Value Chain Model for PSU in Order to Receive Raw Materials from South Research Paper

Value Chain Model for PSU in Order to Receive Raw Materials from South Korea and China - Research Paper Example Having a shared vision enables the workers in all the locations to collaborate in delivering value. The process of receiving spare parts, storage, general inventory control, shipping scheduling should be managed with an aim of cutting any time delays. Immediately an order is registered, a process of simulation from the production plant should be initiated. 1.4 Operations. The assembling, packaging, equipment maintenance, product-testing as well as other activities must be streamlined with an aim of creating efficiency in delivering the final desired product. In fact, all necessary output measures should be aimed at enabling workflow as well as delivery performance to include dependable stock safety levels to avoid delays and understocking. This is where a forecast comes in to ensure the scheduling of end items. In reference to the activities needed to deliver goods to the market, the different locations need to share information as well as to operate in guidance by same policies so as to translate their cooperation into a synergetic relationship. Other areas of key concern are ordered fulfilment, the logistics involved in shipping as well as Material Requirements Planning or Distribution Requirements Planning system. By using a centralized in-formation model any demand changes will be detected well in advance and preemptive measures taken in advance. There need to be many resources committed to wooing buyers to purchase the cutting technology product. On top of that, how the distributors and dealers are selected goes a long way to determine whether sales targets will be achieved or not.  

Unit 5 Individual Project Biology Essay Example | Topics and Well Written Essays - 1250 words

Unit 5 Individual Project Biology - Essay Example The Dichotomous Key (Appendix B) was used to determine the taxonomic category (phylum or class) for each animal picture, and these categories written on Classification Column on the table. The phylum list (Appendix A) for each animal picture were also written in column one; and all steps on column two as used to arriving at the classification for each animal given. The cartilaginous Fish are in class chondricthyes for instance the rays and sharks. Their skeleton is made of cartilage and not the bone. They do not have the lungs and swim bladders. The placodermi fishes are precursors of these fish that are now extinct. They were the first fish to develop paired fins and jaws. (Don, & DeeAnn, 2005). 6. The three types of mammals based on how the young one develops are marsupials, monotremes, and placentals. The monotremes lay eggs; marsupials give birth to underdeveloped young ones and develop them in a pouch such as the koala and kangaroo (Mayr, & Bock, 2002). The placental mammals give birth to adequately mature young ones, feed them via the placenta until they are fully developed in a womb before they are born (Mayr, & Bock, 2002). An example is the humans. Dichotomous means â€Å"divided or cut into two parts.† A dichotomous key is a tool used by scientists to classify organisms into classification categories or taxa. The key is made up of a series of numbered couplets, and within each couplet are two opposing statements which you read, choosing the one that best fits the animal picture. To use the key, you always start at the first couplet (look for a 1 in the first column). Read the two couplet choices (labeled a and b in the second column), and consider them carefully. If you do not know the meaning of a word, as some of these terms are technical, look them up in a reference, a dictionary, or your textbook glossary, perhaps. Again, you

The Renovation of English Vocabulary from Old English to Modern Research Paper

The Renovation of English Vocabulary from Old English to Modern English - Research Paper Example In the transformation of English language from Old English to Modern English, crucial changes have taken place in vocabulary, spelling, and pronunciation which is illustrated by an analysis of these elements in ‘Canterbury Tales’ compared with Modern English equivalents. In the Text 81 from the ‘Canterbury Tales’ one finds several examples of the origins of the vocabulary and a comparison of the original Old English vocabulary and their Modern English equivalents proves how the vocabulary developed overages. The Friar’s Prologue in ‘Canterbury Tales’, for example, opens with the lines: â€Å"This worthy lymytour, this noble free, / He made always a manner louring chiere / Upon the somonour, but for honesty / No vileyns word as yet to him speak he.† (Freeborn) This can be read in the Modern English as follows: â€Å"This worthy limiter, this noble friar, / He turned always a lowering face, and dire, / Upon the summoner, but for cou rtesy / No rude and insolent word as yet spoke he.† (Freeborn) The changes or the developments in each of these items can be easily recognised by the readers and this progress in the vocabulary of the language reflects the general nature of English language which has developed over several periods. In conclusion, the history of English language establishes that the language progressed from Old English to Middle English to Early Modern English and the vocabulary is a major area of language in which variations are more readily noticeable over long stretches of time.

Electoral College System Essay Example for Free

Electoral College System Essay The Electoral College system is a part of the United States Constitution. It has been present since the creation of the nation. There has never been a United States presidential election not determined by the Electoral College system (Kuroda 127). In the first presidential election of 1789 George Washington was awarded 69 electoral votes to win his first term as the first president of the fledgling nation. The idea of eliminating what is seen as an archaic and unwieldy form of election has been considered for years, but what most politicians have found is that it is never easy to amend the United States Constitution, particularly in favor of an unknown. People believe they have a system, that while cumbersome and antiquated, still functions as the founding fathers intended it to do. With some of the founding fathers of the opinion that the average citizen was not well enough informed to make a logical or wise decision as to who should succeed to the highest office in the land, it was thought to be imminently better for a Congress to elect the president. When that idea was defeated, the proponents settled for having a group of unbound electors be sent to the capital each four years, and there decide for the people. Writing in the Federalist Papers, Alexander Hamilton said: It was desirable that the sense of the people should operate in the choice of the person to whom so important a trust was to be confided. This end will be answered by committing the right of making it, not to any pre-established body, but to men chosen by the people for the special purpose, and at the particular conjuncture. (par. 2) And still today, while the electors are faithful to the point that an unfaithful elector is an aberration, the fact remains that electors have options and can, if they wish, simply deny the will of the people (Archives. gov 1). Besides the fact that the nation has had presidential winners who did not win a majority of the popular vote, which in essence denies the will of the people, this system is maintained (Abbott and Levine 21). There is a need for, at the very least, a major over-haul of the system, and possibly a totally new approach, allowing for the direct election of the president by the popular vote of the American people. The arguments in favor of the Electoral College are specious today, particularly in regard to the people being informed enough to make a decision, and for that reason, as well as numerous others, the Electoral College should be discarded in favor of a system which better expresses the will of We the People. The present system has its advocates, and they make some good points in favor of not scraping the Electoral College. They rightly point out that such an act would not only be difficult, requiring a Constitutional amendment, necessitating a two-thirds majority of both house of Congress to agree, but also three-fourths of all the states would also have to acquiesce on the matter. They point out that in the past there have only been 27 amendments to this blueprint of government so well written by the nation’s founders. They also point out that some amendments have proven to be national disasters, such as Amendment 18. This system, they argue, has served the nation for over near 220 years and it simply is not wise to exchange a system which works for an unknown, which could result in chaos or even massive civil disturbance. It offers, they argue, both parity and equity to the smaller states, which would have virtually no voice in a direct election system. Then comes the question of what system would be better. There are several ideas being floated occasionally as trial balloons. The Congressional District method has been proposed. It comes with its own problems, however, and fails to address some of the more troubling aspects of the Electoral College system. This system proposes that each Congressional District be given one vote and allotting the two Senatorial votes as a bonus for the winner of the statewide popular vote. Maine and Nebraska currently use this method. First, this system does not correct one of the perceived flaws of the current system, which is the extraordinarily disproportionate weight given the vote of citizens of less populous states. Under the present system Wyoming is given one electoral vote per 165,000 citizens, while Texas is given one electoral vote per 652,000 citizens. This makes the vote of a Wyoming citizen worth four times that of a Texas citizen. Secondly the Congressional District proposal does not take into account the self-serving gerrymandering which tends to carve up American votes as if in a feudal system, making incumbents virtually bullet-proof, so to speak, and guaranteeing a vote for the party in power when the district was drawn. Frequently Joe Six-pack will grumble and insist that the election should be decided in a winner-take-all popular vote. This system, usually put forth as a â€Å"Direct Vote with Plurality Rule† has its good points and its bad. It harkens back to the days of the Greek city-states, when the citizens of Athens would all gather to directly vote for their candidate. Under this system the Electoral College would be eliminated, which would require the above-mentioned amendment to the United States Constitution, which could take years to effect. Simplistically, this system would award the presidency to the candidate with the most popular votes, irrespective of whether he or she garners a majority. This system would not prevent the spoiler-effect from occurring when third-party candidates dilute the vote of one major party candidate, allowing the other to move ahead in the popular vote. And, in theory, a wide field of candidates could dilute the vote to such an extent that a winner could be declared although only winning a small plurality, should the field be large enough. With this concern, and the necessity to amend the Constitution, there are surely better alternatives.

The bone disorders

The bone disorders Introduction There are many different types of bone disorders and these can have vast implications on a patient suffering from any particular one of these bone disorder. There 7 main categories of bone disorders listed below, each of which will be discussed in detail. Genetic (inherited) disorders, i.e. Achondroplasia, Osteogenesis imperfecta. Nutritional disorders, i.e. Rickets, Osteomalacia. Autoimmune disorders, i.e. Rheumotid Arthritis Degenerative disorders, i.e. Osteoarthritis. Bone tumours, i.e. Primary Bone Cancer, Secondary Bone Cancer. Hormonal disorders, i.e. Osteoporosis. Pagets disease. Genetic (inherited) disorders. Achondroplasia. Achondroplasia is genetic disorder and is the main type of short-limbed dwarfism that takes place in humans, occurring amongst 1 in 15,000 and 40,000 live births. It has been estimated that about 90% of cases of achondroplasia are sporadic, and on average, there is a rise of paternal age at the moment of conception of affected individuals (Vajo et al., 2000). The literal meaning of achondroplasia is without the formation of cartilage, and sufferers have difficulty with bone growth. Achondroplasia affects mainly long bones e.g. legs and arms. It is an Autosomal Dominant Gene Defect (ADGI), and leads to the conversion of cartilage into bone. It occurs when one of the 22 non-sex genes is mutated, and this mutated gene has now been identified to be located on chromosome 4, which is known to be the Fibroblast Growth Factor Receptor 3 (FGFR3). Symptoms; Achondroplasia is typically distinguished by the formation of a long, narrow trunk and short limbs. Some other usual symptoms of achondroplasia include hyperextensibilty of joints in particular at the knees and hands, however the rotation of the elbow is limited as well being unable to fully extend. Sufferers of Achondroplasia normally have a large head, short broad hands, and suffer from hypertonia (poor muscle tone). Spinal cord compression at the cervicalmedullary junction is another typical feature of achondroplasia patients (Horton et al., 2007). The location of the mutated gene associated with achondroplasia was mapped to chromosome 4p16.3 in 1994, and this was followed soon after by the identification of the heterozygous mutations of FGFR3 (Rousseau et al., 1994). It has been further discovered that children that have FGFR3 mutations, they parents generally do not have the FGFR3 mutation, and there has also been a strong association between advanced paternal age, in particular over 35 years of age. Diagnosis; Because the symptoms of achondroplasia are very distinguishable, the diagnosis at birth should not be a problem. However, it has been estimated that about 20% of individuals are not diagnosed with achondroplasia at birth (Trotter et al., 2005). A common method that has been employed and widely used for the diagnosis of achondroplasia is prenatal ultrasound. This method detects effected foetuses in the third trimester of pregnancy. The diagnosis of Achondroplasia can be carried out via CVS (Chronic Villus Sampling), followed by molecular gene tests. CVS is a test that is carried out before birth, in which cells are inspected. Molecular genetic testing is carried out in order to identify possible mutations. Treatment; There is no clear treatment for achondroplasia, and there are many tests that are ongoing in order to do find one. The use of human growth hormone has been proposed as a possible method of treatment. Tests have shown that there was an initial increase in growth rate of subjects with achondroplasia, nevertheless, the long-term benefits of such treatment have not been made clear, and many experts do not recommend it (Horton et al., 1992). In order to increase the stature of achondroplasia patients, surgical limb lengthening is another proposed method to help achondroplasia patients. The typical method compromises of different bones being broken, i.e. femur, tibiae, and humeri, after which orthopaedic appliances are used in order to carry out slow stretching during the healing process. Although this method increases the standing height of the patient, this method is also not recommended due to the many complications arising from it. These complications include, the need of repeated surgeries, wound infections and problems arising from the stretching of skeletal tissue such as blood vessels. Osteogenesis Imperfecta. Osteogenesis imperfecta is a bone disorder causing imperfect bone formation. It effects roughly 1/5,000 to 1/10,000 individuals (Sillence et al., 1979). It occurs as a result of a poor quality of collagen or a lack of collagen production, and can lead to fragile bones that are easily broken and have a low bone mass. Another distinguishable characteristic of osteogenesis imperfecta patients is an s-shaped spine that can eventually break. Osteogenesis imperfecta occurs as a result of mutations in the genes that encode the chains of type I collagen. Type I collagen is the main protein found in bone. Genetically inherited cases of osteogenesis imperfecta normally show very mild symptoms. However, spontaneous cases are often more severe. Symptoms; The symptoms of osteogenesis Imperfecta range in severity, from intrauterine fractures and perinatal lethality, to very mild fractures. Diagnosis; The diagnosis of osteogenesis imperfecta in individuals with a family history of the disease is rather simple, but more difficult in those that do not have a family history. Generally osteogenesis imperfecta is diagnosed clinically, and based on the physical symptoms associated with the disease Osteogenesis imperfecta can be diagnosed via a collagen biopsy test, which is a new method. This test is known to identify 90% of osteogenesis imperfecta cases. Ultrasound is another method that can be used for diagnosis, and can detect more severe types of Osteogenesis imperfecta, even at the foetus phase and also 16 weeks into pregnancy. Test such as those that include culturing cells, and observing the collagen produced can also be carried out, as well as using blood samples to examine mutations of the collagen manufacturing genes. Although these types of tests can be useful in the diagnosis of osteogenesis imperfecta to some extent, they are generally no more than 85% accurate. Treatment; Currently there is no known cure for osteogenesis imperfecta. However particular emphasis has been placed on prevention on injury and maintaining healthy bones particularly in younger children. Supplements of calcium and phosphorus help increase bone density. Also Biophosphates are used, and these are drugs that help decrease the rate of bone resorption. Biophosphates have been clearly shown to prevent bone fractures from occurring and also increasing the bone strength and density. Growth hormones has been previously proposed as a possible treatment for osteogenesis imperfecta (Kruse and Kuhlencordt, 1975). However this has been later dismissed, and although the use of growth hormone in combination with Biophosphates may be a useful treatment, this has not yet been tested. Metal bone plates are also used for patients with more severe fractures, and helps to strengthen and reduce fractures of the affected bones, mainly long bones e.g. arms and legs. Nutritional disorders. Rickets and Osteomalacia. Rickets is a nutritional bone disorder which is found in children. It is known to affect about 1 in 1000 children in the UK alone. A very similar disorder takes place amongst adults and this is known as osteomalacia. Both these disorders occur as a result of abnormal mineralisation (calcification) of bone and cartilage. The body transfers calcium and vitamins from the bone into the blood due to vitamin deficiency i.e. deficiency in Vitamin D and calcium. This demineralisation subsequently leads to bone deformity, and thus the bones become soft and very vulnerable to fractures. There are many reasons that cause vitamin deficiency that subsequently leads to rickets and osteomalacia. Some of which include nutritional deficiency (poor diet), poor lifestyle (lack of exercise), insufficient sunlight exposure (remaining indoors for long periods of time) and abnormal metabolism (liver and kidney disease, chronic renal failure etc) (de Menezes Filho et al., 2006). Another main cause of rickets in children is due to the baby receiving a lack of vitamin D in the womb from the mother who may also be deficient in vitamin D. Symptoms; Symptoms of rickets and osteomalacia include; Growth retardation. Deformities in the upper and lower limbs. Insufficient weight gain in children. High vulnerability to bone fractures. Bone pain. Muscle weakness. Pelvic flattening. Bowing legs. Defects in structure of teeth. Diagnosis; A physical examination will firstly help to identify bone deformities and multiple fractures. A medical history check can also help to identify a possible genetic link. The levels of parathyroid hormone and alkaline phosphate will increase in the blood as a result of deficiency in vitamin D and calcium. These hormones are responsible for the transfer of minerals and vitamins from the blood to the bone. This rise in the bloodstream is a major sign of rickets and osteomalacia, and blood tests carried out to see this elevated rise of these hormones is a good method for diagnosis. X-rays can also show the demineralisation of the bone and reveal any abnormal bone structures. Treatment; Replacing vitamin D, calcium, and other necessary minerals in patients with rickets and osteomalacia is very important, and is the main method of treatment. Babies that received a lack of vitamin D whilst in the womb of their mother, or a shortage from their mothers milk should be given vitamin drops, e.g. Abidec, to help increase their levels of vitamin D. Food rich in Vitamin D and calcium are highly advised, and offer a replacement for their deficiency. These types of food include oily fish (tuna, salmon herrings, mackerels), dairy products (milk, yoghurt), liver, Vitamin supplements can also be prescribed from a doctor. An injection of vitamin D (calciferol) is also available and can last up to a year before another injection is needed. Adequate exposure to sunlight is also highly recommended. Autoimmune disorders. Rheumatoid arthritis (RA). It has been estimated that at least 1 in 100 people suffer from RA, and that in the UK alone there are about 400,000- 500,000 sufferers. It is a chronic inflammatory disease mainly affecting synovial membrane, cartilage and bone. This then can lead to joint destruction, which is typically distinguished by gradual bone erosion, and is the main cause of disability in RA. RA causes the immune system to start producing antibodies, which attack the lining of joints (synovium), and tissues (tendons), and so thus resulting in inflammation and swelling. In response to this, the body releases a special synovium thickening chemical which causes the joint to wear away and loose its shape, and eventually the joint is completely destroyed. RA is also systemic and can spread to other tissues and other parts of the body causing more problems mainly in the hands, feet and spine. In very severe cases the disease can spread to organs and this can be very critical. RA does not occur at a particular age group, and the disorder can develop at any age in sufferers lifetime. However, more commonly RA occurs in patients that are between the ages of 30 to 60 years old. The causes of RA are still relatively unknown, however that have been several theories involving possible genes that can cause RA (Barton and Worthington, 2009). RA may also occur as a result of pollution (bacteria, fungi, viruses). Symptoms; Symptoms of RA include; Swelling of joints. Stiffness, particularly early in the morning. Inflammation. Formation of rheumatoid nodules, which appear on hands, feet and elbows. Flu like symptoms such as fever. Weight loss. Diagnosis; The diagnosis of RA is rather difficult, due to the fact that the main symptoms of RA inflammation and joint stiffness/swelling, and these symptoms can be commonly associated with other diseases/disorders. A full family history is looked at first in order to establish any hereditary traits of RA in the patient. Imaging techniques such as X-rays, CT scans and ultrasound can used to look at rheumatic erosion (the disappearance of bones/joints). However, it can be difficult to diagnose RA in the early stages of the disorder, as there may not be any physical changes during these stages. The cytokines TNF (tumour necrosis factor) and IL-1 (Interlukin-1) are responsible for further inflammation which occurs in people that suffer from RA. Both of these cytokines are present in the joint of people with RA, and checking for the presence of these cytokines at joints is a method used to diagnose RA. ESR (erythrocyte sedimentation rate) is also another blood test that can be used to diagnose RA. It is a measure of the rate in which red blood precipitate in a period of 1 hour, and is a non specific measure of inflammation. The CRP test (C-reactive protein test) is the second most popular diagnosis test for RA. In response to inflammation of tendon/ligaments, the liver produces C-reactive proteins, and this test is used to detect the presence of these proteins in the blood. The antibody RF (Rheumatoid factor) is present in the blood of sufferers of RA. Therefore blood tests to identify the presence of this antibody in the blood, 8 out of 10 times will diagnose a person that is suffering from RA. Treatment; Currently there is no clear treatment for RA, however there a few drugs available that either help relieve some of the symptoms, or to help modify the disorder. Pain killers such as paracetamol and ibuprofen can help relieve some of the symptoms of RA. NSAIDs (non-steroidal anti-inflammatory drugs) are also a set of pain killers e.g. diclofenac, ibuprofen and naproxen, and help to control joint pain and stiffness. Although these drugs help with the symptoms of RA they do not directly impede the development of RA. Furthermore, there are many common side effects associated with NSAIDs including diarrhoea, nausea, increased risk of myocardial infarction etc. Disease modifying anti-arthritic/antirhumatic drugs (DMARDS) are drugs that function by blocking the affect of certain chemicals i.e. TNF following the damage of bone, joints, tendons and ligaments. These drugs not only ease the pain and stiffness related to RA, but also slow the progression of the condition. Maintaining a healthy lifestyle for an individual suffering from RA is also vital as it reduces the chances of further complications arising from the disease. There are also many therapies e.g. acupuncture, hydrotherapy, and also arthroplasty which can significantly help with the pain and joint stiffness linked to the disorder. Degenerative disorders. Osteoarthritis (OA). Osteoarthritis is an age-related disease that ultimately has an effect on each individual, who live onto they senior years (Wong and Carter, 2003). The pain associated with osteoarthritis typically emerges from the degeneration of the cartilage between the joints, as a result of primary osteoarthritis, or from trauma bringing about the loss of cartilage (Temenoff and Mikos, 2000). Given that cartilage demonstrates a poor ability to self-repair, these injuries are sustained for years and can ultimately bring about further degeneration (secondary osteoarthritis) (ODriscoll, 1998). The degeneration of cartilage causes bone ends to become exposed, and the deposition of new osseous tissue on the bone ends. This also reduces the space in the joint cavity and limits movement (Gerard J. Tortora, 2007). The underlying bone also forms osteophytes (spikes) which grow outwards due to the bone compensating for the loss of cartilage, and this hinders joint movement and causes pain. It has been estimated that roughly 36 million Americans are diagnosed with this form of arthritis (Temenoff and Mikos, 2000). Osteoarthritis is also the main reaso n as to why many individuals undergo hip and knee replacement surgery (Wilson et al., 2005), and is also the main cause of mobility impairment in elder individuals (Buckwalter, 1997). Symptoms; Acute pain causing stiffness and lack of joint movement is the main symptom of OA. The capsule surrounding joints become bigger due to inflammation and this reduces mobility, and thus muscles at the joint become weaker. Other symptoms include spasm and contractions in the tendons; accumulation of fluid at joints, muscle weakness, and hardy bone enlargements in small joints i.e. fingers and toes. Diagnosis; There is no single test used to diagnose OA. A physical examination can show a lack of mobility, joint weakness and swelling. X-rays can show the loss of joint space and in extreme cases the presence of osteophytes. Treatment; There is advanced research going into ways to engineer cartilage to help patients suffering from OA, although a major breakthrough has yet been developed. Instead a healthy lifestyle i.e. loss of weight and exercise is highly advised Sufferers are advised to exercise the affected area as this will enable better support for affected joints and strengthen the muscles surrounding the joint. This also helps in increasing the mobility of the joints, balance and posture. Drugs such as NSAIDs (non-steroidal anti-inflammatory drugs) i.e. ibuprofen can help in relieving pain and reducing inflammation. However the long term use of these types of drugs can cause many adverse reactions. Bone tumours. A Bone tumour is the neoplastic growth of tissue in bone i.e. cells in tissue continually dividing resulting in the formation of the tumour, and can be benign or malignant. This tumour can further spread throughout the body via the lymph system. The lymph system contains lymphocytes and phagocytes, and a further function of the lymph system is to remove worn out red blood cells. There are two main categories of bone tumours, primary bone tumours and secondary bone tumours. Primary bone tumours can be localised or can spread (malignant), and these bone tumours derive from within the tissue. Primary tumours can be further divided into benign tumours and cancer. Secondary bone tumours derive from other tumours from a different part of the body and spread to the tissue via the blood. The mutation of the P53 gene which suppresses bone tumour is thought to responsible for the formation of bone tumours; however the exact cause is still not fully known. There are many different types of bone tumours, of which the most common are listed below, including symptoms, diagnosis and treatments. Osteosarcoma- This is the most common type of bone tumour, and as well as Ewings syndrome (see below), is the most aggressive type of bone tumour. It affects people at an early age (5-25years), and is rare in people of above the age of 30. Osteosarcoma is a malignant tumour and eventually will spread throughout the body. It is also known to start in the cavities within the bone, and is it affects long bones mainly the knee. Osteosarcoma is diagnosed via examination and imaging techniques such as MRI or CT scan. Osteosarcoma if usually treated by surgery and chemotherapy before and after the surgery. Ewings Sarcoma- Just like Osteosarcoma, Ewings sarcoma affects people at a young age (5-15 years), and also the survival rate up to 3 years is a 60% chance. Ewings sarcoma in mainly found in the lower extremity, than the upper extremity (Eggli et al., 1993) Some of the symptoms of Ewings disorder include pain and swelling, warmth of the local area, and the appearance of onion skin. Ewings disorder can be diagnosed via MRI and CT scans. Treatments of Ewings disorder include surgery, radiation and multi-drug chemotherapy (Eggli et al., 1993). Chondrosarcoma- This bone tumour affects the chondrocytes of cartilage tissue and subsequently, the tissue eventually becomes cancerous. Chondrosarcoma can occur at any age, and this tumour grows slowly and normally without any pain. Lymphoma- Lymphoma is cancer of lymphatic cells, and usually begins in the lymph node, but can also form in the bones. Multiple Myeloma- This bone tumour occurs as a result of bone marrow cells becoming cancerous and can cause osteolytic bone damage. It usually occurs in people above the age of fifty five, and men are twice more likely to get it than women. The main symptom of multiple myeloma is pain, as well as normochromic anemia, spinal cord compression and renal insufficiency. Multiple myeloma can be diagnosed via MRI and CT scans. Chemotherapy, bone marrow transplant as well as Bisphosphonate drugs are some of the main treatments for multiple myeloma. Osteroid Osteoma- This tumour occurs as a result of the matrix of bone becoming cancerous. It normally occurs twice as often in males than females. It more commonly takes place in the proximal femur, then mainly in the tibia, followed by posterior elements of the spine and the humerus (Bloem and Kroon, 1993). Common symptoms include dull pain which gets worse during the night, an increase in skin temperature, increased sweating and abnormal growth. Radiological scans and CT scans are common methods for diagnosis. Non-steroidal anti-inflammatory drugs are given as part of the treatment for osteroid osteoma as well surgical removal. Osteoblastoma- Osteoblastoma is a benign tumour in bone tissue and occurs when osteoblast cells become cancerous. It is mainly common in children and young adults. Pain and bone mass reduction are the main symptoms of osteoblastoma. Method of diagnosis for osteoblastoma includes x-rays, microscopic examination of osteoblast cells and a biopsy. Surgical removal of the tumour is a common treat for this bone tumour as well as cryosurgery, radiation and chemotherapy. Hormonal disorders. Osteoporosis. Osteoporosis results in bones becoming porous and these pores become bigger (2 times bigger) in cancellous cortical bone. It occurs as a result of a reduction in bone mineral density (bone mineralisation). It is a direct disease of the bone as compared to some of the other bone disorders mentioned above. During osteoporosis the rate of bone renewal is slower than bone breakdown and it commonly affects the hip, wrists and spine. It is estimated that over 3 million people in the UK alone suffer from osteoporosis. There are two main types of osteoporosis (Type I and Type II). Type I osteoporosis occurs mainly in females following menopause. Following menopause there is a deficiency in oestrogen and testosterone and this disorder is known as postmenopausal osteoporosis. Type II is mainly caused by a poor lifestyle i.e. excess smoking and drinking. This leads to a deficiency of calcium and vitamin D as a result of disorders of the intestine. The deficiency may also arise from kidney disorders caused by a poor diet (too much fast foods and fizzy drinks) and excess alcohol consumption. Also people continuously taking drugs mainly corticosteroid drugs will have a loss of bone density. Symptoms; Osteoporosis does not have any specific symptoms; however its main outcome is an increased risk of bone fractures and breaks, and also an increased risk of falling due to fractures of the wrist, spine and hip. Diagnosis Bone mineral density (BMD) test to measure bone mineral density was the first test used to diagnose osteoporosis. There are many different types of BMD tests, the most common being quantitative ultrasound. This is a very good method for diagnosis and is also a much safer approach than x-rays and radiography, which can also be used to diagnose osteoporosis. Blood tests to identify deficiencies in calcium and vitamin D are a further method for diagnosis. Treatments; HRT (Hormone Replacement Therapy) was initially used to treat postmenopausal osteoporosis, however its used was later stopped due to its many side effects e.g. breast cancer, blood clotting, stroke etc. Bisphosphonates can be used to treat osteoporosis and it functions by slowing down the breakdown of bone, in order for the body to cope with bone renewal. Bisphosphonate intolerancy was then later discovered in 20 % of people. Calcitonin drugs are another type of drug used to treat osteoporosis. Calcitonin is produced naturally in the thyroid gland, and calcitonin drugs work by directly inhibiting osteoclast activity. Calcitonin is also found naturally in salmon. Strontium Renelate is another drug that can be used and helps to promote bone renewal. Calcium and vitamin D supplements also help to slow down osteoporosis. Exercise is also highly advised for osteoporosis sufferers and has been shown to maintain or increase bone mineral density especially in postmenopausal women. Pagets disease. Pagets disease is a bone disorder associated with a disorder in bone remodelling, and affects 10% of elderly people (Barker et al., 1980). Furthermore it is more prominent in males than females. In Pagets disease there is an increase in bone remodelling which is also disorganised, and this caused by a primary abnormality of osteoclast cells (Hosking et al., 1996). The bone turnover is increased by 40%, and in addition, bone is grown in areas where bone is not needed and removed from areas where bone is required. Pagets disease is now referred to as osteoclast pagetic disease. In the disorder, the osteoclasts which are bone cells responsible for the removal of bone are targeted. Over a period of time osteoblast activity subsequently increases in response to osteoclast activity, and helps in forming new bone. However, the new bone that is formed is a lot larger and thicker because of the very fast remodelling process, but critically the interior parts of the bone are porous, and a lot more fragile and tender. This therefore makes the bone more venerable to fractures and breaks. Below is an illustration of a particular deformity associated with Pagets disease sufferers (see Figure 2.) Symptoms/complications; Joint pain and bone paint are common symptoms associated with Pagets disease. As the disease progresses the swelling and expansion of the bone leads to the expanding bone becoming weaker. Also the initial symptoms of Pagets disease are not clear but do become clearer over time as the disorder develops. Fractures of long bones e.g. tibia, femur, pelvis, spine, skull are common symptoms of Pagets disease as well as skeletal deformity. Arthritis is a common complication which arises from Pagets disease and occurs mainly in the proximal ends of long bones. A further complication of Pagets disease is Gout. Gout arises from the excessive production of uric acid and salts leading to gouting arthritis, which is a disease of uric acid metabolism. The build up of uric acid and salts in the bloodstream leads to accumulation at the bone joints/cartilage which then causes kidney stones. Bone tumours, and in particular cancellous bone tumour can arise as a result of gout. The dysregulation of bone can also cause an increase in blood circulation and can consequently bring about heart failure. Compression of nerves is also seen in sufferers of Pagets disease and is caused by bone expansion and this brings about complications in movement. Also nerve compression in the skull brings about a loss of hearing and vision. Diagnosis; X-rays is a very clear method to help detect bone expansion, bone loss and bone deformity. Alkaline phosphate which is a by-product of any type of bone disease/disorder is present in the bloodstream, and so blood test can help to identify the presence of these. Treatment; Bisphosphonates and calcitonin are common drugs used to treat Pagets disease. These drugs bind to osteoclast cells and increase their activity, thus reducing their breakdown, and reabsorption of bone into the bloodstream. Pain killers can also be taken to help ease bone pain and neuralgic pain. It is also advised that Pagets disease sufferers should receive adequate sunshine, adequate amounts of vitamin D, and maintain a healthy lifestyle i.e. healthy diet and regular exercise. References Barker, D.J., Chamberlain, A.T., Guyer, P.B., and Gardner, M.J. (1980). Pagets disease of bone: the Lancashire focus. Br Med J 280, 1105-1107. Barton, A., and Worthington, J. (2009). Genetic susceptibility to rheumatoid arthritis: an emerging picture. Arthritis Rheum 61, 1441-1446. Bloem, J.L., and Kroon, H.M. (1993). Osseous lesions. Radiol Clin North Am 31, 261-278. Buckwalter, J.A.a.H.J.M. (1997). Articular Cartilage. Part II: Degeneration and Osteoarthrosis, Repair, Regeneration, and Transplantation. Journal of Bone and Joint Surgery, 612-632. de Menezes Filho, H., de Castro, L.C., and Damiani, D. (2006). Hypophosphatemic rickets and osteomalacia. Arq Bras Endocrinol Metabol 50, 802-813. Eggli, K.D., Quiogue, T., and Moser, R.P., Jr. (1993). Ewings sarcoma. Radiol Clin North Am 31, 325-337. Gerard J. Tortora, B.D. (2007). Principles of Anatomy Physiology 11th Edition Binder Ready Version, 11 edn (John Wiley Sons, 2007). Horton, W.A., Hall, J.G., and Hecht, J.T. (2007). Achondroplasia. Lancet 370, 162-172. Horton, W.A., Hecht, J.T., Hood, O.J., Marshall, R.N., Moore, W.V., and Hollowell, J.G. (1992). Growth hormone therapy in achondroplasia. Am J Med Genet 42, 667-670. Hosking, D., Meunier, P.J., Ringe, J.D., Reginster, J.Y., and Gennari, C. (1996). Pagets disease of bone: diagnosis and management. BMJ 312, 491-494. Kruse, H.P., and Kuhlencordt, F. (1975). On an attempt to treat primary and secondary osteoporosis with human growth hormone. Horm Metab Res 7, 488-491. ODriscoll, S.W. (1998). The healing and regeneration of articular cartilage. J Bone Joint Surg Am 80, 1795-1812. Rousseau, F., Bonaventure, J., Legeai-Mallet, L., Pelet, A., Rozet, J.M., Maroteaux, P., Le Merrer, M., and Munnich, A. (1994). Mutations in the gene encoding fibroblast growth factor receptor-3 in achondroplasia. Nature 371, 252-254. Sillence, D.O., Senn, A., and Danks, D.M. (1979). Genetic heterogeneity in osteogenesis imperfecta. J Med Genet 16, 101-116. Temenoff, J.S., and Mikos, A.G. (2000). Review: tissue engineering for regeneration of articular cartilage. Biomaterials 21, 431-440. Trotter, T.L., Hall, J.G., and American Academy of Pediatrics Committee on, G. (2005). Health supervision for children with achondroplasia. Pediatrics 116, 771-783.

Risks and Benefits of Estrogen plus Progestin in Healthy Postmenopausal

For reasons both practical and political, women’s health has long been neglected as a field of study. This study by the Women’s Health Initiative is the largest investigation of a pertinent women’s issue ever, with 161,809 post-menopausal women enrolled from 1993 to 1998. Designed in the early part of the 1990s, this study consisted several trials, among them low-fat dietary patterns, calcium and vitamin D supplement use, and hormone replacement therapy. The hormone replacement trial experienced such surprising and unpredicted results that the entire trial was stopped early. It was hypothesized that giving post-menopausal women a combination of estrogen and progesterone would prevent coronary heart disease. Thus, a coronary heart disease event such as a heart attack was considered the primary outcome, or stopping point. Intermediate markers were determined to be invasive breast cancer, stroke, pulmonary embolism, endometrial cancer, colorectal cancer, or hip fracture. Hormone replacement therapy has long been an accepted form of treatment for women with age-related diseases like osteoporosis. Thus, when the WHI realized that the women taking estrogen plus progesterone were experiencing 29% more coronary heart disease events (i.e. heart attacks), 41% more strokes, and 26% more breast cancer than those who were receiving the placebo, the study was terminated. While the group of women receiving hormones also experience 37% less colorectal cancer and lower hip fracture rates, it was determined that allowing the trial to run to its finish would not be beneficial overall and would in fact cause increasing harm for stroke, coronary heart disease, and breast cancer. Below is a list of things that were inv... ...nodes; or the cancer has spread to lymph nodes near the breastbone or to other tissues near the breast Stage IV – metastatic breast cancer where the cancer has spread outside the breast to other organs in the body Hormonal Treatments of Breast Cancer Pathologists examine the cancers in the breast for estrogen or progestin. If there are signs of either the patient may be eligible for certain drugs containing special hormones. There are also very uncommon side effects like blood clots, strokes, or uterine cancer that may scare patients from choosing to take it. Venous Thromboembolic Disease A clotting of the blood in the blood vessel associated with deep vein thrombosis and pulmonary embolism. Other Cancers Endometrial- cancer that originates in the endometrial lining of the uterus Colorectal- cancer of the colon or rectum

The Wifes Lament Essay -- Poet Wifes Lament Speaker

The Wife's Lament Over the years, there have been many interpretations of who the speaker of The Wife’s Lament could be. These range from very interesting ideas to ones that seem a little rough around the edges. It is obvious that no sure answer can be found due to the fact that whoever wrote this poem is dead and that the answer will always be in speculation even if it is correct. Hopefully, at the end of this quest I will be slightly more enlightened as to who the true speaker may really be. There are some things that we do know about this poem. It is most often referred to as an elegy because of the mood of mourning and regret. Upon further reading I discovered that this poem is like others of its time period. Many parallels can be seen between The Wife’s Lament and The Wanderer. The Wanderer is a poem about a man that is exiled due to war and details his miserable life in the wintry wilderness. Another poem that resembles The Wife’s Lament is Wulf and Eadwacer. In both of these poems, the speaker is interpreted to be a woman unlike other poems of the time. Wulf and Eadwacer is about a woman who has been involved with two men, the dreaded love-triangle. When the woman was separated from her lover, Wulf, she is taken into the comforting arms of another man, Eadwacer. This causes her much happiness but also pain over the lost love of Wulf. Thus the lament of this woman is very similar to the speaker in The Wife’s Lament. The various interpretations of The Wife’s Lament may argue on who the speaker is, but there is one thing that can not be denied. There is no doubt that this poem is about lamenting exile and the trials the speaker must face due to this exile. No matter who the speaker is, he/she is wroug... ... I think that anyone that reads this poem should be told about this interpretation so that they can at least consider it. The question of who is speaking in The Wife’s Lament will never be answered because there are too many facts that aren’t provided. It would have been wonderful if the poet would have stated straight away that the speaker was a woman or a goddess or any of the other possible people or things. The only thing that readers of this poem can do is take all of these interpretations into consideration and use them to form their own idea of who the speaker is. I am very glad that I was introduced to this work and that I had the possibility to examine the various arguments of who is speaking. I think that when reading any piece of literature it should be looked at in a similar fashion as trying to pick apart who is speaking in The Wife’s Lament.