Accounting and Financial Reporting of Wesfarmers and Woolworths

Question: Talk about the Financial Reporting of Wesfarmers and Woolworths. Answer: Presentation Wesfarmers Built up in 1914 as Western Australian Farmers agreeable, they have reached to discover its place among the greatest recorded organizations in Australia. Their assorted business incorporate the departmental stores, markets, manures and vitality, security items, home enhancements and office supplies. The principle goals of the organization are to give the good come back to their investors. They intend to accomplish this goal through: Satisfying the prerequisites of the clients by offering types of assistance and merchandise on proficient and serious premise. Conveying safe workplace for the representatives with great prizes for execution and open door for additional enhancements. Offering significance to the assurance of condition in which they work Working with uprightness and genuineness while managing outside just as inside the organization. Their authoritative structure uncovers that they have 94 officials and 9 auxiliaries named as Bunnings, Coles Group, Target Australia, Wesfarmer synthetic substances (Kleenheat and CSBP), officeworks, Wesfarmers assets and Wesfarmers Industrial and Safety. During 2016, they have accomplished the accompanying things: They decreased the recurrence pace of absolute recordable injury by 15.2% They attempted to advance the decent variety in the work environment and more than 3300 representatives were perceived as indigenous They improved the straightforwardness under the review program for more than 3200 manufacturing plants under the gracefully chain They had the option to decrease the green house gas emanations by over 2% during the most recent year (Wesfarmers.com.au 2017). Woolworths On 22nd February 1878, first store of Woolworth was set up by Frank Winfield as Woolworths incredible five penny store. They are perhaps the greatest store among Australia and records for 80% of the piece of the pie of Australia. Among the different items they manage, the beverage business incorporates BWS and Dan Murphys primary goal is to convey the accommodation and best an incentive to their clients. They are better known for selling the staple things. Be that as it may, they additionally manage deals of DVDs, magazines, fixed things and at present having in excess of 1000 stores in Australia itself. Their fundamental point is to turn into the most ideal brand for the clients and to accomplish that they have the underneath referenced procedures: Building a tem and store-drove culture for the clients Making the economical energy for deals of nourishments Turning into the lean retailer by framework greatness and start to finish methodology Engaging the portfolio business to build the investors worth Build up their beverage business to convey accommodation and incentive to the clients. Their hierarchical structure uncovers that they have 77 officials and 5 auxiliaries named as Big W, Progressive undertaking, EziBuy, Dan Murphys and Endeavor Drinks. Among others, hardly any outstanding accomplishments by Woolworth are as per the following: They were the first to build up the arrangement of best previously and sell by through furnishing their clients with the sign of the likely time at which the great gulp be reached to them They were the first to accomplish the natural development of the business crop cotton. They were the first to expel however much additives and added substances as could reasonably be expected from the nourishments they manage (Woolworths Online 2017). Distinguishing proof and assessment of financing sources Capital Structure: Wesfarmers Liabilities Sum Sum Current liabilities Exchange and different payables $ 6,491.00 Enthusiasm bearing advances and borrowings $ 1,632.00 Annual assessment payable $ 29.00 Arrangements $ 1,861.00 Subordinates $ 160.00 Other $ 251.00 Absolute current liabilities $ 10,424.00 Non-current liabilities Enthusiasm bearing advances and borrowings $ 5,871.00 Arrangements $ 1,554.00 Subordinates $ 81.00 Other $ 104.00 Absolute non-current liabilities $ 7,610.00 Absolute liabilities $ 18,034.00 Values Sum Sum Given capital $21,937.00 Saved offers $ - 28.00 Held profit $ 874.00 Stores $ 166.00 Absolute values $ 22,949.00 Capital structure Measure of absolute capital $ 40,983.00 Measure of obligation $ 18,034.00 Sum if value $ 22,949.00 Obligation parcel (%) 44% Value parcel 56% From the above table it tends to be recognized that the measure of capital for Wesfarmers worth $ 40,983 million. Out of the absolute capital, $ 18,034 that is 44% has been raised through obligation and $22,949 that is 56% has been raised through value. Further, the influence proportion of the organization that is, (Total obligation/absolute resources) = ($22,949/$40,983) = 44%. It expresses that for each dollar of the benefit of the organization, it needs to raise $0.44 of obligation (Wesfarmers.com.au 2017). Examination of obligation The obligation of the organization is commonly brought up in name of Wesfarmers and is related with corporate assurance. In the event that the obligation is legitimately raised by the joint endeavor or auxiliary, at that point that will have a different course of action for security. The offices related with the bank obligation reserves are exposed to the edge furthest reaches of premium inclusion proportion and least influence. Typically the made sure about obligation can't be in excess of a particular % of absolute resources. Nonetheless, the set % can surpass in some particular cases like procurement (Wesfarmers.com.au 2017). Investigation of value The common portions of Wesfarmers are completely paid and don't have any standard worth. Each offer conveys one democratic vote and is qualified for get profits. The offers don't convey any conditions or uncommon terms that can influence the capital privileges or the salary of the organization and are essentially ordered under value. The saved offers are the common offers that were repurchased by the organization and are held with the end goal of future use. Woolworths Liabilities Sum Sum Current liabilities Exchange and different payables $ 6,266.10 Borrowings $ 490.70 Current assessment payable $ 39.50 Arrangements $ 1,873.50 Liabilities related with resources held available to be purchased $ 202.60 Other monetary liabilities $ 120.30 Complete current liabilities $ 8,992.70 Non-current liabilities Borrowings $ 3,870.90 Arrangements $ 1,382.40 Other $ 294.50 Other monetary liabilities $ 179.80 Complete non-current liabilities $ 5,727.60 Complete liabilities $ 14,720.30 Values Sum Sum Given capital $ 5,347.00 Saved offers $ - 94.80 Held profit $ 3,124.50 Stores $ 93.90 Complete values $ 8,470.60 Capital structure Measure of all out capital $ 23,190.90 Measure of obligation $ 14,720.30 Sum if value $ 8,470.60 Obligation divide (%) 63% Value divide 37% From the above table it very well may be recognized that the measure of capital for Woolworth worth $ 23,190 million. Out of the complete capital, $ 14,720 that is 63% has been raised through obligation and $8,470 that is 37% has been raised through value. Further, the influence proportion of the organization that is, (Total obligation/complete resources) = ($14,720/$23,502.20) = 63%. It expresses that for each dollar of the benefit of the organization, it needs to raise $0.63 of obligation (Woolworths Online 2017). Investigation of obligation The budgetary courses of action are made through the bank advance and the organization can draw the advance whenever with the related loaning understandings. Further, the bank overdraft offices can be drawn whenever. The borrowings of the organization are at first perceived at the reasonable worth less inferable value-based expenses. Subsequently, the borrowings are perceived and recorded at amortized cost. The distinction between recovery worth and cost are perceived under the united articulation for benefit and misfortune during the time of getting. Investigation of value Holders of the conventional offers are empower to get the profits and are qualified for one decision in favor of each offer at the gathering of the investors. In the event of wrapping up the standard investors will stand simply after satisfaction of duty of the loan bosses and every other investor and are entitled for the returns from the liquidation (Woolworths Online 2017). Proportion examination Proportion examination Proportion Recipe Wesfarmers Woolworths Sum Result Sum Result Liquidity and effectiveness Current proportion Current resources 9,684 0.93 7427.00 0.83 Current liabilities 10,424 8992.70 Records receivable turnover Net deals 65,981 27.89 58275.50 70.68 Normal records receivable 2,366 824.55 Productivity Profit for resource proportion Net gain 407 1.00 - 1234.80 - 5.25 All out resources 40,783 23502.20 Profit for deals Net gain 407 0.62 - 1234.80 - 2.12 Deals 65,981 58275.50 Dissolvability Obligation rati

Diversity in AT&T telecommunication company Essay

Assorted variety in AT&T media transmission organization - Essay Example The statement of purpose for AT and T is to interface individuals with their globe, everywhere and show improvement over some other organization. The organization is satisfying the above vision by thinking of new answers for organizations and shoppers, and through driving innovation in the diversion and correspondence industry. Considering this viewpoint, this paper basically looks at decent variety in AT&T Telecommunication Company in the U.S from a wide perspective. Comprehensively, the paper presents a SWOT examination, suggestions, and indeces for the organization. Decent variety in AT&T Telecommunication Company in the U.S AT and T is a media transmission organization that has been in the telecom business for quite a few years. Being a piece of the capital escalated business, AT and T’s residential condition has been great as far as stock and turnover. The triumphant lawful and administrative result saw the consummation of syndication in American communication in the year 1968. AT and T submitted different recommendations including an application for minimal effort instructive TV station (Campbell 28). This application was intended to appear AT and T as the adaptable organization to open interests than some other firm in the business. The FCC controlling on AT and T demand occurred on 14 August 1969 where AT and T was authorized to work. State that the administration guideline was not the explanation regarding why the organization confronted chapter 11. Inside administration was flawed that saw the organization confronted with numerous monetary outrages and the chapter 11. The administration guideline of 1968 was agreeable to AT and T Communications and has been instrumental in forming the household condition the organization works in for quite a while (Brooks 41). The Federal Communications Commission (FCC) set up strong laws, which saw AT and T utilize the chance to develop its piece of the overall industry and extend its client base all a round. With the expectation of supporting the development, AT and T Corporation imbued enormous capitals into its business. AT and T required noteworthy measures of money to back its arrangements of expanding and keeping up its household piece of the overall industry (Borkowski 64). The company’s development plan was a figure from $890 million of every 1984 to $2.76 billion out of 1987. To back its estimates, AT and T started by selling $481 million in like manner stock in 1984 a similar way it had done previously. The offer cost was $47 per share, and AT and T expected to gain by the high incentive at that point. From 1985 to 1989, AT and T sold convertible debentures. Another desire for the organization at the time was to accomplish a piece of the pie of 20% by 1990. The organization understood that to accomplish this it required financing of between $890 million out of 1984 to $2.76 billion by 1987. AT and T money inflows at the time were lacking to help its household cond ition plans. The organization was to raise the funds through different methods (Lawrence 15). This is the place it picked to sell $481 million in value in 1984, and a short time later gave convertible debentures up until 1989 to coordinate its extension plans. Giving those debentures permitted AT and T to change over them into stock giving AT and T an influence to raise more obligation. Thinking about research, AT and T is encountering a serious worldwide condition as new contenders are battling for piece of the overall industry in a venture concentrated business. With the expanded

How to Get Leadership Experience in Your Extracurriculars

Step by step instructions to Get Leadership Experience in Your Extracurriculars SAT/ACT Prep Online Guides and Tips Extracurriculars are a huge piece of your school application, and simply taking an interest in an extracurricular isn't sufficient. Universities don’t need members. Schools need pioneers. On the off chance that you need to stick out, it’s not sufficientto be the leader of a club. Universities need pioneers who takeinitiative and get their objectives achieved. How might you become an effective innovator in your extracurricular? What are acceptable initiative exercises for high schoolers? In this article, I’ll control you through the entire procedure of turning into a fruitful pioneer: from choosing where to center your endeavors to actualizing your arrangement to depicting your accomplishments on a school application. Why Is Leadership Experience Important? Demonstratingleadership is one of the most significant pieces of your school application. It's nearly required to get into a top school, and having incredible administration experience can help make up for another region of your application that isn't exactly as solid as you'd like it to be.Admissions officials like to see understudies take control in their secondary school extracurricular exercises and hotshot their authority abilities. For what reason do confirmations officials care about initiative? Universities trust that the candidates they concede will proceed to be pioneers on their grounds and pioneers out in the world.Colleges need their alumnito have a critical and advantageous effect on the world.Admissions officials utilize your secondary school extracurricular exercises as an approach to pass judgment on the off chance that you have the intrigue and capacity to be a pioneer. What do schools search for in administration experience? As I said previously, essentially having an administration title in one of your extracurriculars isn't sufficient (most high-achievinghigh school understudies have a position of authority in an extracurricular), you should be a pioneer who has an effect. What Is Impact? Effect is having a genuine effect: driving your club to raise $5,000 for bosom malignant growth inquire about, directing your group as commander to the national title, driving your club to gather 1,000 jars of nourishment to give to your neighborhood nourishment back, and so forth. When all is said in done, your effect ought to be quantifiable by a number sum (for example $1,000 raised or 500 understudies went to the occasion) or by meeting a major objective (for example getting to the state or national degree of rivalry). You ought to have the option to state, Under my authority, the understudy board raised $5,000 to make prom free for all understudies or Under my initiative, our math group went from not making the local rivalry to winning the state title. It's imperative to show impactbecause, as I referenced above, most high-accomplishing secondary school understudies will have some position of authority on their application. Relatively few understudies will have made a genuine impact.Impact is hard to accomplish, however I will control you through the procedure in the means beneath. You need to stand apart from different candidates! What Are Ivy League Schools Looking For? On the off chance that you’re planning to go to an Ivy League school, I suggest that you tryto get administration involvement with your primary region of intrigue. What do I mean by that?The Ivy League no longer needs balanced understudies (who do changed exercises, for example, tennis, show, understudy government, and chipping in at a creature cover). By taking an interest in such a wide scope of exercises, incredibly, specific schools (the Ivy League and Stanford) may consider your to be roundedness as an absence of core interest. The Ivy League schools need experts.They need understudies who spend significant time in one general area.For model, if your enthusiasm is dramatization, you should join the show club, do provincial theater, contend in the dramatization classifications with your discourse and discussion group, compose a unique play, as well as volunteer with a children’s theatergroup.Specializing in one zone doesn’t mean just doing one action. In the event that dramatization is your center, don’t simply be an inert individual from your show club. You have to accomplish more than that to intrigue the Ivy League. As I said above, you have to have an effect. Whatever one thing you decide to be a specialist in,I prescribe you likewise attempt to turn into a leaderin that field.If you’re a number 1 positioned tennis player, consider attempting to run for group chief at your school,founding a club to show youngsters how to play tennis, and facilitating a tennis rivalry to fund-raise for bosom cancer.If you’re a mathlete, consider running for a mathlete board position, holding a Pi day pledge drive for a noble cause where you sell pies, and beginning a club to assist understudies with their math schoolwork. Regardless of whether you’re wanting to go to an Ivy League school, you should even now attempt to showleadership and have an effect in your extracurriculars. In the event that you’re not gunning for the Ivy League, you don’t need to stress over concentrating on one zone of expertise.However, you despite everything need administration experience on the grounds that it’s amazing to all universities, and, as I said previously, it can assist you with getting acknowledged or compensate for another territory of your application on the off chance that it isn't exactly as solid as you'd like it to be. What direction do you go to get initiative experience? By what means Can You GetLeadership Experience? On the off chance that universities need to see significant authority experience, you should attempt to get it! Buthow would you be able to turn into a leader?Your originally thought may be to consider customary secondary school authority activitiessuch as being on understudy gathering. Understudy chamber isn't really the best authority experience for all applicants.There are numerous different approaches to showleadership. Beneath, I give you my main four choices: Alternative #1: Become a Board Member, Club President, or Team Captain You can become club president or group commander by getting the hang of whatever the fundamental club movement is, developing associations with partners or other club individuals, and accomplishing more work than is simply required. Show that you're willing to accomplish more work than anticipated by offering to help with the occasions (come early, help with set up/sorting out, help with tidy up, and so forth.). Don’t hope to become club president promptly as a freshman.I prescribe you attempt to stir your way up to turning into a top head in the club. Start in a littler position, for example, secretary or treasurer your rookie or sophomore year, and afterward climb to VP and afterward to president. All during this time you should make associations with colleagues or club individuals and showyou're willing to buckle down. That was my technique to turn into my high school’s understudy government president, and it worked! Choice #2: Starta New Club in Your Area of Interest Prior to establishing another club, conceptualize what you'd need that club to be, concoct thoughts for what the club's motivation would b,e andtalk to individuals with comparative interests to check whether they'd be keen on the club. For more data, read about how to begin a club in high schooland look at our rundown of clubs to begin in secondary school. On the off chance that you’re anxious or uncertain about beginning another club, consider first attempting to design another occasion or venture for a current club.For model, if a math club exists, consider arranging an occasion at which the math club offers free coaching to different understudies battling with math.If your arranged occasion works out positively, you’ll feel significantly more certain and prepared to begin your own club. Choice #3: Lead a Project in Your Area of Interest Prior to driving a task, you should support a present club or noble cause plan an occasion or host a pledge drive. That way you can figure out how to compose an effective occasion or pledge drive. You'll perceive how that individual did it, get counsel, and perceive how fruitful they are. Converse with colleagues about what sort of pledge drive they'd appreciate, and check whether any cohorts would be keen on helping you. Alternative #4: Increase Participation inan Activity So as to have a genuine effect, I'd recommend attempting to get the quantity of members or participants for a club, pledge drive, or comparable occasion over 50 (100 or more is better). Before you endeavor to expand investment, you have to perceive how that occasion or club runs. Offer to help the individual as of now liable for arranging that occasion or the individual who is responsiblefor club enrollment. See what they do that works and what they do that doesn't. Ask individuals who go to club occasions what they preferred, hated, and what proposals they have for development. Contemplate the entirety of this when attempting to expand investment in a club or occasion. DISCLAIMER: I do suggest joining understudy committee if that’s your â€Å"expertise.† If you’re planning to be a political theory major in school and need to be a government official sometime in the not so distant future, feel free to join understudy chamber and make that your â€Å"expertise.† If you need counsel on the most proficient method to run for understudy gathering, look at our other article. Notwithstanding, don’t simply join understudy board to add to your rundown of extracurriculars and to cause yourself to appear to be a pioneer. By what means Should YouDecideWhich Leadership ActivitiestoDo? I've recorded an entire bundle of choices above, however which should you do?Take an opportunity to make a rundown of all the potential administration openings in your general vicinity of interest.Check out my guides to help begin: Skill: Film Potential Leadership Roles: Become a board individual from the film club that presently exists at my school. I like outside movies. I’m going to make a remote film club where we watch another outside film each week and talk about it. I am going to begin a gift drive where I gather people’s old VHSs and DVDs (alongside DVD and VHS players) and give them to a nearby emergency clinic so the patients will have motion pictures to watch. Mastery: Art Potential Leadership Roles: Become a board individual from the craftsmanship club that right now exists at my school. Host an understudy workmanship deal at a nearby exhibition to fund-raise for bosom malignant growth. Compose and

Haemoglobinopathies - Free Essay Example

Abstract Haemoglobinopathies or inherited disorders of haemoglobin are the most common monogenic disorders in humans. Red cell transfusion is a well accepted therapy for clinical management of the most severe form of haemoglobinopathies namely, sickle cell disease (SCD) and ÃŽÂ ²-thalassaemia major. Patients affected by SCD need red blood cell transfusions on a regular basis to reduce morbidity and mortality. The transfusions are administered intermittently to control or prevent a serious complication of SCD, and as a perioperative measure. Or, as a chronic procedure, transfusion strategy is applied to prevent the recurrence, or the first occurrence, of stroke which is a major crisis in SCD, and to manage pulmonary hypertension and other sources of morbidity and mortality. Exchange transfusions are used to reduce the sickle cell haemoglobin (HbS) levels during crisis. Several situations also exist wherein the indication for red cell transfusion is controversial, uncertain, or downright injudicious. Many side effects of transfusion have been identified and methods to overcome them have been developed. Iron overload (remedy: iron chelation), and alloimmunisation (remedy: phenotypical matching of transfused blood) are two notable examples. Association of haemoglobinopathies and neurologic sequelae after transfusion is also known. At the present time, bone marrow transplant is the only curati ve procedure available for both SCD and ÃŽÂ ²-thalassaemia major. Potential therapies involving stem cell transplantation and gene techniques are being vigorously researched. A detailed discussion of the current status of clinical management strategies as applied to inherited haemoglobin-related diseases in particular, sickle cell disease and the thalassaemias, is presented in this paper. 1. Introduction Anaemia is a syndrome characterised by a lack of healthy red blood cells or haemoglobin deficiency in the red blood cells, resulting in inadequate oxygen supply to the tissues. The condition can be temporary, long-term or chronic, and of mild to severe intensity. There are many forms and causes of anaemia. Normal blood consists of three types of blood cells: white blood cells (leucocytes), platelets and red blood cells (erythrocytes). The first generation of erythrocyte precursors in the developing foetus are produced in the yolk sac. They are carried to the developing liver by the blood where they form mature red blood cells that are required to meet the metabolic needs of the foetus. Until the 18th week of gestation, erythrocytes are produced only by liver after which the production shifts to the spleen and the bone marrow. The life of a red blood cell is about 127 days or 4 months (Shemin and Rittenberg, 1946; Kohgo et al., 2008). The main causes of anaemia are blood loss, product ion of too few red blood cells by the bone marrow or a rapid destruction of cells. Haemoglobin, a protein, present in the red blood cells is involved in the transport of oxygen from the lungs to all the other organs and tissues of the body. Iron is an important constituent of the haemoglobin protein structure which is intimately involved in the transport of oxygen. Anaemia is generally defined as a lower than normal haemoglobin concentration. The normal blood haemoglobin concentration is dependent on age and sex, and, according to the World Health Organisation (WHO) Expert Committee Report, anaemia results when the blood concentration of haemoglobin falls below 130 g/L in men or 120 g/L in non-pregnant women (WHO, 1968). However, the reference range of haemoglobin concentration in blood could vary depending on the ethnicity, age, sex, environmental conditions and food habits of the population analysed. According to Beutler and Warren (2006), more reasonable benchmarks for anaemia are 137 g/L for white men aged between 20 and 60 years and 132 g/L for older men. The value for women of all ages would be 122 g/L. Also, the lower limit of normal of haemoglobin concentrations of African Americans are appreciably lower than that of Caucasians (Beutler and Warren, 2006). Besides the well recognised iron deficiency anaemia, several inherited anaemias are also known. These are mostly haemoglobinopathies. Adult haemoglobin is a tetrameric haeme-protein. Abnormalities of beta-chain or alpha-chain produce the various medically significant haemoglobinopathies. The variations in amino acid composition induced genetically impart marked differences in the oxygen carrying properties of haemoglobin. Mutations in the haemoglobin genes cause disorders that are qualitative abnormalities in the synthesis of haemoglobin (e.g., sickle cell disease) and some that are quantitative abnormalities that pertain to the rate of haemoglobin synthesis (e.g., the thalassemias) (Weatherall., 1969). In SCD, the missense mutation in the ÃŽÂ ²-globin gene causes the disorder. The mutation causing sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid 6. The substitution converts a glutamic acid codon (GAG) to a valine codon (GTG). The form of haemoglobin in persons with sickle cell anemia is referred to as HbS. Also, the valine for glutamic acid replacement causes the haemoglobin tetramers to aggregate into arrays upon deoxygenation in the tissues. This aggregation leads to deformation of the red blood cell making it relatively inflexible and restrict its movement in the capillary beds. Repeated cycles of oxygenation and deoxygenation lead to irreversible sickling and clogging of the fine capillaries. Incessant clogging of the capillary beds damages the kidneys, heart and lungs while the constant destruction of the sickled red blood cells triggers chronic anaemia and episodes of hyperbilirubinaemia. Fanconi anaemia (FA) is an autosomal recessive condition, and the most common type of inherited bone marrow failure syndrome. The clinical features of FA are haematological with aplastic anaemia, myelodysplastic syndrome (MDS), and acute myeloid leukaemia (AML) being increasingly present in homozygotes (Tischkowitz and Hodgson, 2003). Cooleys anaemia is yet another disorder caused by a defect in haemoglobin synthesis. Autoimmune haemolytic anaemia is a syndrome in which individuals produce antibodies directed against one of their own erythrocyte membrane antigens. The condition results in diminished haemoglobin concentrations on account of shortened red blood cell lifespan (Sokol et al., 1992). Megaloblastic anaemia is a blood disorder in which anaemia occurs with erythrocytes which are larger in size than normal. The disorder is usually associated with a deficiency of vitamin B12 or folic acid . It can also be caused by alcohol abuse, drugs that impact DNA such as anti-cancer drugs, leukaemia, and certain inherited disorders among others (Dugdale, 2008). Malaria causes increased deformability of vivax-infected red blood cells (Anstey et al., 2009). Malarial anaemia occurs due to lysis of parasite-infected and non-parasitised erythroblasts as also by the effect of parasite products on erythropoiesis (Ru et al., 2009). Large amounts of iron are needed for haemoglobin synthesis by erythroblasts in the bone marrow. Transferrin receptor 1 (TfR1) expressed highly in erythroblasts plays an important role in extracellular iron uptake (Kohgo et al., 2008). Inside the erythroblasts, iron transported into the mitochondria gets incorporated into the haeme ring in a multistep pathway. Genetic abnormalities in this pathway cause the phenotype of ringed sideroblastic anemias (Fleming, 2002). The sideroblastic anemias are a heterogeneous group of acquired and inherited bone marrow disorders, characterised by mitochondrial iron overload in developing red blood cells. These conditions are diagnosed by the presence of pathologic iron deposits in erythroblast mitochondria (Bottomley, 2006).   2. Classification of anaemia Anaemia can be generally classified based on the morphology of the red blood cells, the pathogenic spectra or clinical presentation (Chulilla et al., 2009). The morphological classification is based on mean corpuscular volume (MCV) and comprises of microcytic, macrocytic and normocytic anaemia. (a) Microcytic anaemia refers to the presence of RBCs smaller than normal volume, the reduced MCV ( 82 fL) reflecting decreased haemoglobin synthesis.   Thus, it is usually associated with hypochromic anaemia. Microcytic anaemia can result from defects either in iron acquisition or availability (Iolascon et al., 2009), or disorders of haeme metabolism or globin synthesis (Richardson, 2007). The differential diagnosis for microcytic anaemia includes iron deficiency anaemia (IDA), thalassaemia, ACD, and rarely sideroblastic anaemia (Chulilla et al., 2009). Microcytosis without anaemia is characteristic of thalassaemia trait. The red blood cell distribution width (RDW) obtained with haematological analysers provides the index of dispersion in the erythrocyte distribution curve and complements MCV values. RDW is helpful to differentiate between thalassaemia and IDA. RDW is normal in thalassemia; on the contrary, microcytic anemia with RDW 15 would probably indicate IDA (Chulilla et al., 2009). In macrocytic anaemia, erythrocytes are larger (MCV 98 fL) than their normal volume (MCV = 82-98 fL). Vitamin B12 deficiency leads to delayed DNA synthesis in rapidly growing haematopoietic cells, and can result in macrocytic anaemia. Drugs that interfere with nucleic acid metabolism, such as.hydroxyurea increases MCV ( 110 fL) while alcohol induces a moderate macrocytosis (100-110 fL). In the initial stage, most anaemias are normocytic. The causes of normocytic anaemia are nutritional deficiency, renal failure and haemolytic anemia (Tefferi, 2003). The most common normocytic anaemia in adults is ACD (Krantz, 1994). Common childhood normocytic anaemias are, besides iron deficiency anaemia, those due to acute bleeding, sickle cell anaemia, red blood cell membrane disorders and current or recent infections especially in the very young (Bessman et al., 1983). Homozygous sickle cell disease is the most common cause of haemolytic normocytic anemias in children (Weatherall DJ, 1997a). In practice, the morphological classification is quicker and therefore, more useful as a diagnostic tool. Besides, MCV is also closely linked to mean corpuscular haemoglobin (MCH), which denotes mean haemoglobin per erythrocyte expressed in picograms (Chulilla et al., 2009). Thus, MCV and MCH decrease simultaneously in microcytic, hypochromic anaemia and increase together in macrocytic, hyperchromic anemia. Pathogenic classification of anaemia is based on the production pattern of RBC: whether anaemia is due to inadequate production or loss of erythrocytes caused by bleeding or haemolysis. This approach is useful in those cases where MCV is normal. Pathogenic classification is also essential for proper recognition of the mechanisms involved in the genesis of anaemia. Based on the pathogenic mechanisms, anaemia is further divided into two types namely, (i) hypo-regenerative in which the bone marrow production of erythrocytes is decreased because of impaired function, decreased number of precursor cells, reduced bone marrow infiltration, or lack of nutrients; and (ii) regenerative: when bone marrow upregulates the production of erythrocytes in response to the low erythrocyte mass (Chulilla et al., 2009). This is typified by increased generation of erythropoietin in response to lowered haemoglobin concentration, and also reflects a loss of erythrocytes, due to bleeding or haemolysis. The r eticulocyte count is typically higher. Sickle cell disease is characterised by sickled red cells.   The first report of SCD was published a century ago noting the presence of peculiar elongated cells in blood by James Herrick, an American physician (1910). Pauling et al. (1949) described it as a molecular disease. The molecular nature of sickle haemoglobin (HbS) in which valine is substituted for glutamic acid at the sixth amino acid position in the beta globin gene reduces the solubility of haemoglobin, causing red cells to sickle (Fig. 1). Sickling of cells occurs at first reversibly, then finally as a state of permanent distortion, when cells containing HbS and inadequate amounts of other haemoglobins including foetal haemoglobin, which retards sickling, become deoxygenated (Bunn, 1997). The abnormal red cells break down, leading to anaemia, and clog blood vessels with aggregates, leading to recurrent episodes of severe pain and multiorgan ischaemic damage (Creary et al., 2007). The high levels of inflammatory cytokines in SCD may promote retention of iron by macrophage/reticuloendothelial cells and/or renal cells. SCD care commonly depends on transfusion that results in iron overload (Walter et al., 2009). 3. Pathogenesis of anaemia Anaemia is a symptom , or a syndrome, and not a disease (Chulilla et al., 2009). Several types of anaemia have been recognised, the pathogenesis of each being unique. Iron deficiency anaemia (IDA) is the most common type of anaemia due to nutritional causes encountered worldwide (Killip et al., 2008). Iron is one of the essential micronutrients required for normal erythropoietic function While the causes of iron deficiency vary significantly depending on chronological age and gender, IDA can reduce work capacity in adults (Haas Brownlie, 2001) and affect motor and mental development in children (Halterman et al., 2001). The metabolism of iron is uniquely controlled by absorption rather than excretion (Siah et al., 2006). Iron absorption typically occurring in the duodenum accounts for only 5 to 10 per cent of the amount ingested in homoeostatis. The value decreases further under conditions of iron overload, and increases up to fivefold under conditions of iron depletion (Killip et al., 2008). Iron is ingested as haem iron (10%) present in meat, and as non-haem ionic form iron (90%) found in plant and dairy products. In the absence of a regulated excretion of iron through the liver or kidneys, the only way iron is lost from the body is through bleeding and sloughing of cells. Thus, men and non-menstruating women lose about 1 mg of iron per day while menstruating women could normally lose up to 1.025 mg of iron per day (Killip et al., 2008). The requirements for erythropoiesis   which are typically 20-30 mg/day   are dependent on the internal turnover of iron (Munoz et al., 2009) For example, the amount of iron required for daily production of 300 billion RBCs (20-30 mg) is provided mostly by recycling iron by macrophages (Andrews, 1999). Iron deficiency occurs when the metabolic demand for iron exceeds the amount available for absorption through consumption. Deficiency of nutritional intake of iron is important, while abnormal iron absorption due to hereditary or acquired iron-refractory iron deficiency anemia (IRIDA) is another important cause of unexplained iron deficiency. However, IDA is commonly attributed to blood loss e.g., physiological losses in women of reproductive age. It might also represent occult bleeding from the gastrointestinal tract generally indicative of malignancy (Hershko and Skikne, 2009). Iron absorption and loss play an important role in the pathogenesis and management of IDA. Human iron disorders are necessarily disorders of iron balance or iron distribution. Iron homeostasis involves accurate control of intestinal iron absorption, efficient utilisation of iron for erythropoiesis, proper recycling of iron from senescent erythrocytes, and regulated storage of iron by hepatocytes and macrophages (Andrews, 2008). Iron deficiency is largely acquired, resulting from blood loss (e.g., from intestinal parasitosis), from inadequate dietary iron intake, or both. Infections, for example, with H pylori, can lead to profound iron deficiency anemia without significant bleeding. Genetic defects can cause iron deficiency anaemia. Mutations in the genes encoding DMT1 (SLC11A2) and glutaredoxin 5 (GLRX5) lead to autosomal recessive hypochromic, microcytic anaemia (Mims et al., 2005). Transferrin is a protein that keeps iron nonreactive in the circulation, and delivers iron to cells possessing specific transferrin receptors such as TFR1 which is found in largest amounts on erythroid precursors. Mutations in the TF gene leading to deficiency of serum transferrin causes disruption in the transfer of iron to erythroid precursors thereby producing an enormous increase in intestinal iron absorption and consequent tissue iron deposition (Beutler et al., 2000). Quigley et al. (2004) found a haem exporter, FLVCR, which appears to be necessary for normal erythroid development. Inactivation of FLVCR gene after birth in mice led to severe macrocytic anaemia, indicating haem export to be important for normal erythropoiesis. The anaemia of chronic disease (ACD) found in patients with chronic infectious, inflammatory, and neoplastic disorders is the second most frequently encountered anaemia after iron-deficiency anaemia. It is most often a normochromic, normocytic anaemia that is primarily caused by an inadequate production of red cells, with low reticulocyte production (Krantz, 1994). The pathogenesis of ACD is unequivocally linked to increased production of the cytokines including tumour necrosis factor, interleukin-1, and the interferons that mediate the immune or inflammatory response. The various processes leading to the development of ACD such as reduced life span of red cells, diminished erythropoietin effect on anaemia, insufficient erythroid colony formation in response to erythropoietin, and impaired bioavailability of reticuloendothelial iron stores appear to be caused by inflammatory cytokines (Means, 1996;2003). Although iron metabolism is characteristically impaired in ACD, it may not play a key role in the pathogenesis of ACD (Spivak, 2002). Neither is the lack of available iron central to the pathogenesis of the syndrome, according to Spivak (2002), who found reduced iron absorption and decreased erythroblast transferrin-receptor expression to be the result of impaired erythropoietin production and inhibition of its activity by cytokines. However, reduced erythropoietin activity, mostly from reduced production, plays a pivotal role in the pathogenesis of ACD observed in systemic autoimmune diseases (Bertero and Caligaris-Cappio, 1997). Indeed, iron metabolism as well as nitric oxide (NO), which contributes to the regulation of iron cellular metabolism are involved in the pathogenesis of ACD in systemic autoimmune disorders. Inflammatory mediators, particularly the cytokines, are important factors involved in the pathogenesis of the anaemia of chronic disease, as seen in rheumatoid arthritis anaemia (Baer et al., 1990), the cytokines causing impairment of erythroid p rogenitor growth and haemoglobin production in developing erythrocytes.   Anaemia is also commonly found in cases of congestive heart failure (CHF), again caused by excessive cytokine production leading to reduced erythropoietin secretion, interference with erythropoietin activity in the bone marrow and reduced iron supply to the bone marrow (Silverberg et al., 2004). However, in the presence of chronic kidney insufficiency, abnormal erythropoietin production in the kidney plays a role in the pathogenesis of anaemia in CHF. The myelodysplastic syndromes (MDS) are common haematological malignancies affecting mostly the elderly as age-related telomere shortening enhances genomic instability (Rosenfeld and List, 2000). Radiation, smoking and exposure to toxic compounds e.g., pesticides, organic chemicals and heavy metals, are factors promoting the onset of MDS via damage caused to progenitor cells, and, thereby, inducing immune suppression of progenitor cell growth and maturation. TNF- and other pro-apoptotic cytokines could play a central role in the impaired haematopoiesis of MDS (Rosenfeld and List, 2000). Premature intramedullary cell death brought about by excessive apoptosis is another important pathogenetic mechanism in MDS (Aul et al., 1998).   SCD arising from a point mutation in the ÃŽÂ ²-globin gene and leading to the expression of haemoglobin S (HbS) is the most common monogenetic disorder worldwide. Chronic intravascular haemolysis and anaemia are some important characteristics of SCD. Intravascular haemolysis causes endothelial dysfunction marked by reduced nitric oxide (NO) bioavailability and NO resistance, leading to acute vasoconstriction and, subsequently, pulmonary hypertension (Gladwin and Kato, 2005).    However, a feature that differentiates SCD from other chronic haemolytic syndromes is the persistent and intense inflammatory condition present in SCD. The primary pathogenetic event in SCD is the intracellular polymerisation or gelation of deoxygenated HbS leading to rigidity in erythrocytes (Wun, 2001). The deformation of erythrocytes containing HbS is dependent on the concentration of haemoglobin in the deoxy conformation (Rodgers et al., 1985). It has been demonstrated that sickle monocytes are a ctivated which, in turn, activate endothelial cells and cause vascular inflammation. The vaso-occlusive processes in SCD involve inflammatory and adhesion molecules such as the cell adhesion molecules (CAM family), which play a role in the firm adhesion of reticulocytes and leukocytes to endothelial cells, and the selectins, which play a role in leukocyte and platelet rolling on the vascular wall (Connes et al., 2008). Thus, inflammation, leucocyte adhesion to vascular endothelium, and subsequent endothelial injury are other crucial factors contributing to the pathogenesis of SCD (Jison et al., 2004). 4. Current therapies for clinical management of sickle cell disease including a critical appraisal of transfusion Between 1973 and 2003, the average life expectancy of a patient with SCD increased dramatically from a mere 14 years to 50 years thanks to the development of comprehensive care models and painstaking research efforts in both basic sciences especially molecular and genetic studies, and clinical aspects of SCD (Claster and Vichinsky, 2003). The clinical manifestations of SCD are highly variable. Both the phenotypic expression and intensity of the syndrome are vastly different among patients and also vary longitudinally within the same patient (Ballas, 1998). New pathophysiological insights available have enabled treatments to be developed for the recognised haematologic and nonhaematologic abnormalities in SCD (Claster and Vichinsky, 2003). The main goals of SCD treatment are symptom alleviation, crises avoidance and effective management of disease complications. The strategy adopted is primarily palliative in nature, and consists of supportive, symptomatic and preventative approaches to therapy. Symptomatic management includes pain mitigation, management of vasoocclusive crisis, improving chronic haemolytic anaemia, treatment of organ failure associated with the disease, and detection and treatment of pulmonary hypertension (Distenfeld and Woermann, 2009). The preventative strategies include use of prophylactic antibiotics (e.g., penicillin) in children, prophylactic blood transfusion for prevention of stroke in patients especially young children who are at a very high risk of stroke, and treatment with hydroxyurea of patients experiencing frequent acute painful episodes (Ballas, 2002). Currently, curative therapy for sickle cell anaemia is only available through bone marrow and stem cell transplantation. Hematopoietic cell transplantation using stem cells from a matched sibling donor has yielded excellent results in paediatric patients (Krishnamurti, 2007). Curative gene therapy is still at the exploratory stage (Ballas, 2002). 4.1 Current and potential therapies The potential treatment strategies basically target cellular dehydration, sickle haemoglobin concentrations, endothelial dysfunction, and abnormal coagulation regulation (Claster and Vichinsky, 2003). HbS concentrations are essentially tackled through transfusions while approaches to reduce HbS polymerisation which is the main mechanism for the development of vaso-occlusion include (a) increasing foetal haemoglobin (HbF) concentration using hydroxyurea (Fig. 2), butyrate, or erythropoietin, and (b) preventing sickle cell dehydration using Clotrimazole (Fig. 3) or Mg2+pidolate. Hydroxyurea therapy increases the production of HbF in patients with sickle cell anaemia, and, thereby, inhibits the polymerisation of HbS and alleviates both the haemolytic and vaso-occlusive manifestations of the disease (Goldberg et al., 1990). Recombinant erythropoietin also increases the number of reticulocytes with HbF. Additionally, it has been observed that administration of intravenous recombinant eryt hropoietin with iron supplementation alternating with hydroxyurea enhances HbF levels more than hydroxyurea alone (Rodgers et al., 1993). As SCD is essentially characterized by an abnormal state of endothelial cell activation   that is, a state of inflammation, a pharmacologic approach to inhibit endothelial cell activation has proved clinically beneficial (Hebbel and Vercellotti, 1997). Thus, administration of sulfasalazine which is a powerful inhibitor of activation of nuclear factor (NF)-B, the transcription factor promoting expression of genes for a number of pro-adhesive and procoagulant molecules on endothelium to humans has been found to provide transcriptional regulation of SCD at the endothelium level (Solovey et al., 2001). 4.2 Red blood cell transfusion A key therapy that is applied regularly in the clinical management of patients with SCD is packed red blood cell transfusion. RBC transfusion improves the oxygen-carrying capacity which is achieved by enhancing the haemoglobin levels, causes dilution of HbS concentration thereby, reducing blood viscosity and boosting oxygen saturation. Furthermore, RBC transfusion is helpful in suppressing endogenous production of sickle RBCs by augmenting tissue oxygenation ( Josephson et al., 2007). There are two major types of RBC transfusion therapy: intermittent and chronic which are further classified as prophylactic or therapeutic. Intermittent transfusions are generally therapeutic in nature and administered to control acute manifestations of SCD whereas chronic transfusions are performed as general preventative measures to check complications of SCD. RBC transfusion given as a single dose is termed as simple transfusion. Exchange transfusion involves administration of a larger volume of RBCs replacing the patients RBCs that are simultaneously removed. Details of the various types of RBC transfusion and the major clinical indications for the same in SCD patients are listed in Table 1. 4.3 Indications for intermittent transfusions Indications for intermittent transfusions include acute manifestations of SCD, as indicated in Table 1, that require redressal through therapeutic transfusions. However, under certain circumstances intermittent transfusions could be prophylactic such as for instance, when SCD patients are transfused before specific surgeries viz., those related to pregnancy complications or renal failure (Table 1). Acute Chest Syndrome (ACS) describes a manifestation of SCD in which, due to sickling, infectious and noninfectious pulmonary events are complicated, resulting in a more severe clinical course. The diagnosis is the presence of a new infiltrate on chest radiography that is accompanied by acute respiratory symptoms. ACS accounts for nearly 25% of all deaths from SCD (Vichinsky, 2002). Repeated episodes of ACS are associated with an increased risk of chronic lung disease and pulmonary hypertension (Castro, 1996). The severe pulmonary events occurring in SCD may be precipitated by any trigger of hypoxia (Vichinsky, 2002). Transfusions are very efficacious and provide immediate benefit by reversing hypoxia in ACS. Transfusion of leucocyte-poor packed red cells matched for Rh, C, E, and Kell antigens can curtail antibody formation to below 1% (Vichinsky, 2002). Simple transfusions suffice for less severe cases; however, exchange transfusion is recommended to minimise the risk of increased viscosity. Also, chronic transfusion appears promising for prevention of recurrence in selected patients (Styles and Vichinsky, 1994). In a multicentre ACS trial, prophylactic transfusion was found to almost completely eliminate the risk of pulmonary complications (Vichinsky, 2002). Acute Symptomatic Anaemia arises in SCD as a result of blood loss, increased RBC destruction, suppression of erythropoiesis etc. and is effectively treated with intermittent transfusion of RBCs to relieve symptoms of cardiac and respiratory distress (Josephson et al., 2007). Aplastic Anaemia is commonly caused in SCD on account of infection of haematopoietic precursors in the bone marrow by Parvovirus B19 leading to a steep fall in RBCs. According to Josephson et al. (2007), therapeutic intermittent transfusion of RBCs is again the recommended first-line of treatment to improve total haemoglobin count and prevent cardiac decompensation. However, in those patients who are prone to fluid overload on account of cardiac or renal dysfunction an alternative transfusion strategy is to remove the whole blood and replace it with packed cells while avoiding the addition of excess volume (Josephson et al., 2007). Acute Stroke is a high risk especially in paediatric SCD cases because of elevated cerebral flow. Enormous decline in stroke rate have occurred in children receiving intermittent simple transfusion (Adams et al., 1998). However, the identification of the stroke type would be necessary in all SCD patients in order to determine the appropriate treatment approach since the occurrence of infarctive strokes is higher in children as opposed to a higher incidence of haemorrhagic strokes in adults (Adams, 2003). 4.4 Indications for Chronic Transfusions Prophylactic chronic RBC transfusion every 3 to 4 weeks to maintain HbS levels lower than 30% is crucial for preventing first as well as recurrent strokes in children (Johnson et al., 2007). The transfusions could either be chronic simple transfusion or prophylactic chronic RBC exchange transfusion. Prophylactic chronic transfusions are recommended for patients with chronic renal failure so as to avoid severe symptomatic anaemia and for those patients with SCD undergoing pregnancy with complications. However, prophylactic transfusion is not indicated for SCD patients with normal pregnancy (Tuck et al., 1987). 4.5 Controversial and indeterminate indications for transfusion Several situations also exist wherein the indication for red cell transfusion is controversial, uncertain, or downright injudicious in SCD management. Some examples are indicated in Table 1. According to Hankins et al. (2005), chronic transfusion therapy is helpful in reducing the incidence of strokes in children but not the severity of strokes. In the case of acute priapism, improvement in patients has been observed after exchange or simple transfusion (Rifikind   et al., 1979). Yet, due to the ASPEN syndrome, transfusion therapy currently is only a second-line therapy in the management of priapism ( Miller et al., 1995). RBC transfusion is a vital component in the management of symptoms and complications of SCD. It has drastically reduced the morbidity and mortality of SCD. Yet, immune-related effects such as FNHTRs (Febrile Non-Haemolytic Transfusion Reaction i.e., fever resulting from a blood transfusion) and alloimmunisation to HLAs (Human Leucocyte Antigens),   and nonimmune-related effects e.g., iron overload and transfusion-transmitted infections are serious adverse effects of the transfusion therapy that need to be attended to in SCD patients receiving transfusion (Johnson et al., 2007). Chronic transfusions could result in an inexorable accumulation of tissue iron that could become fatal if not treated (Cohen, 1987). Excess iron damages the liver, endocrine organs, and heart and may be fatal by adolescence (Engle, 1964). 5. Critical review of thalassemias : (i) Molecular pathogenesis The large number of inherited haemoglobin disorders known today include (a) those related to anomalies in the haemoglobin structure e.g., sickle cell disease, and (b) the thalassemias whose hallmark is globin-chain deficiency of one or other of the globin chains of adult haemoglobin in erythroid cells. 5.1 ÃŽÂ ²-Thalassaemias These are a set of genetic disorders inherited as simple codominant traits affecting haemoglobin synthesis. Depending on the haemoglobin chain affected, 2 types of thalassemia are recognised: ÃŽÂ ±-thalassaemia and ÃŽÂ ²-thalassaemia. Homozygous ÃŽÂ ²-thalassaemia is marked by a quantitative deficiency of the ÃŽÂ ²-globin chains in the erythroid cells. A complete absence of the ÃŽÂ ²-globin chains occurs in homozygous ÃŽÂ ²o-thalassaemia whereas in homozygous ÃŽÂ ²+-thalassaemia the ÃŽÂ ²-globin chains are present at less than 30% of normal. Accounting for nearly 90% of the cases, ÃŽÂ ²+-thalassaemia is the most commonly observed form of ÃŽÂ ²-thalassaemia. The condition is termed thalassaemia major when there is microcytic hypochromic anaemia with severe haemolysis, hepatosplenomegaly, skeletal deformities and iron overload. ÃŽÂ ²-thalassaemia homozygotes exhibit severe transfusion-dependent anaemia in the very first year of life. Homozygotic individ uals having a relatively benign clinical phenotype and surviving with or without transfusion are described as thalassaemia intermedia (Weatherall, 1969). The thalassaemias, thus, encompass a wide gamut of clinical disability from intrauterine death to a mild anaemia with no overt symptoms (Weatherall, 1997b). The coexistence of   ÃŽÂ ± -thalassaemia leading to reduction in the synthesis of ÃŽÂ ±-globin chains, and a genetic predisposition to produce high levels of HbF, could be important factors for the extensive phenotypic variability described above (Weatherall, 1996). The milder form of thalassaemia intermedia is the result of a lesser imbalance in globin chain synthesis probably the result of residual ÃŽÂ ² -globin chain synthesis due to mild mutation or due to reduced synthesis of ÃŽÂ ±-globin chains due to co-inheritance of ÃŽÂ ±-thalassaemia (Nadkarni et al., 2001). Persons having the heterozygous form of the disorder are usually asymptomatic but can be recognised by typical abnormalities of red cell morphology (shown in Fig.4) and indices (Spritz and Forget, 1983). Compared to the heterozygous form of ÃŽÂ ²-thalassaemia, a larger imbalance exists in the ÃŽÂ ±- to ÃŽÂ ²-globin chain synthesis in the homozygous ÃŽÂ ²-thalassemia or Cooley anaemia. The excess ÃŽÂ ±-globin chains are liable to precipitate, causing damage to the ÃŽÂ ²-thalassemic red cell membrane and affecting erythropoiesis. Important manifestations of homozygous ÃŽÂ ²-thalassemia are severe chronic microcytic haemolytic anaemia and hepatosplenomegaly due to extramedullary haematopoiesis (Spritz and Forget, 1983). As many as 175-200 molecular mutations affecting the ÃŽÂ ²-globin gene complex are involved in creating the ÃŽÂ ²-thalassaemia syndromes with the resultant altered synthetic ratios of ÃŽÂ ±- to ÃŽÂ ²-globin chains, precipitation of excess unbalanced ÃŽÂ ±-globin chains, and programmed cell death of erythroid precursors (Steinberg and Rodgers, 2001; Gambari, 2010). Hence, the pathogenetic basis of the clinical diversity of the ÃŽÂ ²-thalassaemia syndromes essentially rests with the striking heterogeneity of mutations in the ÃŽÂ ²-globin gene (Thein, 1993). The -158 (C ÃÆ'   T) substitution in the GÃŽÂ ³ gene has been found to be linked to the increase in HbF synthesis leading to less severe disease in thalassaemia intermedia (Gilman and Huisman, 1985; Ragusa et al., 1992). 5.2 Red blood cell transfusion and iron overload Regular RBC transfusions have proved to be efficacious in the treatment of ÃŽÂ ²-thalassemia by nullifying the complications of anaemia and compensatory bone marrow (BM) expansion. However, thalassaemias are also complicated by physiological iron overload which gets exacerbated by blood transfusion and causes various endocrine diseases, liver cirrhosis, cardiac failure and also death (Engle, 1964). Complemented with iron-chelating therapy (e.g., deferoxamine) for iron overload, the prognosis of thalassemia major has become dramatic (Olivieri and Brittenham, 1997).  Ãƒâ€šÃ‚   Recently, the mechanism of iron overload in the absence of transfusion in thalassaemia has been unraveled by Tanno et al. (2007) who observed that the overproduction of the protein GDF15 suppresses the production of the liver protein, hepcidin in thalassaemia patients which eventually leads to an increase in the uptake of dietary iron in the gut. This information could translate into new diagnostic and therapeutic tools in the future. 6. Critical review of thalassemias : (ii) Clinical management therapies ÃŽÂ ²-thalassaemia syndromes are the most common genetic diseases worldwide. Improvements in treatment strategies have resulted in good prognosis. Yet, disease- and treatment-related complications get exacerbated over time, increasing morbidity and curtailing life expectancy of the patients. Currently, the only curative treatment available for thalassaemia is stem cell transplantation (SCT) (Gaziev et al., 2008) which is a gold standard in treating the disease. Many challenges exist for transplantation therapy including graft versus host disease (GVHD), rejection of the donated stem cells, and infections while a major limitation for SCT is finding HLA-matched blood-related donors viz., siblings. Currently available high-resolution HLA-typing could minimise rejection and GVHD by matching major as well as minor HLA (Gaziev et al., 2008). The advanced techniques of HLA-typing can also identify unrelated but suitable voluntary donors. Intermittent red blood cell transfusion is the recommended mode of treatment for people who have moderate or severe thalassaemias. ÃŽÂ ²-thalassemia major, or Cooleys anaemia require regular blood transfusions. 6.1 Emerging Therapies Gene therapy for treatment of thalassaemia is still evolving. Research is focussed on finding a potential treatment of ÃŽÂ ² -thalassemia based on globin gene transfer. One of the aims of the genetic research is to trigger the production of HbF in adults to make up for the lack of healthy adult haemoglobin. The molecular mechanisms that initiate the change in gene expression during the switch from foetal (HbF) to adult (HbA) have been partially elucidated. Several chemical compounds able to reactivate HbF synthesis in vitro and in vivo in adult bone marrow have been identified (Testa, 2009). Induction of HbF to treat thalassaemia is a novel therapeutic strategy especially for those patients who are resistant to conventional therapy that is, regular blood transfusions and chelation therapy (Gambari, 2010). In view of the fact that gene therapy could be inaccessible to many because of biological/genetic as well as economic constraints (Gambari, 2010), chemical inducers are being extensively studied. Hydroxyurea has already been used as HbF inducer in both moderate and severe forms of ÃŽÂ ²-thalassaemia (Testa, 2009). Some of the potential inducers of HbF are histone deacetylase inhibitors, DNA-binding drugs and inhibitors of the mammalian target of rapamycin or mTOR pathway (Gambari and Fibach, 2007). Also, according to Gambari and Fibach (2007) chemical inducers need to be used with caution since many of those used so far were potentially cytotoxic. Accelerated apoptosis has been observed in the erythroid progenitors of patients with ÃŽÂ ²-thalassaemia major (Silva et al., 1996). The hormone erythropoietin (Epo), which is the principal regulator of red blood cell production, is known to interact with high-affinity receptors on the surface of erythroid progenitor cells and promote cell viability. Epo has been shown to repress apoptosis via Bcl-XL and Bcl-2 during proliferation and differentiation of erythroid progenitors (Silva et al., 1996). Hence, recombinant human erythropoietin (rHuEpo) could have potential application in the treatment of transfusion-dependent thalassaemia patients as it promotes the differentiation and proliferation of erythroid cells, and stimulates the production of HbF (Makis et al., 2001). 7. Conclusion Inherited haemoglobinopathies including sickle cell disease and thalassaemias result from genetic abnormalities in the synthesis of globin protein chains. Sickle cell disease (SCD) is caused by structural defects in the haemoglobin molecule while thalassaemias occur due to reduced or absent globin chain. Only bone marrow or haematopoietic stem cell transplantation can cure patients with either disease. Clinical management of SCD generally involves supportive therapy consisting of pain relief, fluids and antibiotics, and folic acid supplements. Red cell transfusion is currently a well accepted therapy for clinical management of inherited haemoglobinopathies including SCD and the thalassaemias. 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Hershko C Skikne B, 2009, Pathogenesis and management of iron deficiency anaemia: Emerging role of Celiac disease, Helicobacter pylori, and autoimmune gastritis, Seminars in Hematology, 46 (4): 339-350.Iolascon A, De Falco L. Beaumont C, 2009, Molecular basis of inherited microcytic anemia due to defects in iron acquisition or heme synthesis, Haematologica 94(3): 395-408. Jison ML, Munson PJ, Barb JJ et al., 2004, Blood mononuclear cell gene expression profiles characterize the oxidant, hemolytic, and inflammatory stress of sickle cell disease, Blood, 104(1): 270-280.   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Killip S, Bennett JM Chambers MD, 2008, Iron deficiency anemia, American Family Physician, 75(5): 671-678. Kohgo Y, Ikuta K, Ohtake T. et al., 2008, Body iron metabolism and pathophysiology of iron overload, Int J Hematol. 88(1): 7-15. Krantz SB, 1994, Pathogenesis and treatment of the anemia of chronic disease, Am J   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Med Sci.,307(5): 353-359. the art, Expert Opinion on Biological Therapy, 7(2): 161-172. Josephson CD, Su LL, Hillyer KL, et al., 2007, Transfusion in the Patient With Sickle Cell Disease: A Critical Review of the Literature and Transfusion Guidelines, Transfusion Medicine Reviews, 21(2): 118-133. MakisAC, ChaliasosN, Hatzimichael EC et al., 2001, Recombinant human   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   erythropoietin therapy in a transfusion-dependent ÃŽÂ ²-thalassaemia major patient,   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Annals of Haematology, 80(8):492-495. Means RT Jr., 1996, Advancement in the anemia of chronic disease: A cytokine- mediated anemia, Stem Cells, 13(1): 32-37. Means RT Jr., 2003, Recent developments in the anemia of chronic disease, Current   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Hematology Reports, 2(2):116-121. Miller S, Rao S, Dunn K, et al., 1995, Priapism in children with sickle cell disease, J   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Urol, 154:844- 847. Mims MP, Guan Y, Pospisilova D, et al., 2005, Identification of a human mutation of DMT1 in a patient with microcytic anemia and iron overload, Blood,105:1337- 1342. MuÃÆ' ±oz M, Villar I GarcÃÆ' ­a-Erce JA, 2009, An update on iron physiology, World J Gastroenterol, 15(37): 4617-4626. Nadkarni A, Gorakshakar AC, Lu CY, et al., 2001, Molecular pathogenesis and clinical variability of ÃŽÂ ²-thalassaemia syndromes among Indians, American Journal of Haematology, 68:75-80. Olivieri NF Brittenham GM, 1997, Iron-chelating therapy and the treatment of   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   thalassaemia, Blood, 89(3): 739-761 Pauling L, Itano HA, Singer SJ, et al., 1949,   Sickle cell anemia: a molecular disease, Science, 110(2865):543-548. Quigley JG, Yang Z, Worthington MT, et al. 2004, Identification of a human heme exporter that is essential for erythropoiesis, Cell, 118:757-766. Ragusa A, Lambardo M, Beldjord C, et al., 1992, Genetic epidemiology of ÃŽÂ ²- thalassaemia in Sicily: do sequences 58 to the GÃŽÂ ³ gene and 58 to the ÃŽÂ ² gene interact to enhance HbF expression in ÃŽÂ ² -thalassemia?, Am J Hematol, 40:199-206. Richardson M, 2007, Microcytic anemia, Pediatrics in Review, 28:5-14. Rifikind S, Waisman J, Thompson R, et al., 1979, RBC exchange pheresis for priapism in sickle cell disease, JAMA, 242:2317 2318. Rodgers GP, Noguchi CT, Schechter AN, 1985, Irreversibly sickled erythrocytes in sickle cell anemia: A quantitative reappraisal, Am J Hematol., 20(1): 17-23. Rodgers GP, Dover GJ, Uyesaka N, et al., 1993, Augmention by erythropoietin of the fetal-hemoglobin response to hydroxyurea in sickle cell disease, NEJM, 328(2): 73- 80. Rosenfeld C List A, 2000, A hypothesis for the pathogenesis of myelodysplastic syndromes: implications for new therapies, Leukemia, 14(1): 2-8. Ru YX, Mao BY, Zhang FK et al., 2009, Invasion of erythroblasts by Plasmodium vivax: A new mechanism contributing to malarial anaemia, Ultrastruct. Pathol., 33(5):236-42.   Shemin, D. Rittenberg D, 1946, The life span of the human red blood cell, J Biol Chem, 166: 627-636. Siah CW, Ombiga J, Adams LA, et al., 2006, Normal iron metabolism and the pathophysiology of iron overload disorders, Clin Biochem Rev. 27:5-16. Silva M, Grillot D, Benito A, et al., 1996, Erythropoietin can promote erythroid progenitor survival by repressing apoptosis through Bcl-XL and Bcl-2. Blood, 88:1576-1582. Sokol RJ, Booker DJ Stamps R, 1992, The pathology of autoimmune haemolytic anaemia, J Clin Pathol., 45: 1047-1052. Spivak, JL, 2002, Iron and the anemia of chronic disease, Oncology, 16(9 Suppl 10):25- 33. Spritz RA Forget BG, 1983, The thalassemias: molecular mechanisms of human genetic disease, Am J Hum Genet., 35:333-361. Steinberg MH Rodgers GP, 2001, Pharmacologic modulation of foetal haemoglobin, Medicine, 80:328-344. Styles LA Vichinsky E, 1994, Effects of a long-term transfusion regimen on sickle cell- related illnesses, J Pediatr., 125:909-911. Tanno T, Bhanu NV, Oneal PA et al., 2007, High levels of GDF15 in thalassemia   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   suppress expression of the iron regulatory protein hepcidin, Nature   Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   Medicine, 13:1096 1101. Tefferi A, 2003, Anaemia in adults: a contemporary approach to diagnosis, Mayo Clin   Proc.78:1274-1280. Testa U, 2009, Fetal hemoglobin chemical inducers for treatment of   Haemoglobinopathies, Ann Hematol. 88:505-528. Thein SL, 1993, ÃŽÂ ²- Thalassaemia. In: Higgs DR Weatherall DA, editors, Baillieres clinical haematology: the hemoglobinopathis, Vol 6, Bailliere Tindall, London, p151-175. Tischkowitz MD Hodgson SV, 2003, Fanconi anaemia, J Med Genet 2003;40:1-10 doi:10.1136/jmg.40.1.1 Tuck S, James C, Brewster E, et al., 1987, Prophylactic blood transfusions in maternal sickle cell syndromes, Br J Obstet Gynaecol., 94:121 125. Walter PB, Harmatz P Vichinsky E, 2009, Iron metabolism and iron chelation in sickle cell disease, Acta Haematol., 122(2-3):174-183. Weatherall DJ, 1969, The genetics of the thalassaemias, British Medical Bulletin, 25(1): 24-29. 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High School And Selective Honors Programs - 983 Words

One of the biggest myths in my high school was that the people in the top ten rank were the smartest students in the city. That because we were considered to be the best school in the city(another issue in and of itself), they were the ones that were going to be accepted into the high ranking universities and selective honors programs. But what most of my classmates (and myself at first) failed to see, was that the truth was actually very different. When one took a step back and actually looked at the credentials and scores of the people in the top ten rank when compared to the rest of the class, it became exceedingly obvious that the numbers don’t support the notion that they are the â€Å"elite† scholars of the school. Many of the â€Å"elite† were there for one reason only, they knew how to play the system by picking the easiest teachers for each subject. 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Role of Women in Ancient Roman Society Essay - 1341 Words

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Policies & Procedures to Promote the behviour of childern & Yound Peop

Questions: 1.1 Summarise the policies and procedures of the setting relevant to promoting children and young peoples positive behaviour 1.2 Evaluate how the policies and procedures of the setting support children and young people to: a) feel safe 1.2 Evaluate how the policies and procedures of the setting support children and young people to: b) make a positive contribution 1.2 Evaluate how the policies and procedures of the setting support children and young people to: c) develop social and emotional skills 1.2 Evaluate how the policies and procedures of the setting support children and young people to: d) understand expectations and limits 1.3 Explain the benefits of all staff consistently and fairly applying boundaries and rules for children and young peoples behaviour in accordance with the policies and procedures of the setting 2.1 Explain the benefits of actively promoting positive aspects of behaviour 3.5 Explain the sorts of behaviour or discipline problems that should be referred to others and to whom these should be referred 4.1 Recognise patterns and triggers which may lead to inappropriate behavioural responses and take action to pre-empt, divert or diffuse potential flash points. Answers: 1.1 Summarise the policies and procedures of the setting relevant to promoting children and young peoples positive behaviour ? The policies and procedures of setting relevant for promoting children and young peoples positive behavior are as follows: Behavior policy: It tells the guidelines on how the behavior of the pupils has to be managed. Code of conduct: It is a set of rules that the peoples should follow and how they should behave. Children are to be advised to strictly follow it (Angela et al, 2007). Rewarding: Acknowledging and rewardingchildren for their positive behavior helps to maintain the decorum. Punishment: punishingthe children for inappropriate behavior and charging a fine for the adults wrong behavior. Attendance: Making a rule that proper attendance is necessary for the institution or any setting helps in building up a positive lifestyle. Dealing with conflict and inappropriate behaviour: It would tell on how to handle the more difficult behaviors (Scott et al, 2008). Itis also important that pupils understand the behaviour policy of the setting so that they have a clear idea of how bad behaviour will be dealt with if they choose to go against rule or behave in an inappropriate manner. 1.2 Evaluate how the policies and procedures of the setting support children and young people to: a) feel safe: The policies are kept keeping the view that every single individual and child respected, considered equal and a friendly environment is made so as to make them feel safe. Punishment and no acceptance to wrong behavior also helps the people and the children to feel safe in the setting (Tincani, 2007). b) make a positive contribution: Rewarding and acknowledging the people and the children for their positive behavior is what makes a positive mind set and encourage the individuals to do more good deeds. c) develop social and emotional skills: Following up the behavioral guidelines and a code of conduct among everyone helps to develop the social skills by increasing positive communication (Walker et al, 2005). Attaining respect and encouragement from others and the settings helps in attaching emotionally with the environment and the people (Cancio Johnson, 2007). d) understand expectations and limits: The behavioral policy and the code of conduct explains the children and the people the fact that what quality of behavior is expected from them and also help them to understand their limits. It also tells what is allowed and what is not allowed and also the difference between right and wrong deeds and behaviour. 1.3 Explain the benefits of all staff consistently and fairly applying boundaries and rules for children and young peoples behaviour in accordance with the policies and procedures of the setting The benefits of all staff consistently and fairly applying boundaries and rules for children and young peoples behaviour in accordance with the policies and procedures of the setting are as follows: A peaceful and healthy environment encourages the staff to maintain the decorum of the setting and encourages children to follow them (Hawken Johnston, 2009). Sincerity and obedience among the children benefits the staff as they dont have to be after the children for everything (Sugai et al, 2000). No conflicts and no wrong behaviours are encouraged so the staff does not have to deal up with bad behaviors like mood swings. Positive behavior among the children helps the staff to be in the setting for a long time with a peace of mind. 2.1 Explain the benefits of actively promoting positive aspects of behaviour Positive behavior is linked to giving resect to others. The benefits is that it teaches to have a self control on oneself and to consider the feelings of others. It tells what kind of behavior is required by others and what kind of behavior is acceptable. It also tells how to build up positive social relationship with others by behaving appropriately. Positive behavior heals an individual to learn the basic principles of humanity. At the same side the positive behavior is continued among the children when they are awarded and praised in front of their friends and public (Stewart et al, 2005). Some more features of promoting positive behavior is that it also develops a sense of warmth, love and emotions between the individuals. If a child or an individual behaves in a positive way to others than the bond and attachment relation develops on its own between them. The benefit of positive behavior also lie in the fact it helps to know about ones expectation and limits and others too. The person who has a positive behavior benefits as the hope in them never dies so chances of success are even more. The individuals are also loved and resected by everyone in the society does development of a good self image is also an advantage (Koegal et al, 2011). 3.5 Explain the sorts of behaviour or discipline problems that should be referred to others and to whom these should be referred There are situations when the children do not show a positive behavior. There can be number of reasons for this like sometimes they are just trying to test of their limits. But on the same side it is the staffs duty to recognize the when the child is in need to be referred. The signs show that there is a need of extra support or not. The type of behaviors that are to be referred to others are as follows: When the child do any danger to himself or others. When the staff is itself dealing with a personal problem. When the situations are uncontrollable and the child is not at all listening. When an incident is serious enough to warrant the involvement of a senior member of staff. The situations decide what kind of referral is to be used and when (Tobin Sugai, 2005). The referral can be as support from another staff member. In some cases special support is required like a support of a supervisor, support from the staff who has already dealt with the same issue, a support from a senior management team if the situation is intolerable and cannot be controlled up in any way. In some situation parent support and guidance can also be required so as to promote positive behavior in the child at all times. 4.1 Recognise patterns and triggers which may lead to inappropriate behavioural responses and take action to pre-empt, divert or diffuse potential flash points Observation is the first thing that helps in recognizing the inappropriate behavioral responses. Like for example noticing any abnormal behavior with friends, not paying attention in studies or not interested to play out. These are some of the signs that tells the child is not behaving in a proper way. Observing the signs and the reason behind the abnormal behavior is also very important. For example if a child is fighting than what happened jus before that which has lead the child to behave in appropriately. In case of small kids diverting their minds is of most help. If a small kid is not behaving appropriately than diverting him/her in some other activity diverts their mind and they forget about the way they were behaving. In kids who are little grown ups sharing their feelings and guiding them towards the solution is what that helps to abolish inappropriate behaviors. Cueing: Cueing is a common behavior management technique. Choose one specific trigger to work on and then come up with some kind of hand signal or phrase that will serve as an alert to the child that the trigger is present. This allows you to make the child aware of the trigger subtly in social situations. Once you have alerted him, hell have the chance to self-correct, or in other words, respond using the new plan you came up with, with minimal help from you. Cueing works at home as well (Rhodges et al, 2011). References Angela Waguespack, Terrence Vaccaro Lauren Continere (2006). Functional Behavioral Assessment and Intervention with Emotional/Behaviorally Disordered Students: In Pursuit of State of the Art. International Journal of Behavioral Consultation and Therapy, 2 (4), 463474. [1 Cancio, E. Johnson, J.W. (2007). Level Systems Revisited: An Impact Tool For Educating Students with Emotional and Behavioral Disorders. International Journal of Behavioral Consultation and Therapy, 3 (4), 512527 Hawken, L.S. and Johnston, S.J. (2008). Preventing Severe Problem Behavior in Young Children: The Behavior Education Program. Journal of Early and Intensive Behavior Intervention, 4 (3), 599613. Koegel, L. K., Koegel, R. L. Dunlap, G.(2011) (Eds.), Positive Behavioral support: Including people with difficult behavior in the community (pp. 381-402). Baltimore: Paul H. Brookes Rhodes, Virginia; Stevens, Douglas and Hemmings, Annette (15 April 2011). "Creating Positive Culture in a New Urban High School". High School Journal. Spring 2011 94 (3): 8294. 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