reasonable approach to the idea of gaining knowledge. With out sensory perception feeding us, we have nothing to base our knowledge on. We have been born with blank slate, but are still equipped with reason as human beings. One can relate scientific discoveries to sensory perceptions because all scientific knowledge comes from observations. One cannot call something a scientific discovery if it does not have evidence to back up their hypotheses. The evidence used does not come from innate knowledge, but from observation, touching, hearing, smelling, tasting. If, according to Plato and Descartes, basic science and math were innately known, then science would not improve. If science were innate, scientists would not have a job, and everyone wouldn’t be arguing about their beliefs. Science is constantly discovering something new, constantly realizing that something once thought as true, turned out to be false. For example, Einstein’s Theory of Relativity is based on mathematical structures and therefore is valid in the eyes of a rationalist. But if this knowledge were innate it would automatically have to be true. Scientists just recently have discovered subatomic particles that defy the theory of relativity, as these particles move faster than the speed of light. If this is the case, it is impossible to say that innate knowledge is the only truth. The whole world would have to be in agreement and collectively accept things as they are, and the world is nothing like that. We can all agree to this because we have all gained knowledge through the use of our senses. Knowledge itself is something that we as humans are still discovering, questioning and experiencing in our own way. John Locke helps us to see that knowledge is something gained individually, in our own ways, in our own time. We all have something in common and that is our ability to use our senses in such ways that we have been able to create magnificent pieces of art, unravel the mysteries of the universe, invent new and convenient strategies for the human race and so on. All this made possible by the pursuit of knowledge. Works cited Books Hutchins, Robert Maynard// Rene Descartes// Baruch Spinoza. Great Books of the Western World: Descartes Spinoza. Chicago: Encyclopedia Britannica, 1952. Print. Locke, John. An Essay Concerning Human Understanding. Ed. Kenneth Winkler. Hackett Publishing Company, 1996. Velasquez, Manuel. â€Å"Chapter 5: The Source of Knowledge. † Philosophy. 10th ed. Belmont: Thomas Wadsworth, 2008. 320-33. Print. Websites Albert. â€Å"Criticisms to Descartes’ Cogito  « Albert’s PHI101/103 Weblog. Albert’s PHI101/103 Weblog. 1 Apr. 2008. Web. 20 Jan. 2012. http://ajfphi. wordpress. com/2008/04/01/criticisms-to-descartes-cogito/. â€Å"John Locke – Philosopher – Biography. † The European Graduate School – Media and Communication – Graduate Postgraduate Studies Program. 2010. Web. 20 Jan. 2012. http://www. egs. edu/library/john-locke/biography/. Uzgalis, William, â⠂¬Å"John Locke†, The Stanford Encyclopedia of Philosophy (Winter 2010 Edition), Edward N. Zalta  (ed. ), URL = http://plato. stanford. edu/archives/win2010/entries/locke/. How to cite The Validity of Knowledge, Papers

Foundation The Human Services Disciplines â€Myassignmenthelp.Com

Question: Discuss About The Foundation The Human Services Disciplines? Answer: Introduction: The following report intends to review the positioning of a local enterprise in Australia in the sector of health and their functions. The selected organizations for the report include National Rural Health Alliance Inc. and Carers Victoria. The prominent highlights that could be observed in the report refer to the implications of organization description and the underpinning values for the operations for the organizations (Battistoni, 2017). Other prominent dimensions that are addressed in the report also refer to the identification of challenges and risk factors for the organization in the domain of providing healthcare services (Boley, et al., 2014). The concluding section of the report would evaluate the ability of the two organizations to address the future trends that could be anticipated in context of the health sector and the suitable positioning of the organizations in accordance with references to relevant theory and empirical data. Description of organizations: The description of the organizations that are considered for evaluation in this report refer to the observation of their legal structure, nature of organization and the management structures implemented by them. National Rural Health Alliance Inc (NRHA) could be classified as a non-government organization intended for promoting healthcare initiatives in rural and remote areas (Buchbinder, Rivkin-Fish Walker, 2016). The NRHA is formed from the alliance of 37 member bodies which are national organizations comprising of examples such as consumer groups, health professional associations, service providers and representatives from the aboriginal health sector. The organization renders its operations through a comprehensive management structure implying the involvement of council, board and staff in accomplishing the organizations objectives. The structure of NRHAs operations is characterized by the role of The Board in governance. Furthermore, the implications of managing staff in the organization could be accounted as feasible description of the management style of the organization in which the principle responsibility for management is vested in the Chief Executive Officer of the organization (Burger, 2013). The staff of NRHA is facilitated with the opportunities to provide their contributions in terms of progress policy development and preparing discussion papers regarding the collaboration and advocacy implications integral for the alliance. Carers Victoria could be assumed as a non-profit organization inclined to deliver care and support services to individuals suffering from disabilities, chronic condition, terminal illness or elderly individuals. The activities of the organization are coordinated with different government initiatives alongside support from organizations required for improving the lives of families which avail care services across Victoria (Gitlin Lyons, 2013). The organization was established in 1992 and presently the organization has over 5000 members that comprise of carers, support groups, organizations and former carers. The organizations legal typology can be described as a non-profit organization which is dependent on an assorted funding base that is facilitated primarily by the Australian Government and Victorian state government (Lecca, et al., 2014). The organization also obtains substantial support from the government in terms of financial grants through the approaches of supported accommodation and effective consultation. The management structure of the organization is supervised by a board of directors while the workforce is liable to report to the CEO of the agency. Underpinning values: The underpinning values or motivation for the organizations to deliver care services could be identified in context of inferences drawn from the vision statement of the organizations. The primary underpinning value that can be observed in the case of Carers Australia is the vision for an Australia where the activities of carers are valued and supported. The organization recognizes the large scale transformational change in the community sector that is derived from the drastic changes introduced in the contexts of disability, mental health, non-profit sectors and elderly care (Lucas Villegas, 2013). The organizations determination for increase political as well as public awareness pertaining to issues involved in care services is responsible for developing advocacy for personal care services alongside provision of support to carers in order to look after their loved ones. The type of program delivery in the health sector adopted by Carers Victoria could be described through a depiction of essential elements such as geographical areas, client groups and the associated demographic details. The geographical area served by the organization is observed in the state of Victoria (Manlove, et al., 2016). The classification of client groups could be identified among individuals that are afflicted with disabilities, mental illness, elderly individuals and chronic illnesses. The strategic approach followed by Carers Victoria presently is aligned with five basic priorities which help the organization to support the health and wellbeing of service users. The strategic priorities established by the organization refer to the creation of a flexible system for care service providers, facilitating support to care providers and develop their competences for care and development of expert knowledge pertaining to carers and the services included in care and implementing it appropriately (Martin, 2016). The abilities of the organization to improve community awareness and involvement in order to pave amiable paths for care givers to provide services effectively should also be developed as a part of the strategic goals of the organization (Monette, Sullivan DeJong, 2013). The requirement for sustainable growth is ensured by Carers Victoria through acquisition and retention of a competent workforce and the use of contemporary agile systems. The underpinning value that can be identified in context of National Rural Health Alliance Inc. (NRHA) is vested in the vision statement of the organization to establish good health and wellbeing in rural and remote areas of Australia. The program delivery of NRHA is primarily vested for client groups identified in the rural areas of Australia (Neukrug, 2016). The strategic approach followed by NRHA is based on certain specific priorities which could be identified in the implementation of evidence based approaches, improvement of health outcomes for aboriginal communities, acquisition of long term funding that could sustain the core activities of the organization in context of influence, advocacy and policy development as well as reduction of the improving statistics in suicides, mental health and suicide attempts observed in rural and remote areas of Australia. The examples of activities implemented by the organization to deliver its programs in the health sector through a long term rural and remote health plan characterized with performance indicators to observe and report the changes observed in the health sector in rural and remote Australia (Oberle, et al., 2013). Challenges and risk factors: The challenges and risk factors that could influence the operations of Carers Victoria and NRHA could be identified through a detailed analysis of the macro environment for the organizations in the healthcare industry in Australia. The instability in the political framework presents formidable concerns for organizations in the sector of healthcare that can be validated on the grounds of the dependency of healthcare industry on the combined efforts of the state as well as federal governments. The probabilities of conflicts between state and federal government could lead to the concerns of limited accountability of agencies and formidable pressure in terms of cost on the organizations. Political reforms could imply the shifting of cost responsibility to state governments thereby creating disruption in provision of voluntary and non-profit care services (Schoech, et al., 2013). Furthermore, organizations such as NRHA and Carers Australia should anticipate the impact that can be rendered by the introduction of regulatory policies or legislations according to the Commonwealth state agreements on order to address the associated risks effectively (Smith, et al., 2013). The challenges posed for the healthcare industry in Australia from the perspective of economic aspects of the macro environment could be identified in the consistently increasing costs of medical improvements and the concerns for managing the distribution of funds in public and private sector organizations. Another challenging factor that could be perceived in the social aspect of the macro environment for the healthcare industry in Australia could be observed in the concerns of the sector to maintain the health and well being of an ageing population. The major constraint in this case could be identified in the formal restriction of budgets as well as the increasing costs for healthcare services (Summers, 2015). The projected estimates of population in Australia suggest that by 2053, almost 21% of the population would be aged over 65. The demographic variations noted in a specific population alongside the proliferation of new disease patterns with an ageing population alongside the growth in the prominence of chronic diseases. Technological breakthroughs, on the other hand present feasible opportunities in the form of sophisticated diagnostic facilities, resources for care services and management of serious afflictions. However, it is imperative to observe the challenges in context of technology aspect of the macro environment which include cost as well as the integration of technology into the existing infrastructure of care service provision (Woodside McClam, 2014). The impact of healthcare technologies as a burden on the federal budgets could also be accounted as a profound technological risk factor for non-profit organizations associated with the healthcare sector. The legal changes pertaining to operations of non profit organizations in the healthcare sector, the distribution of funding and precedents for employment of care service providers can be assumed as risk factors for the two organizations identified for this report. Environmental changes would have minimal impact on the performance of Carers Victoria and NRHA apart from the effect of global climate change on the national economy thereby causing roadblocks for efficient operations of the healthcare industry. The review of issues from the macro environment of healthcare industry in Australia could also be complemented with an illustration of other probable risk factors for the two organizations such as the issues with supply and distribution of workforce in the healthcare sector that could lead to depreciation in the quality and safety of health services. Predictions and organizational planning: Based on the analysis of the healthcare sector in Australia, certain significant trends could be derived for the future. The primary factors which would be driving change in the future scenarios of the healthcare industry refer to the development of technological advancements in medical devices and related apparatus as well as the ageing population of the country. Furthermore the distribution of healthcare budgets between state and federal governments could lead to formidable challenges for focussing on the specific requirements of population. The ageing population would lead to explicit outcomes in the future such as escalation in the demand for services and utilization of resources (Schoech, et al., 2013). The future predictions in context of the healthcare industry in Australia could also imply a drastic shift towards provision of resources for chronic diseases from the provision of acute care resources which could lead to the proliferation of risk factors especially among younger population and lower socio-economic regions. The implications of cost and restrictions on time would be responsible for the inclination of the propensity of care service providers towards providing care services rather than emphasizing on the risk factors and associated challenges. The complexity of technological advancements integrated in the healthcare sector in Australia could be problematic for care service providers especially in context of managing holistic requirements of the patient alongside maintaining updated knowledge of the distinct specialities (Monette, Sullivan DeJong, 2013). The information asymmetry could lead to prominent issues such as confusion among care service providers for referring to specialists as well as the competence and quality of service facilitated by them. The positioning of the individual organizations for addressing the challenges, risk factors and future trends in the healthcare sector in Australia could be illustrated as follows. NRHA is positioned to accomplish the objective of integrating health sector intelligence for inducing necessary changes and innovation in rural and remote areas of Australia. The emphasis of the organization on the improvement of health outcomes for individuals in the Aboriginal communities could be accounted as strategic positioning that enables the organization to focus on a specific client segment thereby reducing ambiguities in outcomes of programs implemented by NRHA (Gitlin Lyons, 2013). The organization also improvises its process outcomes in terms of information system through ensuring universal access to credible voice and data services. The process outcomes involve references to integration of specialized healthcare services with on-the-ground primary healthcare services. Carers Victoria is strategically positioned to address the future trends in the domain of healthcare in Australia through expanding its support base for carers by improving the revenue base, awareness regarding carers and care services and secured seed funding from the Victorian state government for improving online resources and e-learning platform (Lucas Villegas, 2013). Conclusion: The report presented a reflection on two organizations operating in the healthcare sector in Australia i.e. Carers Victoria and NRHA. The profound highlights of the report could be identified in the description of the organizations and their functioning, types of approach adopted by them for delivering services, potential challenges and risk factors and the strategic planning measures adopted by the organizations to address the predictions regarding future trends in the healthcare industry. References Battistoni, R. M. (2017).Civic engagement across the curriculum: A resource book for service-learning faculty in all disciplines. Stylus Publishing, LLC. Boley, B. B., McGehee, N. G., Perdue, R. R., Long, P. (2014). Empowerment and resident attitudes toward tourism: Strengthening the theoretical foundation through a Weberian lens.Annals of Tourism Research,49, 33-50. Buchbinder, M., Rivkin-Fish, M., Walker, R. L. (Eds.). (2016).Understanding Health Inequalities and Justice: New Conversations Across the Disciplines. UNC Press Books. Burger, W. R. (2013).Human services in contemporary America. Cengage Learning. Gitlin, L. N., Lyons, K. J. (2013).Successful grant writing: Strategies for health and human service professionals. Springer Publishing Company. Lecca, P. J., Quervalu, I., Nunes, J. V., Gonzales, H. F. (2014).Cultural competency in health, social human services: Directions for the 21st century. Routledge. Lucas, T., Villegas, A. M. (2013). Preparing linguistically responsive teachers: Laying the foundation in preservice teacher education.Theory Into Practice,52(2), 98-109. Manlove, K. R., Walker, J. G., Craft, M. E., Huyvaert, K. P., Joseph, M. B., Miller, R. S., ... Cross, P. C. (2016). One Health or Three? Publication Silos Among the One Health Disciplines.PLoS biology,14(4), e1002448. Martin, L. L. (2016).Financial management for human service administrators. Waveland Press. Monette, D. R., Sullivan, T. J., DeJong, C. R. (2013).Applied social research: A tool for the human services. Cengage Learning. Neukrug, E. S. (2016).Theory, practice, and trends in human services: An introduction. Cengage Learning. Oberle, D., Barros, A., Kylau, U., Heinzl, S. (2013). A unified description language for human to automated services.Information systems,38(1), 155-181. Schoech, D., Boyas, J. F., Black, B. M., Elias-Lambert, N. (2013). Gamification for behavior change: Lessons from developing a social, multiuser, web-tablet based prevention game for youths.Journal of Technology in Human Services,31(3), 197-217. Smith, L. M., Case, J. L., Smith, H. M., Harwell, L. C., Summers, J. K. (2013). Relating ecoystem services to domains of human well-being: Foundation for a US index.Ecological Indicators,28, 79-90. Summers, N. (2015).Fundamentals of case management practice: Skills for the human services. Nelson Education. Woodside, M. R., McClam, T. (2014).An introduction to the human services. Cengage Learning Underpinning values: