Anaemia overview and treatment - Free Essay Example

Sample details Pages: 26 Words: 7802 Downloads: 6 Date added: 2017/06/26 Category Statistics Essay Did you like this example? 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. Don’t waste time! Our writers will create an original "Anaemia overview and treatment" essay for you Create order 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, production 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, anaemia of chronic disorders (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 p robably indicate IDA (Chulilla et al., 2009). In macrocytic anaemia, erythrocytes are larger (MCV 98 fL) than their normal volume (MCV = 82-98 fL). Vitamin B12 deficiency leads to delayed DNA synthesis in rapidly growing hematopoietic cells, and can result in macrocytic anemia. Drugs that interfere with nucleic acid metabolism, such as.hydroxyurea increases MCV ( 110 fL) while alcohol induces a moderate macrocytosis (100-110 fL). In the initial stage, most anaemias are normocytic. The causes of normocytic anaemia are nutritional deficiency, renal failure and haemolytic anemia (Tefferi, 2003). The most common normocytic anaemia in adults is anaemia of chronic disease (ACD) (Krantz, 1994). Common childhood normocytic anaemias are, besides iron deficiency anaemia, those due to acute bleeding, sickle cell anemia, red blood cell membrane disorders and current or recent infections especially in the very young (Bessman et al., 1983). Homozygous sickle cell disease is the most common cause of 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 anemia and increase together in macrocytic, hyperchromic anemia. Pathogenic classification of anaemia is based on the production pattern of RBC: whether anaemia is due to inadequate production or loss of erythrocytes caused by bleeding or haemolysis. This approach is useful in those cases where MCV is normal. Pathogenic classification is also essential for proper recognition of the mechanisms involved in the genesis of anaemia. Based on the pathogenic mechanisms, anaemia is further divided into two types namely, (i) hypo-regenerative in which the bone marrow production of erythrocytes is decreased because of impaired function, decreased number of precursor cells, reduced bone marrow infiltration, or lack of nutrients; and (ii) regenerative: when bone marrow upregulates the production of erythrocytes in response to the low erythrocyte mass (Chulilla et al., 2009). This is typified by increased generation of erythropoietin in response to lowered haemoglobin concentration, and also reflects a loss of 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 (Hb S) in which valine is substituted for glutamic acid at the sixth amino acid position in the beta globin gene reduces the solubility of Hb, causing red cells to sickle (Fig. 1). Sickling of cells occurs at first reversibly, then finally as a state of permanent distortion, when cells containing HbS and inadequate amounts of other haemoglobins including foetal haemoglobin, which retards sickling, become deoxygenated (Bunn, 1997). The abnormal red cells break down, leading to anaemia, and clog blood vessels with aggregates, leading to recurrent episodes of severe pain and multiorgan ischaemic damage (Creary et al., 2007). The high levels of inflammatory cytokines in SCD may promote retention of iron by macrophage/reticuloendothelial cells and/or renal cells. SCD care commonly depends on transfusion that results in iron overload (Walter et al., 2009). 3. Pathogenesis of anaemia Anaemia is a symptom , or a syndrome, and not a disease (Chulilla et al., 2009). Several types of anaemia have been recognised, the pathogenesis of each being unique. Iron deficiency anaemia (IDA) is the most common type of anaemia due to nutritional causes encountered worldwide (Killip et al., 2008). Iron is one of the essential micronutrients required for normal erythropoietic function While the causes of iron deficiency vary significantly depending on chronological age and gender, IDA can reduce work capacity in adults (Haas Brownlie, 2001) and affect motor and mental development in children (Halterman et al., 2001). The metabolism of iron is uniquely controlled by absorption rather than excretion (Siah et al., 2006). Iron absorption typically occurring in the duodenum accounts for only 5 to 10 per cent of the amount ingested in homoeostatis. The value decreases further under conditions of iron overload, and increases up to fivefold under conditions of iron depletion (Killip et al., 2008). Iron is ingested as haem iron (10%) present in meat, and as non-haem ionic form iron (90%) found in plant and dairy products. In the absence of a regulated excretion of iron through the liver or kidneys, the only way iron is lost from the body is through bleeding and sloughing of cells. Thus, men and non-menstruating women lose about 1 mg of iron per day while menstruating women could normally lose up to 1.025 mg of iron per day (Killip et al., 2008). The requirements for erythropoiesis   which are typically 20-30 mg/day   are dependent on the internal turnover of iron (Munoz et al., 2009) For example, the amount of iron required for daily production of 300 billion RBCs (20-30 mg) is provided mostly by recycling iron by macrophages (Andrews, 1999). Iron deficiency occurs when the metabolic demand for iron exceeds the amount available for absorption through consumption. Deficiency of nutritional intake of iron is important, while abnormal iron absorption due to hereditary or acquired iron-refractory iron deficiency anemia (IRIDA) is another important cause of unexplained iron deficiency. However, IDA is commonly attributed to blood loss e.g., physiological losses in women of reproductive age. It might also represent occult bleeding from the gastrointestinal (GI) tract generally indicative of malignancy (Hershko and Skikne, 2009). Iron absorption and loss play an important role in the pathogenesis and management of IDA. Human iron disorders are necessarily disorders of iron balance or iron distribution. Iron homeostasis involves accurate control of intestinal iron absorption, efficient utilisation of iron for erythropoiesis, proper recycling of iron from senescent erythrocytes, and regulated storage of iron by hepatocytes and macrophages (Andrews, 2008). Iron deficiency is largely acquired, resulting from blood loss (e.g., from intestinal parasitosis), from inadequate dietary iron intake, or both. Infections, for example, with H pylori, can lead to profound iron deficiency anemia without significant bleeding. Genetic defects can cause iron deficiency anaemia. Mutations in the genes encoding DMT1 (SLC11A2) and glutaredoxin 5 (GLRX5) lead to autosomal recessive hypochromic, microcytic anaemia (Mims et al., 2005). Transferrin is a protein that keeps iron nonreactive in the circulation, and delivers iron to cells possessing specific transferrin receptors such as TFR1 which is found in largest amounts on erythroid precursors. Mutations in the TF gene leading to deficiency of serum transferrin causes disruption in the transfer of iron to erythroid precursors thereby producing an enormous increase in intestinal iron absorption and consequent tissue iron deposition (Beutler et al., 2000). Quigley et al. (2004) found a haem exporter, FLVCR, which appears to be necessary for normal erythroid development. Inactivation of FLVCR gene after birth in mice led to severe macrocytic anaemia, indicating haem export to be important for normal erythropoiesis. The anaemia of chronic disease (ACD) found in patients with chronic infectious, inflammatory, and neoplastic disorders is the second most frequently encountered anaemia after iron-deficiency anaemia. It is most often a normochromic, normocytic anaemia that is primarily caused by an inadequate production of red cells, with low reticulocyte production (Krantz, 1994). The pathogenesis of ACD is unequivocally linked to increased production of the cytokines including tumour necrosis factor, interleukin-1, and the interferons that mediate the immune or inflammatory response. The various processes leading to the development of ACD such as reduced life span of red cells, diminished erythropoietin effect on anaemia, insufficient erythroid colony formation in response to erythropoietin, and impaired bioavailability of reticuloendothelial iron stores appear to be caused by inflammatory cytokines (Means, 1996;2003). Although iron metabolism is 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).   Sickle cell disease (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 activated which, in turn, activate endothelial cells and cause vascular inflammation. The vaso-occlusive processes in SCD involve inflammatory and adhesion molecules such as the cell adhesion molecules (CAM family), which play a role in the firm adhesion of reticulocytes and leukocytes to endothelial cells, and the selectins, which play a role in leukocyte and platelet rolling on the vascular wall (Connes et al., 2008). Thus, inflammation, leucocyte adhesion to vascular endothelium, and subsequent endothelial injury are other crucial factors contributing to the pathogenesis of SCD (Jison et al., 2004). 4. Current therapies for clinical management of sickle cell diseaseincludingacritical appraisal of transfusion Between 1973 and 2003, the average life expectancy of a patient with SCD increased dramatically from a mere 14 years to 50 years thanks to the development of comprehensive care models and painstaking research efforts in both basic sciences especially molecular and genetic studies, and clinical aspects of SCD (Claster and Vichinsky, 2003). The clinical manifestations of SCD are highly variable. Both the phenotypic expression and intensity of the syndrome are vastly different among patients and also vary longitudinally within the same patient (Ballas, 1998). New pathophysiological insights available have enabled treatments to be developed for the recognised haematologic and nonhaematologic abnormalities in SCD (Claster and Vichinsky, 2003). The main goals of SCD treatment are symptom alleviation, crises avoidance and effective management of disease complications. The strategy adopted is primarily palliative in nature, and consists of supportive, symptomatic and preventative approaches to therapy. Symptomatic management includes pain mitigation, management of vasoocclusive crisis, improving chronic haemolytic anaemia, treatment of organ failure associated with the disease, and detection and treatment of pulmonary hypertension (Distenfeld and Woermann, 2009). The preventative strategies include use of prophylactic antibiotics (e.g., penicillin) in children, prophylactic blood transfusion for prevention of stroke in patients especially young children who are at a very high risk of stroke, and treatment with hydroxyurea of patients experiencing frequent acute painful episodes (Ballas, 2002). Currently, curative therapy for sickle cell anaemia is only available through bone marrow and stem cell transplantation. Hematopoietic cell transplantation using stem cells from a matched sibling donor has yielded excellent results in paediatric patients (Krishnamurti, 2007). Curative gene therapy is still at the exploratory stage (Ballas, 2002). Current and potential therapies The potential treatment strategies basically target cellular dehydration, sickle haemoglobin concentrations, endothelial dysfunction, and abnormal coagulation regulation (Claster and Vichinsky, 2003). HbS concentrations are essentially tackled through transfusions while approaches to reduce HbS polymerisation which is the main mechanism for the development of vaso-occlusion include (a) increasing foetal haemoglobin (HbF) concentration using hydroxyurea (Fig. 2), butyrate, or erythropoietin, and (b) preventing sickle cell dehydration using Clotrimazole (Fig. 3) or Mg2+pidolate. Hydroxyurea therapy increases the production of HbF in patients with sickle cell anaemia, and, thereby, inhibits the polymerisation of HbS and alleviates both the haemolytic and vaso-occlusive manifestations of the disease (Goldberg et al., 1990). Recombinant erythropoietin also increases the number of reticulocytes with HbF. Additionally, it has been observed that administration of intravenous recombinant eryt hropoietin with iron supplementation alternating with hydroxyurea enhances HbF levels more than hydroxyurea alone (Rodgers et al., 1993). As SCD is essentially characterized by an abnormal state of endothelial cell activation   that is, a state of inflammation, a pharmacologic approach to inhibit endothelial cell activation has proved clinically beneficial (Hebbel and Vercellotti, 1997). Thus, administration of sulfasalazine which is a powerful inhibitor of activation of nuclear factor (NF)-B, the transcription factor promoting expression of genes for a number of pro-adhesive and procoagulant molecules on endothelium to humans has been found to provide transcriptional regulation of SCD at the endothelium level (Solovey et al., 2001). Red blood cell transfusion : a critical appraisal A key therapy that is applied regularly in the clinical management of patients with SCD is packed red blood cell transfusion. RBC transfusion improves the oxygen-carrying capacity which is achieved by enhancing the haemoglobin levels, causes dilution of HbS concentration thereby, reducing blood viscosity and boosting oxygen saturation. Furthermore, RBC transfusion is helpful in suppressing endogenous production of sickle RBCs by augmenting tissue oxygenation ( Josephson et al., 2007). There are two major types of RBC transfusion therapy: intermittent and chronic which are further classified as prophylactic or therapeutic. Intermittent transfusions are generally therapeutic in nature and administered to control acute manifestations of SCD whereas chronic transfusions are performed as general preventative measures to check complications of SCD. RBC transfusion given as a single dose is termed as simple transfusion. Exchange transfusion involves administration of a larger volume of RBCs replacing the patients RBCs that are simultaneously removed. Details of the various types of RBC transfusion and the major clinical indications for the same in SCD patients are listed in Table 1. SCD (Source: Josephson et al., 2007) Indications for Intermittent transfusions Indications for intermittent transfusions include acute manifestations of SCD, as indicated in Table 1, that require redressal through therapeutic transfusions. However, under certain circumstances intermittent transfusions could be prophylactic such as for instance, when SCD patients are transfused before specific surgeries viz., those related to pregnancy complications or renal failure (Table 1). Acute Chest Syndrome (ACS) describes a manifestation of SCD in which, due to sickling, infectious and noninfectious pulmonary events are complicated, resulting in a more severe clinical course. The diagnosis is the presence of a new infiltrate on chest radiography that is accompanied by acute respiratory symptoms. ACD accounts for nearly 25% of all deaths from SCD (Vichinsky, 2002). Repeated episodes of ACS are associated with an increased risk of chronic lung disease and pulmonary hypertension (Castro, 1996). The severe pulmonary events occurring in SCD may be precipitated by any trigger of hypoxia (Vichinsky, 2002). Transfusions are very efficacious and provide immediate benefit by reversing hypoxia in ACS. Transfusion of leucocyte-poor packed red cells matched for Rh, C, E, and Kell antigens can curtail antibody formation to below 1% (Vichinsky, 2002). Simple transfusions suffice for less severe cases; however, exchange transfusion is 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). Indications for Chronic Transfusions Prophylactic chronic RBC transfusion every 3 to 4 weeks to maintain HbS levels lower than 30% is crucial for preventing first as well as recurrent strokes in children (Johnson et al., 2007). The transfusions could either be chronic simple transfusion or prophylactic chronic RBC exchange transfusion. Prophylactic chronic transfusions are recommended for patients with chronic renal failure so as to avoid severe symptomatic anaemia and for those patients with SCD undergoing pregnancy with complications. However, prophylactic transfusion is not indicated for SCD patients with normal pregnancy (Tuck et al., 1987). Controversial and indeterminate indications for intermittent or chronic transfusion According to Hankins et al. (2005), chronic transfusion therapy is helpful in reducing the incidence of strokes in children but not the severity of strokes. In the case of acute priapism, improvement in patients has been observed after exchange or simple transfusion (Rifikind   et al., 1979). Yet, due to the ASPEN syndrome, transfusion currently is only a second-line therapy in the management of priapism ( Miller et al., 1995). RBC transfusion is a vital component in the management of symptoms and complications of SCD. It has drastically reduced the morbidity and mortality of SCD. Yet, immune-related effects such as FNHTRs and alloimmunisation to HLAs,   and nonimmune-related effects e.g., iron overload and transfusion-transmitted infections are serious adverse effects of the transfusion therapy that need to be attended to in SCD patients receiving transfusion (Johnson et al., 2007). Chronic transfusions could result in an inexorable accumulation of tissue iron that could become fatal if not treated (Cohen, 1987). Excess iron damages the liver, endocrine organs, and heart and may be fatal by adolescence (Engle, 1964). 5. Critical review of thalassemias : (i) Molecular pathogenesis The large number of inherited haemoglobin disorders known today include (a) those related to anomalies in the haemoglobin structure e.g., sickle cell disease, and (b) the thalassemias whose hallmark is globin-chain deficiency of one or other of the globin chains of adult haemoglobin in erythroid cells. 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). (Source: Weatherall, 1997b) 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). 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 antigens (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. Emerging Gene 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). Chemical inducers of foetal haemoglobin 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 (HDAC) inhibitors, DNA-binding drugs and inhibitors of the 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. Erythropoietin suppression of apoptosis 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. 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. Cases with severe complications such as stroke, acute chest syndrome or frequent painful sickling crises are treated with hydroxyurea. Intermittent red cell transfusion is administered to most patients, pre-surgery and in specific cases of severe complications. The only cure available currently for ÃŽÂ ²-thalassaemia major is afforded by 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) 14- 39. Adams R, McKie V, Brambilla D, et al., 1998, Stroke prevention trial in sickle cell anaemia, Control Clin Trials 19:110- 129. Andrews NC, 1999, Disorders of iron metabolism, N Engl J Med, 341:1986-1995. Andrews NC, 2008, Forging a field: the golden age of iron biology, Blood, 112(2): 219-230. Anstey NM, Russel B, Yeo TW et al., 2009, The pathophysiology of vivax malaria, Trends Parasitol., 25(5):220-227. Aul C, Bowen DT Yoshida Y, 1998, Pathogenesis, etiology, and epidemiology of myelodysplastic syndromes, Haematologica, 83(1): 71-86. Ballas SK, 1998, Sickle cell disease: clinical management, Baillieres Clinical   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Haematology, 11 (1): 185-214. Ballas SK, 2002, Sickle cell anaemia: progress in pathogenesis and treatment, Drugs, 62(8):1143-1172. Bertero MT Caligaris-Cappio F, 1997, Anemia of chronic disorders in systemic autoimmune disease, Haematologica, 82(3):375-81. Bessman JD, Gilmer PR Gardner FH, 1983, Improved classification of anemias by MCV and RDW, Am J Clin Pathol 80:322-326. Beutler E, Gelbart T, Lee P, et al., 2000, Molecular characterisation of a case of Atransferrinemia, Blood, 96:4071-4074. Beutler E Waalen J, 2006, The definition of anemia: what is the lower limit of normal of the blood hemoglobin concentration?, Blood, 107(5): 1747-1750. Bottomley SS, 2006, Congenital sideroblastic anemias, Curr Hematol Rep., 5(1):41-49. Bunn HF, 1997, Pathogenesis and treatment of sickle cell disease, N Engl J   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Med.337(11):762-769. Castro O, 1996, Systemic fat embolism and pulmonary hypertension in sickle cell Disease, Hematol Oncol Clin North Am. 10(6):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, 96:3624-3629 Chulilla JAM, ColÃÆ' ¡s MSR MartÃÆ' ­n MG, 2009, Classification of anemia for gastroenterologists, World J Gastroenterol. 15(37): 4627-4637. Claster S and Vichinsky, EP, 2003, Managing sickle cell disease, BMJ,327:1151- 1155. Cohen AR, 1987, Management of iron overload in the paediatric patient, Haematol Oncol Clin North Am., 521-544. Connes P, Hue O, Tripette J et al., 2008, Blood rheology abnormalities and vascular cell adhesion mechanisms in sickle cell trait carriers during exercise, Clinical Hemorheology Microcirculation, 39(1-4): 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 DC, 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 MA, Erlandson M Smith CH, 1964, Late cardiac complications of chronic, severe, refractory anaemia with haemochromatosis, Circulation, 30:698-705. Fleming MD. 2002. The genetics of inherited sideroblastic anemias, Semin Hematol.    39:270-281. Gambari R, 2010, Foetal haemoglobin inducers and thalassaemia: novel achievements, Blood Transfus. 8(1): 5-7. Gambari R Fibach E, 2007, Medicinal chemistry of foetal haemoglobin inducers for treatment of beta-thalassaemia, Curr Med Chem.14:199-212. Gaziev J, Sodani P Lucarelli C, 2008, Haematopoietic stem cell transplantation in thalassaemia, Bone Marrow Transplantation, 42, S41. Gilman JG Huisman THJ, 1985, A sequence variation associated with elevated foetal GÃŽÂ ³globin production. Blood 66:783-787. Gladwin MT Kato GJ, 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 MA, Brugnara C, Dover GJ et al., 1990, Treatment of sickle cell anaemia with Hydroxyurea and erythropoietin, NEJM, 323(6): 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 JS, Kaczorowski JM, Aligne CA et al., 2001, Iron deficiency and cognitive achievement among school-aged children and adolescents in the United States, Pediatrics, 107: 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. Krishnamurtià ¢Ã¢â€š ¬Ã…’ L, 2007, Hematopoietic cell transplantation for sickle cell disease: state of 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 erythropoietin therapy in a transfusion-dependent ÃŽÂ ²-thalassaemia major patient, 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 suppress expression of the iron regulatory protein hepcidin, Nature 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.

Charlotte Brontes Jane Eyre Jane Eyres Artwork Essay

Jane Eyres Artwork Each picture told a story; mysterious often to my undeveloped understanding and imperfect feelings, yet ever profoundly interesting. --Jane Eyre (9) There is something extraordinary and spiritual about Jane Eyres artwork. In her story, Janes solitary pastime sometimes operates as an outlet of past or present pain, and often offers her a chance to deal with unpleasant memories and emotions. Janes art transcends her isolation by bringing her into contact with others who see it; it serves as a bridge over the chasm between her desire to be alone and her need for companionship, which is demonstrated by key scenes in the novel that include a viewing of her art. This struggle between isolation†¦show more content†¦Fairfaxs verbal description (169). She claims that it is madness in all women to let a secret love kindle within them, and resolves to reject imagination and resign herself to reason; at that point, she decides that she could never be the object of Mr. Rochesters affections (168-9). Jane treats herself as her own pupil, and criticizes herself for abandoning sense and resolution and vows to have them for the moment, a fter which she falls asleep easily (170). This scene is curiously like the first time Jane resolves to produce art while a young girl at Lowood, except the focus of that former moment was strictly on the imagination, where Jane was content to imagine the spectacle of my ideal drawings, after which she also fell contentedly asleep (78). Because Jane does not want to abandon sense and reason, her portraits at this point are based on reality; she uses Mrs. Fairfaxs descriptions in conjunction with socially constructed native theories of the time to develop what she thinks Blanche Ingram should look like. In other words, one of the biggest conventions of this novel regarding Victorian women is brought out in the moment Jane paints this portrait?conventional views of how they should look, and, in reality, what Jane is not. She is not allowing herself to have dreams of a better life with Rochester, much like St. John not able to bring himself toShow MoreRelatedPainting Analysis in Jane Ey re3436 Words   |  14 PagesDrawing a Breath of Fresh Eyre From the opening chapter of Charlotte Brontà «Ã¢â‚¬â„¢s Jane Eyre the reader becomes aware of the powerful role that art plays. There is something extraordinary about the pictures Jane admires from other artists, as well as the work she creates herself. Her solitary pastime often operates as an outlet of pain, either past or present, and offers her the opportunity to deal with unpleasant emotions and memories. Jane’s art transcends her isolation by bringing her into contact

Symbols in Their Eyes Were Watching God Free Essays

Symbols in Their Eyes Were Watching God In Zora Neale Hurston’s Their Eyes Were Watching God, many different symbols are used to express Janie’s longing for love and acceptance. Each symbol is related to the condition of Janie’s life at that time. Janie is very beautiful and innocent to the ways of men and sexuality. We will write a custom essay sample on Symbols in Their Eyes Were Watching God or any similar topic only for you Order Now Janie has her first sexual feelings one afternoon beneath a pear tree. She sees a â€Å"bee sinking into the sanctum of a bloom; the thousand sister calyxes arch to meet the love embrace (Hurston 11)† and she comments on how happy the tree must be to have such a feeling. Janie believes she is privy to a â€Å"revelation (Hurston 11)† and she thinks â€Å"So this [is] a marriage (Hurston 11)! † The pear tree and the bee working together in harmony represent new love and desire for Janie. She realizes she has neither in her life but she thinks about the possibilities for the future and she â€Å"[feels] a pain remorseless sweet that [leaves] limp and languid (Hurston 11). † Janie has been sheltered her whole life and is seeking to feel some of what she saw with the pear tree and the bee. She asks herself â€Å"where are the singing bees for [me] (Hurston 11)? Not being able to come up with an answer Janie goes to the â€Å"front gate†¦ waiting for the world to be made (Hurston 11). † Janie sees Johnny Taylor and desire from what she sees wells up in her and she kisses him over the gate. The inside of the gate for Janie represents restriction and separation. Janie’s first kiss is with Johnny in the confines of he r yard. Janie’s grandmother, Nanny, sees the kiss and forces Janie to marry Logan Killicks. The gate also represents seeking for Janie. After her marriage fails, Janie â€Å"begins to stand by the gate and expect things (Hurston 25). It is at this gate that she meets Joe â€Å"Jody† Stark. Janie leaves â€Å"out of the front gate and turned south (Hurston 32)† as she leaves Logan for Joe â€Å"the change was bound to do her good (Hurston 32). † Janie marries Joe Stark and he becomes the mayor of Eatonville. Joe has a very different idea of life for Janie. He wants her to sit and be proper, to be seen and not heard. Janie becomes a clerk in his store. The town gathers on the porch of the store and Janie listens but does not join in the conversations. She is required to be inside working. The porch represents xclusion for Janie and community for everyone else. Janie realizes that â€Å"the wife of the mayor was not just another woman†¦she couldn†™t get but so close to most of them in spirit (Hurston 46). † On this porch an unusual thing happens. One of the townsmen’s mule( Matt Bonner’s mule) was getting old and Matt did not treat him very well. He did not feed the mule often. The mule got loose and the townspeople caught up to him and were â€Å"goosing him in the sides (Hurston 56)† for fun. Janie got upset at the little â€Å"regard for helpless things (Hurston 57),† that the towns people were showing. Mayor Stark saw this and bought the mule so he could rest. The mule in the story represents Janie. Although the mule was old, tired, and a source for ridicule among the town the horse still had a â€Å"more spirit left than body (Hurston 56). † After Mayor Stark dies, Janie sees life brand new. She starts to dress differently. She wears her hair free. She socializes with the town. Janie also falls in love again. She meets a younger man named Vergible Woods known as â€Å"Tea Cake. † Tea Cake represents inclusion, the unknown, and unconditional love for Janie. Janie was now socializing with the town but she still was not included. Tea Cake asks her to play checkers and she is so excited. â€Å"Somebody thought it natural for her to play. [That] was even nice (Hurston 96). † She even compares him to her longing. She thinks that he â€Å"could be a bee to her blossom —- a pear tree blossom in the spring (Hurston 106). † Janie goes on to marry Tea Cake and they have some bumps along their road but Janie ultimately finds what she was searching for under the pear tree. How to cite Symbols in Their Eyes Were Watching God, Papers

Digital Communication in Organizations-Free-Samples for Students

Question: Discuss about the Digital Communication in Organizations. Answer: Introduction Communication is a process that helps to transfer information and knowledge as well as it helps to build up understanding between two or more peoples. The organization is a place where a different type of people work together and it is essential for an organization to use proper communication strategy so that stable and healthy relationships among the employees can be visualized. Communication strategies have changed day by day and in the present digital era, digital communication is one of the best ways to communicate in an organization. This paper provides detail information about digital communication along with the Australian culture and use of digital communication in Australia. This paper also discusses in detail digital communication strategy, implementation of digital communication as well as advantages and disadvantages of using digital communication in an organization. Main Context Digital Communication Communication is an essential part of management function that helps employees and organization to be in a healthy relationship. Communication is carried out in many forms, like verbal communication, written communication, gesture communication and so on. In the present day where technologies have advanced very much, organizations also have started to use digital communication (Lapidoth, 2017). This digital communication is a process of transferring message and information with the help of technology and electronic devices. The most important part of this communication is Internet, websites, email, video meeting and all sorts of things that are used to exchange information by electronic machines. In previous years people used letters, phones as well as personal meeting to communicate but in present day with the changing world where people are mostly involved in social media and the internet is the best way to use digital communication in organizations (Duck, and McMahan, 2017). Digit al communication involves the process of instant messaging by the internet, group messaging, chatrooms, social media, internal blog, etc. This also plays an important role for a business as this help to communicate locally as well as overseas also. The uses of the internet, virtual meeting, video conferencing, email, etc all provide a vast network to communicate anyplace in the world (Viterbi, and Omura, 2013). This is the future of an organization and this help organization to develop as people are able to communicate effortlessly with each other throughout the world. Australian Culture Australia is a society of multi cultural where one can get Muslim, Buddhist, and Christians. Australian communicates in a very color full way and in the workplace they call each other by their names rather by greeting them as sir or madam. Australian like to communicate in the most straightforward way and for that their business meeting also did not continue for a prolonged time (Jensen, 2013). With the help of digital communication in their organization, they are able to perform more effectively than before. They like to work in a group and that is the reason they formed organization group while working and involves every employee in this group. This helps them to communicate with each other in a most effective way. Australian is very much intended to improve their production and motivate their employees so they use an innovative form of communication strategy which helps them to motivate their employees. A healthy communication is very much important to keep healthy relationships w ith employees and Australians are very much positive toward this type of communications (Cornelissen, and Cornelissen, 2017). Digital Communication Strategy to improve workplace Digital communication strategy or communication strategy in an organization is very helpful to motivate their employees, evaluate a working situation and make a proper plan for using digital strategy (Leonardi, 2013). This strategy actually helps employees to get connected with the organization and deliver their thoughts along with their issues directly to the organization. Different organizations from a different type of communication strategy and this are done after evaluating organization internal condition. Communication always helps to bind people together and allow working smoothly in a group. Some strategies that the organization can use are; using social media in an organization to communicate with employees, then forming organization group and performing instant message or group message, then by internal blogs of organization and much more. The organization has to select their strategy in such a way that this helps them to improve their productivity along with their organiza tion bond (Koles, and Nagy, 2014). Sometimes it is best for an organization to form organization group like the manager's group, then the entire managers have their own group with their team members and so on with the discussion forum as well as chatrooms in an organization. This helps to connect everyone directly with an organization and whatever issue they are facing or any message is directly sent to the group members (Beal, and Flynn, 2015). This strategy is best to implement in a workplace to improve productivity, motivate employees along with that improve communication in an organization. Implementing Digital Communication in the Workplace To implement digital communication in a workplace it is important that organization should use the internet (Colbert, 2016). For digital communication, the internet is most essential part as this help to communicate locally as well as overseas also. In implementing group messaging or instant messaging help employees to directly communicate with their boss or managers. In this type of group message, people are not allowed to message individually and this reduce negative and grouping mentality in a workplace, as everyone has to text in the official group and if anyone is having any type of issue then that will also be discussed in an official group message. Along with this group messaging, an organization can implement the process of video conferencing and online task. This will help to communicate with other organization of different country and also will enhance chances of performing a task at home for employees. |With the help of digital communication, all the employees will be to stay connected with organization every time rather they are in an organization or not. Implementing this type of communication in an organization is very helpful for every individual employee along with the organization (Georgakopoulou, and Spilioti, 2015). If employees are satisfied and motivated to upgrade their performance then the organization will also upgrade to one level. In the present day of the digital era, this communication system is a lifeline for an organization. This type of communication will also help to deliver work on time as well as deliver any information to the right person without any intermediate. For example; if a manager of a company wants to provide some news they do not need to say that to their department managers rather they have the ability to directly send a message to the entire employees of an organization. This is the power of digital communication in an organization. Advantages Disadvantages of Digital Communication Instant Messaging Advantages: This help to see a presence of official colleagues' for any instant situation help. This allows seeking help immediately from team members. Disadvantages: Most of the time people ignore busy notice for which they ping as well as disturbed others. People have to use there do not disturb option so that no one is able to message them. Email Advantages: This provides help to send message or files or task to one another or in a group. This can be operated from PC, Laptop or smartphones (Skovholt, 2014). Disadvantages: Maximum numbers of people use email if it is not necessary also. This is not an easy communication process as people have to wait a long time for a reply. Phone Advantages: This help to communicate verbally with anyone around the world. This provides help for employees to express their feelings and communicate easily with others. Disadvantages: Sometimes if the person is not available then leaving message is the last option for employees which is not actually a quick resolution for any problem. Sometimes the place is so noisy that making a call is the biggest challenge for the employees. Group Messaging Advantages: All the colleagues are able to communicate at a time, and if anyone wants to share some information they no need to message everyone differently. Helps to increase the bond between employees and enhance their performance to work in a group. Disadvantages: Sometimes it becomes difficult to share crucial information on group message. It is a time killing process as everyone will be texting and no one has time to read the entire message in the group. Video Conferencing Advantages: This allows person to communicate with each other visually without traveling. This enables to see the facial expression as well as people's reaction over the computer through the internet (Akaiwa, 2015). Disadvantages: This is a complicated process at some time as people feel awkward to communicate with this type of process. Conclusion Digital communications have many advantages as well as disadvantages also but this is considered as one of the best ways to communicate. This paper concludes that digital communication help to communicate within the least period of time and also this allows people to communicate anywhere in the world without traveling. This help to motivate employees and improve working condition of the firm as with these employees are able to connect directly with their managers and higher authorities in the organizations. Reference List Akaiwa, Y., 2015.Introduction to digital mobile communication. John Wiley Sons. Retrieved from: https://books.google.co.in/books?hl=enlr=id=y3xXCQAAQBAJoi=fndpg=PA543dq=Advantages+%26+Disadvantages+of+Digital+Communicationots=dxM0rSWz1nsig=JqUVCoW0tRdrXOunI3UBp1K3RLg#v=onepageqf=false https://muse.jhu.edu/article/665692/summary Beal, C.D., and Flynn, J., 2015. Toward the digital water age: Survey and case studies of Australian water utility smart-metering programs. Utilities Policy,32, pp.29-37. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://www.sciencedirect.com/science/article/pii/S0957178714000976 Colbert, A., Yee, N., and George, G., 2016. The digital workforce and the workplace of the future. Academy of Management Journal,59(3), pp.731-739. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://amj.aom.org/content/59/3/731.extract Cornelissen, J. and Cornelissen, J.P., 2017.Corporate communication: A guide to theory and practice. Sage. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://books.google.co.in/books?hl=enlr=id=Ju60DQAAQBAJoi=fndpg=PP1dq=digital+communication+in+organisationsots=eVfJ0iWd7Osig=atdKuQ0q2E2Hy0u13ZZHAEKQGC0#v=onepageq=digital%20communication%20in%20organisationsf=false Duck, S. and McMahan, D.T., 2017.Communication in Everyday Life: The Basic Course Edition with Public Speaking. SAGE Publications. Retrieved from: https://books.google.co.in/books?hl=enlr=id=StyqDQAAQBAJoi=fndpg=PP1dq=Advantages+%26+Disadvantages+of+Digital+Communication+in+the+workplaceots=MFFo4DVYevsig=NECpvKORbnVhg0A-OQuH7DZmLJg#v=onepageq=Advantages%20%26%20Disadvantages%20of%20Digital%20Communication%20in%20the%20workplacef=false https://muse.jhu.edu/article/665692/summary Georgakopoulou, A. and Spilioti, T. eds., 2015.The Routledge handbook of language and digital communication. Routledge. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://books.google.co.in/books?hl=enlr=id=ofMsCgAAQBAJoi=fndpg=PP1dq=digital+communication+in+the+workplaceots=XObJBbsD6Esig=6n74IwqksFBuVV8bNBn-DVuC8Do#v=onepageq=digital%20communication%20in%20the%20workplacef=false Jensen, K.B. ed., 2013.A handbook of media and communication research: Qualitative and quantitative methodologies. Routledge. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://books.google.co.in/books?hl=enlr=id=uQLgCgAAQBAJoi=fndpg=PP1dq=digital+communication+in+organisationsots=SjJ_1auXhMsig=86ZzLrdI0edi62dDLvUEHGNxgaA#v=onepageqf=false Koles, B. and Nagy, P., 2014. Virtual worlds as digital workplaces: Conceptualizing the affordances of virtual worlds to expand the social and professional spheres in organizations.Organizational Psychology Review,4(2), pp.175-195. Retrieved from: https://journals.sagepub.com/doi/abs/10.1177/2041386613507074 https://muse.jhu.edu/article/665692/summary Lapidoth, A., 2017.A foundation in digital communication. Cambridge University Press. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://books.google.co.in/books?hl=enlr=id=6oTuDQAAQBAJoi=fndpg=PR16dq=Digital+communicationots=i-PLh7G7GUsig=P7H9vBkx03JrKQaekKUDZROa_SQ#v=onepageq=Digital%20communicationf=false Leonardi, P.M., Huysman, M. and Steinfield, C., 2013. Enterprise social media: Definition, history, and prospects for the study of social technologies in organizations.Journal of Computer?Mediated Communication,19(1), pp.1-19. Retrieved from:https://muse.jhu.edu/article/665692/summaryhttps://onlinelibrary.wiley.com/doi/10.1111/jcc4.12029/full Skovholt, K., Grnning, A., and Kankaanranta, A., 2014. The Communicative Functions of Emoticons in Workplace E?Mails::?.Journal of Computer?Mediated Communication,19(4), pp.780-797. Retrieved from: https://onlinelibrary.wiley.com/doi/10.1111/jcc4.12063/full https://muse.jhu.edu/article/665692/summary Viterbi, A.J., and Omura, J.K., 2013. Principles of digital communication and coding. Courier Corporation. Retrieved from:https://books.google.co.in/books?hl=enlr=id=oGbDAgAAQBAJoi=fndpg=PP1dq=Digital+communicationots=hKu3mNXNFXsig=gMDZg86VHxHmow96YXhGOV4K3XI#v=onepageq=Digital%20communicationf=false https://muse.jhu.edu/article/665692/summary

One Love free essay sample

As he approaches me, he cheerfully greets me saying â€Å"Hey, how are you?†, and warmly shakes my hand. A bit unsure of my new surroundings, I give a shy response with a timid handshake. He asks, â€Å"Would you come this way please?† I slowly stand up and he leads me out of the waiting room and we start walking through a maze of hallways. There are classrooms on both sides of me. Finally, we reach his room and step inside. I look around and see a drum set, a marimba, and two drum thrones that are facing each other. The room seems small, and I wonder how all of this equipment is able to fit inside such a tiny room. On the walls, I see posters with pictures of famous musicians, most of whom have gone before us. Because of my uneasiness about this unfamiliar place, I was a bit doubtful about taking drum lessons here. We will write a custom essay sample on One Love or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page Little did I know that this classroom in Meridian Music Studios in Carmel, Indiana, would serve as a place that holds some of my life’s greatest experiences. It is a place where I learned much more than just the art of music. To me, a hero is someone that a person looks up to and has a lot of respect for. It is someone that has made a profound impact on another’s life, and does so much without expecting repayment. Walking down the street, one might think that Wade Parish is just another â€Å"average joe†. He doesn’t have a superman cape or a jet pack. Standing at six feet tall, with broad shoulders, any other person would think he’s another ordinary guy going to work. Dressed in dark blue jeans and a sweater or jacket, he looks like another ordinary person. However, his long dark hair as well as his artsy yet contemporary style of clothing accurately expresses his independent outlooks on life. Wade forms his own views on life and refuses to conform to others’ beliefs. He carries on this independency in his music as well. â€Å"The silent space that we instill in music is sometimes more powerful than the music itself† He would often tell me this to relay the mess age that music is not about how fast you can play. Instead, it is about the emotions that musicians express to the audience. The musical creativity that Wade expresses is just as admirable as his overall non-conforming attitude toward today’s society. One of Wade’s favorite quotes is â€Å"Carpe Diem†. I see him live by this quote each and every day. He knows that every day is his, and sees that each day is an opportunity to do something worthwhile. He knows that the days that he has are limited, so he chooses to live each one to the fullest. In our interview, he explains to me that many people are driven by materialistic things such as money, cars, and success. The most important thing in one’s life is doing what you love. â€Å"Do what you love and you will never work a day in your life†. Another admirable trait that Wade possesses is the passion that he has for music. Wade has always told his students, to follow their dreams and do what is most important to them. He too follows this philosophy. Wade first moved out of his parents’ house when he was 18 and had taken ordinary jobs such as a waiter and a landscaper. However, he soon came to be unhappy with these jobs because they interfered with the schedule that he had with his band. If his employers refused to give him time off to play at shows, he would easily quit the position he held. Wade started to play the drums when he was 14. Even though he was a poor academic student, he worked hard in the field of music. For someone to love a hobby so much that they would quit their job just to pursue it is a truly courageous action. He would also reduce the amount of time that he spent with other hobbies, such as motorcycle racing, so he would be able to play more music. Wade would look hypocritical if he told his s tudents to follow their dreams when he himself did not do that. This is what makes him most respectable. Not only did he take a risk financially, but he followed his dream which makes him one of the most successful people I know. The final trait that I really admire in Wade is the sense of love that he shows everyone. When teaching, he never gives up on his students. Even if they themselves give up, he still sees the talent that they have and tries to get them to see it too. One time, while I was in a lesson, I was being a little too hard on myself. I had had a rough day and I was expecting to be perfect. The more I played, the more I became upset. Finally, Wade told me to stop and we would play something else. So, he went over to his stereo and turned on â€Å"One Love† by Bob Marley. That’s when he told me to drum to that song. I drummed to that song for 20 minutes and afterward I felt very relaxed. That’s when he explained that I am not a bad drummer. I was actually his only student that could do that. I had a lot more confidence after that because what he said about my great skills meant a lot. â€Å"I believe that everyone wants to be loved, but they show this desire in warped ways.† When he told me this, it really showed me that there is no such thing as purely evil people. We all need each other when we are hurt, and some people just don’t know how to ask for support. Whether we choose to see it or not, there will always be at least one person that unexpectedly walks into our lives and makes a profound impact that we are most certainly not expecting. For me, that person was Wade. I can only hope that everyone will come to see the values that others unconsciously instill in us, and hopefully cherish them. Above all else, Wade taught me to follow my dreams and do exactly what I love. After I met Wade, I realized life is wasted when one does not do what they love. â€Å"Do what you love and you’ll never work a day in your life†.

SAT Syllabus What’s on the Exam and How to Prep

SAT Syllabus What’s on the Exam and How to Prep SAT / ACT Prep Online Guides and Tips Are you taking the SAT soon but aren’t sure what to expect?Not to worry! This guide will give you an in-depth look at the SAT syllabus and what to expect on the exam. For each section of the SAT, I’ll explain the format of the section, thetypes of questions you’ll see, and the skills it tests.At the end of this guide, I'll also go over the top tips you need to know when preparing for the SAT to help you achieve your highest score. Overview of the SAT Before we start looking in-depth at the SAT syllabus, let’s first get a broad overview of what the SAT covers.There are three main sections on the SAT: Reading, Writing and Language, and Math. There is also an optional essay. More information about each section is available in the chart below. Section Minutes Given Number of Questions Reading 65 52 Writing and Language 35 44 Math 80 58 Essay (Optional) 50 1 Total 3 hours, 50 minutes (3 hours without the essay) 154 (+1 essay prompt) The SAT sections will always go in this order, beginning with Reading and ending with (if you choose to take it), the SAT Essay.The Math section is divided into two groups, the first where you can’t use a calculator (25 minutes and 20 questions), and the second, where a calculator is allowed (55 minutes and 38 questions). Below, for each section of the SAT, I’ll explain what subjects it covers. SAT Reading Number of Questions Minutes Given Time Per Question 65 52 75 seconds Format The SAT Reading section consists of passages with 52 multiple-choice questions. In this section, there will be four individual passages and one passage pair, which means there will be about 10-12 questions for each passage/passage pair.At least one of the passages will have graphics, such as tables, graphs, and charts accompanying it.Each passage, or passage pair set, will be at about 500 to 750 words. There will be at least one passage from each of the following topics: U.S. or world literature U.S. founding document or a text inspired by one Social science (such as economics, psychology, sociology, etc.) Science (Earth science, biology, chemistry, or physics) Types of Questions All questions on SAT Reading are multiple choice with four answer choices. There areeight main different questions types you may see in this section. Big Picture/Main Idea These questions ask about the overall purpose of the passage, such as what is the passage about, what is it trying to accomplish, or what the point of it is. The main purpose of each passage is to A) compare brain function in those who play games on the Internet and those who browse on it. B) report on the problem-solving skills of individuals with varying levels of Internet experience. C) take a position on increasing financial support for studies related to technology and intelligence. D) make an argument about the effects of electronic media use on the brain. Little Picture/Detail This type of question will usually refer to a specific line or phrase within a passage and ask you about a specific detail, such as what a particular phrase means or why the author chose to mention something. In the context of the passage, the author’s use of the phrase â€Å"her light step flying to keep time with his long stride† (line 3) is primarily meant to convey the idea that A)Ethan and Mattie share a powerful enthusiasm.B) Mattie strives to match the speed at which Ethan works.C)Mattie and Ethan playfully compete with each other.D)Ethan walks at a pace that frustrates Mattie. Inference Inference questions will ask you to deduce the meaning of a line or phrase from the passage or the entire passage itself. Even though you’ll have to do some interpretation on these questions, they all have to have one objectively correct answer with evidence in the passage you can use to support your choice. The passage most strongly suggests that Adelita used which of the following to navigate her 9,000-mile journey? A)The current of the North Atlantic gyre.B) Cues from electromagnetic coils designed by Putman and Lohmann.C) The inclination and intensity of Earth's magnetic field.D)A simulated "magnetic signature" configured by Lohmann. Vocabulary in Context For these questions, you’ll be asked to define a specific word in the question. Be careful, because sometimes common words are used in unusual ways and you have to correctly identify the definition used in the passage. As used in line 38, â€Å"intense† most nearly means A) emotional.B)concentrated.C) brilliant.D) determined. Function Function questions refer to how a phrase or sentence works within a passage and what effect it has on the passage. The analogy in the final sentence of Passage 2 has primarily which effect? A) It uses ornate language to illustrate a difficult concept. B) It employs humor to soften a severe opinion of human behavior. C) It alludes to the past to evoke a nostalgic response. D) It criticizes the view of a particular group. Author Technique The questions will ask you to analyze the author’s tone, style, perspective and/or attitude. For paired passages, you may have to compare author techniques between the two passages. During the course of the first paragraph, the narrator’s focus shifts from A) recollection of past confidence to acknowledgment of present self-doubt. B) reflection on his expectations of life as a tradesman to his desire for another job. C) generalization about job dissatisfaction to the specifics of his own situation. D) evaluation of factors making him unhappy to identification of alternatives. Evidence Support Evidence support questions refer back to a previous question and ask you to provide evidence for your answer. For example, if you were asked an author technique question, after it there may be an evidence support question asking you to identify which lines in the passage support your answer to the author technique question. 1. The description in the first paragraph indicates that what Ethan values most about Mattie is her A)fitness for farm labor.B)vivacious youth.C) receptive nature. D) freedom from worry. 2. Which choice provides the best evidence for the answer to the previous question? A) Lines 1-4(â€Å"Mattie... farm†) B) Lines 4-8 (â€Å"He had... anyhow†) C) Lines 8-10 (â€Å"But it... hearth†) D) Lines 11-13 (â€Å"She had... will†) Data Interpretation These questions refer to the diagrams, charts or graphs included with some of the passages. You’ll have to analyze the information the graphics present. 1. How does the graph support the author’s point that internal waves affect ocean water dynamics? A) It demonstrates that wave movement forces warmer water down to depths that typically are colder. B) It reveals the degree to which an internal wave affects the density of deep layers of cold water. C) It illustrates the change in surface temperature that takes place during an isolated series of deep waves. D) It shows that multiple waves rising near the surface of the ocean disrupt the flow of normal tides. Skills Tested There are three main skills tested in SAT Reading, all of which relate back to critical reading skills. Command of Evidence Being able to find evidence in a passage to support the answer to a question, understand how authors support their claims, and interpret diagrams. Words in Context Using clues from the passage to identify the meaning of a particular word and understanding how the word’s the author chooses affects tone, style, and meaning. Analysis in History/Social Science and Science Being able to examine hypotheses, interpret data, consider implications in passages that cover the subjects of history, social studies, and science. SAT Writing and Language Number of Questions Minutes Given Time Per Question 44 35 48 seconds Format Like the Reading section, all questions in the SAT Writing and Language are based on passages. This section contains four passages with 11 questions following each passage. Passages will cover either Careers, Social Studies, Humanities, or Science. Careers passages could discuss trends or debates in major professional fields, such as medicine, technology, or business. Social studies passages might focus on topics from history, anthropology, psychology, political science, or sociology. Humanities passages could feature an author or explore trends in literature, drama, art, music, or dance. Science passages will focus on Earth science, biology, chemistry, or physics. There is no fiction writingin this section, instead, passages will either be argument-based, explanatory, or nonfiction narrative, and at least one passage will be accompanied by a chart, graph, or table.For SAT Writing and Language, each of the passages will be filled with punctuation, word choice, sentence structure, and organization errors. Your job will be to identify and correct those errors in the questions. Types of Questions Like SAT Reading, all questions on SAT Writing and Language are multiple choice with four answer choices. Questions in this section will ask you about four main ideas.About 24 questions will focus on Command of Evidence, Words in Context, and Expression of Ideas, and about 20 questions will be on Standard English Conventions. Command of Evidence You’ll be asked to improve how the passages develop and present ideas and information to the reader. For example, when reading a passage you should understand how an argument could be strengthened or a detail added to improve clarity. Words in Context For some questions, you’ll need to improve the word choice used in the passage in order to improve tone, style, and/or clarity. Expression of Ideas You’ll need to be able to understand how a passage is structured and the point it is trying to make. Questions testing this skill may ask you to analyze how the passage’s message or organization could be improved. Standard English Conventions These questions test your grammar skills, such as sentence structure, usage, punctuation, verb tense, parallel construction, subject-verb agreement, and comma use. Skills Tested Sixteenmain skills are tested on this section, focusing on focusing on the development and organization of ideas and effective language use as well as grammar rules. Agreement Concision Conventional expression Logical sequence Modifiers Parallel Structure Possessives Precision Pronouns Punctuation Sentence function Sentence structure Style and tone Syntax Transition Verb Tense SAT MATH Number of Questions Minutes Given Time Per Question No Calculator 25 20 75 seconds Calculator 55 38 77 seconds Format SAT Math is divided into two sections, depending on whether or not a calculator is allowed. During the first section, when you cannot use a calculator, you’ll have 25 minutes to answer 15 multiple-choice questions and 5 grid-in questions. For the second section, when you can use a calculator, you’ll have 55 minutes to answer 30 multiple-choice questions and 8 grid-ins, including an Extended Thinking problem. Types of Questions Multiple Choice The majority of questions on SAT Math will be your standard multiple-choice questions where you’re presented with a problem and have to choose the best answer from four answer choices. Aaron is staying at a hotel that charges $99.95 per night plus tax for a room. A tax of 8% is applied to the room rate, and an additional onetime untaxed fee of $5.00 is charged by the hotel. Which of the following represents Aaron’s total charge, in dollars, for staying x nights? A)(99.5 + 0.08x) + 5B)1.08(99.5x) + 5C) 1.08(99.5x + 5)D)1.08(99.5 + 5)x Grid In On SAT Math, 22% of questions will be grid-ins. On these questions, instead of choosing the correct answer from a list of options, you’ll have to solve the problem and enter your own answer on the grid provided in the answer sheet. Ifwhat is one possible value of Extended Thinking A few of your questions will be part of an Extended Thinking problem. The Extended Thinking problem will appear as part of the grid-ins, typically near the end of the section. You’ll see a graph, table, or word problem and have to answer several questions about it. Extended Thinking questions often focus on real-world situations. An international bank issues its Traveler credit cards worldwide. When a customer makes a purchase using a Traveler card in a currency different from the customer’s home currency, the bank converts the purchase price at the daily foreign exchange rate and then charges a 4% fee on the converted cost. Sara lives in the United States, but is on vacation in India. She used her Traveler card for a purchase that cost 602 rupees (Indian currency). The bank posted a charge of $9.88 to her account that included the 4% fee. 1. What foreign exchange rate, in Indian rupees per one U.S. dollar, did thebank use for Sara’s charge? Round your answer to the nearest whole number. 2.A bank in India sells a prepaid credit card worth 7,500 rupees. Sara canbuy the prepaid card using dollars at the daily exchange rate with no fee,but she will lose any money left unspent on the prepaid card. What is theleast number of the 7,500 rupees on the prepaid card Sara must spendfor the prepaid card to be cheaper than charging all her purchases onthe Traveler card? Round your answer to the nearest whole number ofrupees. Skills Tested SAT Math covers 24 main topics, within four main subject areas. Over half of the questions will be on algebra, while a maximum of 10% of the questions will focus on Additional Topics such as geometry and trigonometry. Basic Algebra Linear functions Single variable equations Systems of linear equations Absolute value Advanced Algebra Manipulating polynomials Quadratic equations Dividing polynomials Exponential functions Function notation Solving exponential equations Systems of equations with nonlinear equations Problem Solving and Data Analysis Ratios and proportions Scatterplots and graphs Categorical data and probabilities Experimental interpretation Median, median, mode, standard deviation Additional Topics Coordinate geometry - lines and slopes Coordinate geometry - nonlinear functions Geometry - circles Geometry - lines and angles Geometry - solid geometry Geometry - triangles and polygons Trigonometry Complex numbers SAT Essay Number of Questions Minutes Given Time Per Question 1 essay 50 50 minutes Format The SAT Essay is the only optional section of the exam. If you decide to take it, you’ll have 50 minutes to plan and write one complete essay. Types of Questions You’ll be given a passage by an author who has taken a stance on a particular issue, and you’ll need to analyze how the author builds her argument, what the strengths and weaknesses of the argument are, and how the argument could be improved. You won’t be taking your own stance on the issue. Skills Tested The major skill you are graded on for the essay is your ability to analyze an argument and understand how evidence and rhetorical devices contribute to an argument.While you’ll want your essay to be clear and easy to understand, a few minor spelling and grammar errors won’t lose you points, so you don’t have to worry about your essay being technically perfect. How to Use ThisSAT Syllabus Now you're an expert on the SAT syllabus, but how does this information help you? First, knowing what's on the SAT will make you feel more comfortable on exam day. You'll know the format, content, and types of questions you'll be asked. This can help you feel more prepared and help reduce test anxiety. Second, understanding the SAT syllabus can significantly help withyour SAT studying. When you know what subjects are tested on the SAT, you'll know what to focus on during your preparation, and you're less likely to skip material you should know or study material that won't be on the test. Additionally, when you take practice tests and are looking to see where you got most of your answers wrong, you can easily pinpoint which area(s) you should work on. Maybe your SAT Math score was lower than you wanted it to be, but where exactly were you making mistakes? Did you get all the algebra questions correct but struggled with geometry? Then you can focus primarily on studying geometry questions. Knowing what's tested on the SAT will help you pinpoint the areas where you need to improve and increase the effectiveness of your studying. How to Prepare for the SAT Knowing the SAT syllabuswill help you become more comfortable and familiar with the exam, which will likely help your score. Follow these three additional tips to be sure you’re getting the most out of your SAT prep. Create a Study Plan Before you begin in-depth preparation for the SAT, you’ll want to create a study plan.A study schedule can help you know when you’re supposed to be studying and can keep you on track.Setting aside a regular time to study each day or week, such as weekdays from 8:00-9:30 or Sundays from 12:00-4:00, will make it easier to study because you’ll know ahead of time when you should be studying and can fit the rest of your schedule around it. You should include regular goals in your study schedule that you hope to meet, such as, â€Å"I want to understand how to answer geometry questions by the end of the weekend,† or â€Å"I want to raise my math score ten points by the end of the month.†Setting these goals can help encourage you to study and ensure you are on track to meet your goal scores. Use High-Quality Study Materials Your studying is only going to be as effective as the prep materials you use, so be sure to use the right materials for you.A high-quality prep book can be one of the best resources you use. Check out some of the best SAT prep books here. A good prep book will effectively explain the content tested on the exam, have high-quality practice questions similar to those on the real SAT, and include full-length practice exams (discussed more below). Take Complete Practice Exams During your studying, you’ll want to take at least one (and ideally at least threeto four) complete practice SATs.Taking complete practice SATs is important because it gives you the most realistic idea of what the real SAT will be like. You’ll learn how taking a test for several hours affects you and if you get tired and distracted towards the later sections. Also, after you score your exam, you’ll have a good idea of how well you’d do on the actual SAT, and you can use this information to identify which areas you should focus on for future studying. Be sure to take your SAT under realistic testing conditions. That means take the test all in one sitting, timed, and with minimal distractions.Try to use official practice tests since they’ll be the closest to the real SAT. We have links to several free and official SAT practice tests you can use. Conclusion Knowing the SAT syllabuswill help you know what to expect for the test and how to prepare.Each of the three main sections of the SAT covers multiple subject areas and contains several question types. There is also an optional essay at the end of the test. To prepare for the SAT, be sure to create a study plan early on, use high-quality study materials, and take full-length practice tests to get a good idea of the progress you’ve made. What's Next? Wondering what a good SAT score is? Learn how to set a score goal based on the schools you want to get into. Thinking about using Khan Academy for SAT prep?Khan Academy can be a great resource if you know how to use it correctly. Read our guide to learn how to make the best use of Khan Academy! Want to learn more about the new SAT? We have a complete guide to the revised SATthat goes over exactly what changed, what stayed the same, and how it affects you. Want to improve your SAT score by 160 points?We have the industry's leading SAT prep program. Built by Harvard grads and SAT full scorers, the program learns your strengths and weaknesses through advanced statistics, then customizes your prep program to you so you get the most effective prep possible. Check out our 5-day free trial today: