Truman, The Ideal Man Essay Example For Students

Truman, The Ideal Man? Essay In the same motion as putting on his jacket Truman reaches for his suitcase. He walks through his perfect house nice, tidy and spacious. Exiting the front door he sees his neighbors across the road  Morning Truman, Morning, and in case I dont see ya good afternoon, good evening and goodnight.  The white picket fences run down the street further then the eye can see its a perfect street of perfect houses with perfect neighbors in a perfect world. This isnt one of your typical Jim Carey movies; its a Peter Weir (Director) masterpiece. Truman Burbank (Jim Carey) plays a middle class husband who lives in a world inside a world. He lives in a studio where everything is fake and everyone fakes who they are. He is married to a fake wife and works for a fake company. He is unaware that his life is broadcast around the world twenty-four hours a day seven days a week. The only thing real in his life is him and his emotions. We will write a custom essay on Truman, The Ideal Man? specifically for you for only $16.38 $13.9/page Order now The Truman show appears to be placed in a very definitive discourse The middle class, double income, one or no child discourse. The discourse is so obvious throughout the film cause it works on the stereotypical views that we all hold. Living in a beautiful neighborhood were everyone knows everyone and get along with no problems, the beautiful houses but not mansion that look alike to the one next door and the highways of white picket fences that bring a sense of purity to the whole place. This is all the features of a middle class family or couple. Its what everyone wants but little can have. The film boarders on being very much like a normal soapie it goes through the lives of a middle class family showing off there highs and lows and the riches they earn an excellent example would be Neighbors. Neighbors focuses on middle class families living on Ramsey Street and just like the Truman show shows each and every part of there lives everyday. A movie duplicate of the Truman show would be American Beauty. The main character lives in a white picket world, he defies his reality by escaping what everyone else has set for him and his life. All this links give a deeper look into a middle class life and how its always controlled by an outer factor. The obvious foregrounding present is the White picket fence world a perfect world with everything that we all want, stability, nice jobs, nice house and nice neighborhood. The whats privileged is what we dont see the reality of the whole thing the crime, the homeless, the problems families face its all not shown in the light, all kept away to make it a happy lifestyle with not a problem in the world. In the crucial scene, which also happens to be one of the last scenes of the film, Truman defies his reality and finally comes to the end of his search for meaning.  Truman literally sails to the end of his world finding out the real truth behind his life when he finally gets to talk to Christof (Ed Harris) the creator of the Truman Show. The music and sound play a large part in the emotional side of the film. When Truman touches the wall of stadium and starts punching it all you can hear is the music and no sound of crying or pounding. This allows the audience to reflect on what is happening and to make up there own emotions. The camera work in relation to where Truman is standing is always looking down at him to signify that when Christof speaks that he is a higher being living up to his name of Christ_of Truman. The lighting also helps in this cause as its bright and a beautiful day to represent the beginning of a new life, in this case Trumans new life in the real world. The dialogue in this scene is where most people finally find out the truth behind the whole film: .u87da81a82d64b5b8ebef93ee8162e0f1 , .u87da81a82d64b5b8ebef93ee8162e0f1 .postImageUrl , .u87da81a82d64b5b8ebef93ee8162e0f1 .centered-text-area { min-height: 80px; position: relative; } .u87da81a82d64b5b8ebef93ee8162e0f1 , .u87da81a82d64b5b8ebef93ee8162e0f1:hover , .u87da81a82d64b5b8ebef93ee8162e0f1:visited , .u87da81a82d64b5b8ebef93ee8162e0f1:active { border:0!important; } .u87da81a82d64b5b8ebef93ee8162e0f1 .clearfix:after { content: ""; display: table; clear: both; } .u87da81a82d64b5b8ebef93ee8162e0f1 { display: block; transition: background-color 250ms; webkit-transition: background-color 250ms; width: 100%; opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #95A5A6; } .u87da81a82d64b5b8ebef93ee8162e0f1:active , .u87da81a82d64b5b8ebef93ee8162e0f1:hover { opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #2C3E50; } .u87da81a82d64b5b8ebef93ee8162e0f1 .centered-text-area { width: 100%; position: relative ; } .u87da81a82d64b5b8ebef93ee8162e0f1 .ctaText { border-bottom: 0 solid #fff; color: #2980B9; font-size: 16px; font-weight: bold; margin: 0; padding: 0; text-decoration: underline; } .u87da81a82d64b5b8ebef93ee8162e0f1 .postTitle { color: #FFFFFF; font-size: 16px; font-weight: 600; margin: 0; padding: 0; width: 100%; } .u87da81a82d64b5b8ebef93ee8162e0f1 .ctaButton { background-color: #7F8C8D!important; color: #2980B9; border: none; border-radius: 3px; box-shadow: none; font-size: 14px; font-weight: bold; line-height: 26px; moz-border-radius: 3px; text-align: center; text-decoration: none; text-shadow: none; width: 80px; min-height: 80px; background: url(https://artscolumbia.org/wp-content/plugins/intelly-related-posts/assets/images/simple-arrow.png)no-repeat; position: absolute; right: 0; top: 0; } .u87da81a82d64b5b8ebef93ee8162e0f1:hover .ctaButton { background-color: #34495E!important; } .u87da81a82d64b5b8ebef93ee8162e0f1 .centered-text { display: table; height: 80px; padding-left : 18px; top: 0; } .u87da81a82d64b5b8ebef93ee8162e0f1 .u87da81a82d64b5b8ebef93ee8162e0f1-content { display: table-cell; margin: 0; padding: 0; padding-right: 108px; position: relative; vertical-align: middle; width: 100%; } .u87da81a82d64b5b8ebef93ee8162e0f1:after { content: ""; display: block; clear: both; } READ: Christian symbolism, especially images that refer to the crucifixion of Christ, is present throughout The Old Man and the Sea EssayIam the creator of a TV show that gives hope, joy and inspiration to millions  and Truman finally finds out the truth about himself:  Was nothing real?  You were real thats what made you so good to watch. Listen to me Truman theres no more truth out there then there is in the world I created for you. Same lies, same deceit but in my world you have nothing to fear. I know you better then you know yourself. The whole film runs around lies and deceit wrapped up in a pretty cover of a white picket fenced world. The world couldnt exist for long as it was too perfect and in time it all fell apart. We all want to have a double income family, live in a beautiful house, get along with our neighbors but for Truman that wasnt enough he wanted everything else that came along with life, the problems and pains. So when the end drew nearer he got what he wanted in one way and the other.

Difference Between Celsius and Centigrade

Difference Between Celsius and Centigrade Depending on how old you are, you might read 38 °C as 38 degrees Celsius or 38 degrees centigrade. Why are there two names for  °C and whats the difference? Heres the answer: Celsius and centigrade are two names for essentially the same temperature scale (with slight differences). The centigrade scale is divided into degrees based on dividing the temperature between which water freezes and boils into 100 equal gradients or degrees. The word centigrade comes from centi- for 100 and grade for gradients. The centigrade scale was introduced in 1744 and remained the primary scale of temperature until 1948. In 1948 the CGPM (Conference General des Poids et Measures) decided to standardize several units of measurement, including the temperature scale. Since the grade was in use as a unit (including the centigrade), a new name was chosen for the temperature scale: Celsius. Key Takeaways: Celsius vs. Centigrade The Celsius scale is a type of centigrade scale.A centigrade scale has 100 degrees between the freezing and boiling points of water.The original Celsius scale actually had a boiling point of 0 degrees and freezing point of 100 degrees. It ran in the opposite direction of the modern scale! The Celsius scale remains a centigrade scale in which there are 100 degrees from the freezing point (0 °C) and boiling point (100 °C) of water, though the size of the degree has been more precisely defined. A degree Celsius (or a Kelvin) is what you get when divide the thermodynamic range between absolute zero and the triple point of a specific type of water into 273.16 equal parts. There is a 0.01 °C difference between the triple point of water and the freezing point of water at standard pressure. Interesting Facts About Celsius and Centigrade The temperature scale created by Anders Celsius in 1742 was actually the reverse of the modern Celsius scale. Celsius original scale had water boil at 0 degrees and freeze at 100 degrees. Jean-Pierre Christin independently proposed at a temperature scale with zero at the freezing point of water and 100 was the boiling point (1743). Celsius original scale was reversed by Carolus Linnaeus in 1744, the year in which Celsius died. The centigrade scale was confusing because centigrade was also the Spanish and French term for a unit of angular measurement equal to 1/100 of a right angle. When the scale was extended from 0 to 100 degrees for temperature, centigrade was more properly hectograde. The public was largely unaffected by the confusion. Even though the degree Celsius was adopted by international committees in 1948, weather forecasts issued by the BBC continued to use degrees centigrade until February 1985!

Technology and culture class Essay Example | Topics and Well Written Essays - 250 words - 1

Technology and culture class - Essay Example Still, Ullman feels that man is not able to live without computers, and expresses her love for the programmer’s world. Bill Joy, in his book, writes that technology has endangered human species though the introduction of robotics, genetic engineering, and nanotechnology. Like Ullman, Joy has also stated the repercussions of letting machines do all the work, since it will lead to humans not doing any work in future, and all decisions will be made by machines. This brings human beings at mercy of machines. He admits that since machine made decisions are and will continue to be better that human decisions, man will continue to rely on machines, which is fatal for man’s independence in the long run. So, we see that both Ullman and Joy have talked about repercussions of computers, while admitting to their usefulness at the same time; but unlike Ullman, Joy has quoted works of famous people to support his argument, as he thinks that his argument relates to a minority of

Normalization of Deviance CJ403 WK 6 Research Paper

Normalization of Deviance CJ403 WK 6 - Research Paper Example Vaughan cited the space shuttle Challenger disaster as an example. It led to the loss of 7 crew members because of the failure of the vehicle’s O-ring seal. There were already apparent flaws regarding its design in the early stages of the project. The first time that it was damaged, experts found a way to repair it. However, intermittent failures occurred in the testing stages. Besides the evident danger, the engineers decided that the Challenger was ready to be launched with â€Å"acceptable risk†. Then, after it fragmented 73 seconds into its flight, they were completely staggered. Basing on the aforementioned discussions, both the offender and the organization share the responsibilities. Using the Challenger example, the engineers on the project should have been sensitive enough while the observers and other individuals in NASA should have pointed out the obvious concerns. Since the offender is mostly unaware of the gravity of the situation, the organization must take aggressive measures. Hence, stopping the normalization of deviance is quite important in preventing mishaps. Astronaut Mullane (2009) specifically identifies several ways on how to deal with this phenomenon. It is significant to be acquainted with one’s susceptibility to it. Furthermore, planning the work and working the plan must be a religion. It is also valuable to contemplate on one’s instincts and to review past mistakes as well as near-misses. In general, the normalization of deviance has negative effects. If left unchecked, sizeable losses may ensue. Thus, individuals must be vigilant in addressing this social concern. Those who are affected must be wise. And those who are uninvolved must be courageous enough to point out the

Entrepreneurial Innovations Research Paper Example | Topics and Well Written Essays - 750 words

Entrepreneurial Innovations - Research Paper Example In addition, the wide-ranging availability of the Internet for performing business-related tasks of the businesses, sellers, and buyers is the primary reason behind the development of electronic commerce (or simply e-commerce). Actually, â€Å"electronic commerce is the method of selling and purchasing services and goods and products performed electronically by means of computerized business transactions over the Internet, networks, and other digital technologies† (Laudon & Laudon, 1999, p. 25; Stair & Reynolds, 2003, p. 19). There are different kinds of innovations in the context of IT, which can be implemented by an organization to upgrade their business processes. For instance, an organization can automate their business process, implement an e-commerce portal or use the Internet for marketing strategies and so on. Innovation in the context of organizational change also plays a significant function in the business organizations. No matter, whether a business organization is going to formulate or launch a new product, or going to introduce a new service, or going to invent and put into practice a technological invention that can change the business processes or a new management tool or technique, innovation, and organizational change helps the business organization develop and put into operation a business strategy and infrastructure. In fact, many business organizations invest a higher proportion of their finances in forming and implementing an innovation strategy than others.  

Leukopenia And Leukemia Risk Factors Biology Essay

Leukopenia And Leukemia Risk Factors Biology Essay A clinical condition, known as leukopenia occasionally occurs in which the bone marrow produces very few white blood cells, leaving the body unprotected against many bacteria and other agents that might invade the tissues. Normally, the human body lives in symbiosis with many bacteria, because all the mucous membranes of the body are constantly exposed to large numbers of bacteria. The mouth almost always contains various spirochetal, pneumococcal, and streptococcal bacteria, and these same bacteria are present to a lesser extent in the entire respiratory tract. The distal gastrointestinal tract is especially loaded with colon bacilli. Furthermore, one can always find bacteria on the surfaces of the eyes, urethra, and vagina. Any decrease in the number of white blood cells immediately allows invasion of adjacent tissues by bacteria that are already present. Within 2 days after the bone marrow stops producing white blood cells, ulcers may appear in the mouth and colon, or the person might develop some form of severe respiratory infection. Bacteria from the ulcers rapidly invade surrounding tissues and the blood. Without treatment, death often ensues in less than a week after acute total leukopenia begins. Irradiation of the body by x-rays or gamma rays, or exposure to drugs and chemicals that contain benzene or anthracene nuclei, is likely to cause aplasia of the bone marrow. Indeed, some common drugs, such as chloramphenicol (an antibiotic), thiouracil (used to treat thyrotoxicosis), and even various barbiturate hypnotics, on very rare occasions cause leukopenia, thus setting off the entire infectious sequence of this malady. After moderate irradiation injury to the bone marrow, some stem cells, myeloblasts, and hemocytoblasts may remain undestroyed in the marrow and are capable of regenerating the bone marrow, provided sufficient time is available. A patient properly treated with transfusions, plus antibiotics and other drugs to ward off infection, usually develops enough new bone marrow within weeks to months for blood cell concentrations to return to normal. Leukemia Leukemia is a cancer of one class of white blood cells in the bone marrow, which results in the proliferation of that cell type to the exclusion of other types. Leukemia appears to be a clonal disorder, meaning one abnormal cancerous cell proliferates without control, producing an abnormal group of daughter cells. These cells prevent other blood cells in the bone marrow from developing normally, causing them to accumulate in the marrow. Because of these factors, leukemia is called an accumulation and a clonal disorder. Eventually, leukemic cells take over the bone marrow. This reduces blood levels of all nonleukemic cells, causing the many generalized symptoms of leukemia. Types of Leukemia Leukemia is described as acute or chronic, depending on the suddenness of appearance and how well differentiated the cancerous cells are. The cells of acute leukemia are poorly differentiated, whereas those of chronic leukemia are usually well differentiated. Leukemia is also described based on the proliferating cell type. For instance, acute lymphoblastic leukemia, the most common childhood leukemia, describes a cancer of a primitive lymphocyte cell line. Granulocytic leukemias are leukemias of the eosinophils, neutrophils, or basophils. Leukemia in adults is usually chronic lymphocytic or acute myeloblastic. Long-term survival rates for leukemia depend on the involved cell type, but range to more than 75% for childhood acute lymphocytic leukemia, which is a remarkable statistic for what was once a nearly always fatal disease. Risk Factors for Developing Leukemia Risk factors for leukemia include a genetic predisposition coupled with a known or unknown initiator (mutating) event. Siblings of children with leukemia are 2 to 4 times more likely to develop the disease than other children. Certain abnormal chromosomes are seen in a high percentage of patients with leukemia. Likewise, individuals with certain chromosomal abnormalities, including Down syndrome, have an increased risk of developing leukemia. Exposures to radiation, some drugs that depress the bone marrow, and various chemotherapeutic agents have been suggested to increase the risk of leukemia. Environmental agents such as pesticides and certain viral infections also have been implicated. Previous illness with a variety of diseases associated with hematopoiesis (blood cell production) has been shown to increase the risk of leukemia. These diseases include Hodgkin lymphoma, multiple myeloma, polycythemia vera, sideroblastic anemia, and myelodysplastic syndromes. Chronic leukemia may sometimes transform into acute leukemia. Clinical Manifestations Acute leukemia has marked clinical manifestations. Chronic leukemia progresses slowly and may have few symptoms until advanced. Pallor and fatigue from anemia. Frequent infections caused by a decrease in white blood cells. Bleeding and bruising caused by thrombocytopenia and coagulation disorders. Bone pain caused by accumulation of cells in the marrow, which leads to increased pressure and cell death. Unlike growing pains, bone pain related to leukemia is usually progressive. Weight loss caused by poor appetite and increased caloric consumption by neoplastic cells. Lymphadenopathy, splenomegaly, and hepatomegaly caused by leukemic cell infiltration of these lymphoid organs may develop. Central nervous system symptoms may occur. Diagnostic Tools Laboratory findings include alterations in specific blood cell counts, with overall elevation or deficiency in white blood cell count variable, depending on the type of cell affected. Bone marrow tests demonstrate clonal proliferation and blood cell accumulation. Cerebral spinal fluid is examined to rule out central nervous system involvement. Complications Children who survive leukemia have an increased risk of developing a new malignancy later on in life when compared to children who have never had leukemia, most likely related to the aggressiveness of chemotherapeutic (or radiological) regimens. Treatment regimens, including bone marrow transplant, are associated with temporary bone marrow depression, and increase the risk of developing a severe infection that could lead to death. Even with successful treatment and remission, leukemic cells may still persist, suggesting residual disease. Implications for prognosis and cure are unclear. Treatment Multiple drug chemotherapy. Antibiotics to prevent infection. Transfusions of red blood cells and platelets to reverse anemia and prevent bleeding. Bone marrow transplant may successfully treat the disease. Blood products and broad spectrum antibiotics are provided during bone marrow transplant procedures to fight and prevent infection. Immunotherapy, including interferons and other cytokines, is used to improve outcome. Therapy may be more conservative for chronic leukemia. The treatments described earlier may contribute to the symptoms by causing further bone marrow depression, nausea, and vomiting. Nausea and vomiting may be controlled or reduced by pharmacologic and behavioral intervention. Anthocyanins (chemicals with known antioxidant and liver protecting properties) isolated from the plant Hibiscus sabdariffa are being studied as chemopreventive agents in that they cause cancer cell apoptosis (death) in human promyelocytic leukemia cells. Anemia Anemia is a condition in which there is a reduced number of red blood cells or decreased concentration of hemoglobin in those cells or both. Anemia is often a manifestation of some disease process or abnormality within the body. Although there are many causes of anemia, the actual mechanism by which the anemia results is generally due to (1) excess loss or destruction of red blood cells and (2) reduced or defective production of red blood cells. Anemias may be classified according to cause or effect on red cell morphology Size changes Normocytic anemia RBC size is unchanged Example: Blood loss anemia Macrocytic anemia RBC size is increased Example: B12/folic acid deficiency anemia Microcytic anemia RBC size is reduced Example: Iron deficiency anemia Color changes (due to altered hemoglobin content) Normochromic Normal hemoglobin concentration Hypochromic Reduced hemoglobin concentration Example: Iron deficiency anemia may be classified as a microcytic, hypochromic anemia as both red blood cell size and hemoglobin content are reduced General manifestations of anemia A major feature of anemia is a reduced capacity for the transport of oxygen to tissues. This reduced oxygen delivery can result in the following: Ischemia Fatigability Breathlessness upon exertion Exercise intolerance Pallor Increased susceptibility to infection Types of anemia Hemolytic anemia Anemia that results from excess destruction of red blood cells (hemolysis). Factors that may cause hemolysis include the following: Autoimmune destruction of red blood cells Certain drugs (example: quinine) or toxins Cancers such as lymphoma and leukemia Rheumatoid arthritis Certain viral infections (parvovirus) Parasitic infections (malaria) Blood loss anemia Anemia that results from acute blood loss. With acute loss of large amounts of blood, shock is the major concern. With chronic loss of smaller amounts of blood, iron deficiency is a chief concern. Causes of acute and chronic blood loss may include the following: Trauma and hemorrhage Malignancy Peptic ulcers Iron-deficiency anemia Iron-deficiency anemia is a major cause of anemia worldwide. It can occur as a result of iron-deficient diets. Vegetarians are at particular risk for iron deficiency as are menstruating or pregnant women due to increased requirement for iron. Iron-deficiency anemia may also result from poor absorption of iron from the intestine or persistent blood loss (e.g., ulcers, neoplasia). Because iron is the functional component of hemoglobin, lack of available iron will result in a decreased hemoglobin synthesis and subsequent impairment of red blood cell oxygen-carrying capacity. Cobalamin-deficiency or folate-deficiency anemia Cobalamin (vitamin B 12) and folic acid are essential nutrients required for DNA synthesis and red cell maturation, respectively. Deficiency of these nutrients will lead to the formation of red blood cells that are of abnormal shape with shortened life spans due to weakened cell membranes. One important cause of vitamin B 12 deficiency is pernicious anemia that results from a lack of intrinsic factor production by the gastric mucosa. Intrinsic factor is required for normal absorption of vitamin B 12 from the intestine. Any intestinal abnormalities (e.g., neoplasia, inflammation) that interfere with the production of intrinsic factor can lead to vitamin B 12 deficiency. Folic acid deficiency most commonly results from poor diet, malnutrition or intestinal malabsorption. Inherited anemia Anemia may also result from genetic defects in red blood cell structure or function. Two common genetic disorders of erythrocytes are sickle cell anemia and thalassemia. Both of these disorders result from abnormal or absent genes for the production of hemoglobin. Sickle cell disease Sickle cell disease is a group of autosomal recessive disorders characterized by abnormal hemoglobin production. In the United States the highest prevalence of sickle cell disease is in blacks with a reported incidence of approximately 1 in 500 births. Sickle cell disease has several patterns of inheritance that determine the severity of the disease in afflicted individuals. In the homozygous form of the disease, most of the hemoglobin formed is defective and the clinical presentation is most severe. With the heterozygous form of the disease, less than half of the red cell hemoglobin is affected and the presentation is significantly milder. Individuals may also inherit the sickle cell trait and be carriers of the defective hemoglobin gene without significant clinical manifestations. Manifestations of sickle cell disease: The abnormal hemoglobin formed in sickle cell disease results from a substitution mutation of a single amino acid. This mutation causes the deoxygenated hemoglobin to clump and become abnormally rigid. The rigidity of the defective hemoglobin deforms the pliable red blood cell membrane and causes erythrocytes to take on sickled or half-moon appearance. The degree of sickling that occurs is determined by the amount of abnormal hemoglobin within the red blood cell and only occurs when the abnormal hemoglobin is deoxygenated. As a result of their elongated shape and rigidity, affected blood cells do not pass easily through narrow blood vessels. Hemolysis of sickled red blood cells is also common. The spleen is a major site of red cell hemolysis since the blood vessels found within this organ are narrow and convoluted. As a result of the sluggish blood flow, many tissues and organs of the body are eventually affected by this disorder. Specific manifestations may include the following: Impaired oxygen-carrying capacity resulting in fatigue, pallor Occlusion of blood vessels leading to ischemia, hypoxia, pain Organ damage Splenomegaly due to increased destruction of red blood cells in this organ Jaundice as a result of increased amounts of hemoglobin released into circulation Increased risk of infection and possible septicemia due to stagnation of blood Thalassemia Thalassemia is a genetic disorder characterized by absent or defective production of hemoglobin ÃŽÂ ± or ÃŽÂ ² chains. As with sickle cell anemia, afflicted individuals may be heterozygous for the trait and have a milder presentation of the disease or homozygous and have a more severe form of the disorder. The ÃŽÂ ² form of thalassemia (defective formation of ÃŽÂ ² hemoglobin chains) is most common in individuals from Mediterranean populations, whereas the ÃŽÂ ± form of thalassemia (defective formation of ÃŽÂ ± hemoglobin chains) occurs mostly in Asians. Both the ÃŽÂ ± and ÃŽÂ ² forms of thalassemia are common in blacks. Manifestations of thalassemia In heterozygous individuals enough normal hemoglobin is usually synthesized to prevent significant anemia. In these individuals symptoms of anemia may appear only with exercise or physiologic stress. Homozygous individuals are often dependent on frequent transfusions to treat the resulting severe anemia. Children affected with the homozygous form may suffer severe growth retardation. The widespread hypoxia that can result from impaired oxygen-carrying capacity leads to erythropoietin-induced increases in hematopoiesis that can eventually affect the structure of the long bones. Severe anemia may also lead to congestive heart failure and marked hepatosplenomegaly. Excessive hemolysis of red blood cells may occur in severe forms of the disease due to overproduction of the normal hemoglobin subunit. Iron deposits from increased absorption and frequent transfusions may injure the liver and heart as well. Treatment of sickle cell anemia and thalassemia Individuals with inherited anemia should avoid physiologic stresses that might exacerbate hypoxia. Infections should be avoided and promptly treated if they occur to prevent a possible hypoxic crisis. Proper immunizations and vaccinations should be administered to lessen the chance of infection. Frequent transfusions of normal erythrocytes are commonly used in individuals with severe forms of inherited anemia during periods of crisis. These individuals are at risk for iron accumulation as well as contracting blood-borne pathogens such as hepatitis and HIV from improperly screened blood. Bone marrow transplant may be utilized effectively to cure patients with genetic anemias; however, the procedure carries considerable risk of its own. Aplastic anemia Aplastic anemia results from a lack of red blood cell production by the bone marrow. If erythrocyte stem cell precursors are lacking or destroyed, the process of erythropoiesis will be severely impaired. Aplastic anemia may result from a congenital defect in stem cell production or can be caused by exposure to agents that damage the bone marrow such as Chemicals (organic solvents, heavy metals), radiation, toxins, HIV infection, chemotherapeutic drugs and certain antibiotics (Chloramphenicol). Drug-induced aplastic anemia is usually a dose-dependent phenomenon. The clinical manifestations of aplastic anemia will depend on the extent to which hematopoiesis is impaired. General symptoms of anemia such as pallor, fatigue and lethargy can occur initially. Bleeding in the skin and from the nose, mouth and body orifices may also occur from a lack of platelet production by the abnormal bone marrow. Increased susceptibility to infection is also seen as a result of diminished white blood cell production. The underlying cause of the aplastic anemia needs to be identified and further exposure prevented. Treatment should also include avoidance of physiologic stresses and infection. Transfusions are effective for temporarily improving oxygen-carrying capacity. In severe cases, bone marrow transplant may offer a cure. Polycythemia Polycythemia is a disorder in which the number of red blood cells in circulation is greatly increased. There are two categories of polycythemia: relative and primary. Relative polycythemia results from an increase in the concentration of red blood cells due to a loss of plasma volume. In contrast, primary polycythemia (polycythemia vera) is caused by excessive proliferation of bone marrow stem cells. Polycythemia vera is a rare neoplastic disorder that occurs in men between the ages of 40 and 60. A secondary form of polycythemia may occur from excess erythropoietin production as a physiologic response to hypoxia. Secondary polycythemia may be seen in individuals living at high altitudes, in chronic smokers or in people with chronic obstructive pulmonary disease. Manifestations Increased blood volume and viscosity Increased risk of thrombus Occlusion of small blood vessels Hepatosplenomegaly from pooling of blood Impaired blood flow to tissues (ischemia) Treatment Increasing fluid volume in relative polycythemia Periodic removal of blood to reduce viscosity and volume in primary polycythemia Chemotherapy or radiation to suppress activity of bone marrow stem cells in polycythemia vera Thrombocytopenia (Purpura) Thrombocytopenia represents a decrease in the number of circulating platelets (usually less than 100,000/mm3). It can result from decreased platelet production by the bone marrow, increased pooling of platelets in the spleen, or decreased platelet survival caused by immune or nonimmune mechanisms. Dilutional thrombocytopenia can result from massive transfusions because blood stored for more that 24 hours has virtually no platelets. Decreased platelet production can result from suppression or failure of bone marrow function, such as occurs in aplastic anemia, or from replacement of bone marrow by malignant cells, such as occurs in leukemia. Infection with human immunodeficiency virus (HIV) suppresses the production of megakaryocytes. Radiation therapy and drugs such as those used in the treatment of cancer may suppress bone marrow function and reduce platelet production. There may be normal production of platelets but excessive pooling of platelets in the spleen. The spleen normally sequesters approximately 30% to 40% of the platelets. However, as much as 80% of the platelets can be sequestered when the spleen is enlarged (splenomegaly). Splenomegaly occurs in cirrhosis with portal hypertension and in lymphomas. Decreased platelet survival is an important cause of thrombocytopenia. In many cases, premature destruction of platelets is caused by antiplatelet antibodies or immune complexes. The antibodies can be directed against self-antigens (autoimmunity) or against nonself platelet antigens (from blood transfusions). Autoimmune thrombocytopenias include idiopathic thrombocytopenic purpura and HIV-associated thrombocytopenias. Decreased platelet survival may also occur as the result of mechanical injury associated with prosthetic heart valves. Drug-Induced Thrombocytopenia Some drugs, such as quinine, quinidine, and certain sulfa-containing antibiotics, may induce thrombocytopenia. These drugs act as a hapten and induce antigen-antibody response and formation of immune complexes that cause platelet destruction by complement-mediated lysis. In persons with drug-associated thrombocytopenia, there is a rapid fall in platelet count within 2 to 3 days of resuming use of a drug or 7 or more days (i.e., the time needed to mount an immune response) after starting use of a drug for the first time. The platelet count rises rapidly after the drug use is discontinued. The anticoagulant drug heparin has been increasingly implicated in thrombocytopenia and, paradoxically, in thrombosis. The complications typically occur 5 days after the start of therapy and result from production of heparin-dependent antiplatelet antibodies that cause aggregation of platelets and their removal from the circulation. The antibodies often bind to vessel walls, causing injury and thrombosis. The newer, low-molecular-weight heparin has been shown to be effective in reducing the incidence of heparin-induced complications compared with the older, high-molecular-weight form of the drug. Idiopathic Thrombocytopenic Purpura Idiopathic thrombocytopenic purpura, an autoimmune disorder, results in platelet antibody formation and excess destruction of platelets. The IgG antibody binds to two identified membrane glycoproteins while in the circulation. The platelets, which are made more susceptible to phagocytosis because of the antibody, are destroyed in the spleen. Acute idiopathic thrombocytopenic purpura is more common in children and usually follows a viral infection. It is characterized by sudden onset of petechiae and purpura and is a self-limited disorder with no treatment. In contrast, the chronic form is usually seen in adults and seldom follows an infection. It is a disease of young people, with a peak incidence between the ages of 20 and 50 years, and is seen twice as often in women as in men. It may be associated with other immune disorders such as acquired immunodeficiency syndrome (AIDS) or systemic lupus erythematosus. The condition occasionally presents precipitously with signs of bleeding, often into the skin (i.e., purpura and petechiae) or oral mucosa. There is commonly a history of bruising, bleeding from gums, epistaxis (i.e., nosebleeds), and abnormal menstrual bleeding. Because the spleen is the site of platelet destruction, splenic enlargement may occur. Diagnosis usually is based on severe thrombocytopenia (platelet counts Treatment includes the initial use of corticosteroid drugs, often followed by splenectomy and the use of immunosuppressive agents. Thrombotic Thrombocytopenic Purpura Thrombotic thrombocytopenic purpura (TPP) is a combination of thrombocytopenia, hemolytic anemia, signs of vascular occlusion, fever, and neurologic abnormalities. The onset is abrupt, and the outcome may be fatal. Widespread vascular occlusions consist of thrombi in arterioles and capillaries of many organs, including the heart, brain, and kidneys. Erythrocytes become fragmented as they circulate through the partly occluded vessels and cause the hemolytic anemia. The clinical manifestations include purpura and petechiae and neurologic symptoms ranging from headache to seizures and altered consciousness. Although TTP may have diverse causes, the initiating event seems to be widespread endothelial damage and activation of intravascular thrombosis. Toxins produced by certain strains of Escherichia coli (e.g., E. coli O157:H7) are a trigger for endothelial damage and an associated condition called the hemolytic-uremic syndrome. Treatment for TTP includes plasmapheresis, a procedure that involves removal of plasma from withdrawn blood and replacement with fresh-frozen plasma. The treatment is continued until remission occurs. With plasmapheresis treatment, there is a complete recovery in 80% to 90% of cases. Fibrinogen Deficiency Factor I (or fibrinogen) deficiency is a very rare inherited disorder with complications that vary with the severity of the disorder. It is not well known, even among health professionals. Discovery Factor I deficiency was described for the first time in 1920 by Fritz Rabe and Eugene Salomon. These two German physicians are credited with discovering the disorder. They studied the case of a 9-year-old boy who presented unexplained bleeding problems from birth. Blood tests finally demonstrated the absence of fibrinogen in the childs blood. His parents were first cousins, but they showed no bleeding problems. The two researchers established that it was an inherited disorder often found in subjects whose parents were blood relatives. Since then, knowledge about the condition has advanced considerably. What is Fibrinogen? Fibrinogen, also called Factor I, is a blood plasma protein produced by the liver that plays an important role in blood coagulation. Blood coagulation is a process in which several components of the blood form a clot. When blood escapes from a rupture in a blood vessel, coagulation is triggered. Several proteins, called coagulation factors, go into action to produce thrombin. The thrombin then converts fibrinogen to fibrin. Fibrin produced from fibrinogen is the main protein in a blood clot. It surrounds the cells in the blood and plasma and helps form the clot. The resulting clot, which is stabilized by Factor XIII, remains intact from 10 to 14 days, the time required for healing to take place. When there is a problem with fibrinogen, i.e., either it is missing or it does not function properly, the clot has difficulty forming. This can result in hemorrhaging or thrombosis. The normal volume of fibrinogen in the blood is from 2 to 4 g/l (grams/litre). The amount of fibrinogen in blood can be measured from a blood sample. The following diagram was devised by a Toronto laboratory technician. It shows the stages in clot formation in a way that makes it easier to understand the theoretical notions explained above. Types of Fibrinogen Deficiency There are three types of deficiency: Afibrinogenemia: (absence of fibrinogen) In this type of factor I deficiency, there is a complete absence of fibrinogen. The fibrinogen level is Hypofibrinogenemia (lower than normal level) Dysfibrinogenemia (improper functioning) Transmission of Fibrinogen Deficiency Fibrinogen deficiency is a very rare inherited bleeding disorder. It is transmitted from parent to child at conception. The disorder is caused by an abnormal gene. It affects both men and women, as well as people of all races and ethnic origins. Every cell of the body contains chromosomes. A chromosome is a long chain of a substance called DNA. DNA is organized in 30,000 units: these are called genes. The genes determine physical characteristics, such as eye colour. In the case of fibrinogen deficiency, one of the genes involved is defective. The defective gene in fibrinogen deficiency is located on a chromosome that is not responsible for the childs sex (autosomal). As a result, both girls and boys can be affected equally. Afibrinogenemia (absence of fibrinogen) This is a recessive disorder, which means that both parents must be carriers. In order for a person to inherit fibrinogen deficiency, he must receive two defective genes, one from the mother and the other from the father. A carrier is a person who has only one of the two defective genes, but is not affected by the disorder: the second gene enables just enough fibrinogen to be made for good coagulation. The fibrinogen level will be lower than normal, but there will be no symptoms of the disorder. Hypofibrinogenemia and dysfibrinogenemia These are inherited disorders that can be either dominant or recessive. Dominant means that a single parent can transmit the disorder if he or she is a carrier. Recessive means that both parents must be carriers of the disorder in order to transmit it. Symptoms Afibrinogenemia (absence of fibrinogen) In congenital afibrinogenemia (fibrinogen level Other types of bleeding have been described: bruises bleeding from the gums epistaxis (nosebleeds) gastrointestinal hemorrhage genito-urinary hemorrhage intra-cranial hemorrhage rupture of the spleen and hemorrhage in the spleen About 20% of those suffering from afibrinogenemia present hemarthroses (bleeding in the joints). Because of this particular feature, the disorder may be confused with hemophilia A or B. Hypofibrinogenemia (lower than normal level) Bleeding in hypofibrinogenemia is much like what is seen in afibrinogenemia. It can be more or less serious, depending on fibrinogen levels, which can vary from 0.2 to 0.8 g/L of plasma. The higher the fibrinogen level, the less bleeding. The lower the fibrinogen level, the more bleeding. Dysfibrinogenemia (improper functioning) In dysfibrinogenemia, the quantity of fibrinogen is normal, which means between 2 and 4 g/L. Bleeding can vary depending on how the fibrinogen is functioning. Bleeding may: be absent (no symptoms) show a tendency toward hemorrhage (as described in afibrinogenemia) show a tendency toward thrombosis How to Recognize Bleeding It is strongly recommended that people who suffer from afibrinogenemia or severe hypofibrinogenemia learn to recognize the signs and symptoms of bleeding that could threaten their lives or the integrity of a limb, so they can react adequately and in a reasonable time. The information below describes the main types of bleeding that may occur in someone with a coagulation disorder. Bleeding that affects the head, neck, thorax (chest) or abdomen can be life-threatening and may require immediate medical attention. Bear in mind that this kind of bleeding can occur either following an injury or spontaneously (without injury). Head The brain, which is protected by the skull, controls all bodily functions that are essential to life. Bleeding in the brain is very serious. Signs and symptoms: Heada

psychology Essay -- essays research papers

As described, there are 10 different perspectives of early psychology. These perspectives are: Structuralism, functionalism, Gestalt psychology, Behavioral, psychodynamic, humanistic, physiological, evolutionary, cognitive, and cultural and diversity. I will only be looking at three of these perspectives still in common use today here is a summary of each. The behavioral perspective "focuses on the observable behaviors; thus it does not speculate about mental processes such as thinking." (Davis and Palladino, 2005).Unlike the other approaches, the behavioral perspective accentuates how it is important to learn and understand and doesn't focus on coconscious. B. F. Skinner, a well known psychologist, was a strong advocate of this thinking. He has since been called the "greatest contemporary psychologist" (Fowler, 1990). Skinner basically took an easy angle on his methods. "Behavior changes as a result of consequences (Bjork, D. W., 1997). When it comes down to it, Skinner teaches basic skills. When applying this type of psychology to young children you will see immediate results and these can be long standing results. However, in young children, this method will not give the parent ay idea of the motivations or thoughts behind that bad behavior. Only reinforcing the correct behaviors will do nothing to help parents or teachers better understand the feelings of the child or the internal factors that have contributed to this behavior. Behaviorism works well in conjunction with the other theories below to help parents and teachers gain a more complete understanding of not only their children’s behaviors but â€Å"why† they choose to behave in a certain way. The humanistic perspective "emphasizes free will and an individual’s control of their own behavior." (Davis and Palladino, 2005).This was more of a human approach to psychology which was to look at and study humans by the choices they make. Laboratory specimens can not possibly equate to what a human can achieve deeming any laboratory experiment illogical. Instead of developing principals about their theories, they concluded that each individual is their own being. Humanistic psychologists believe in the inherent â€Å"good† nature of all people. &nbs... ...ng the humanistic approach to reinforce their own decision making can teach a child to make the correct decisions and also give a more positive view of those choices no matter what they are. At any age the cognitive approach can be used to help children learn to recall information they have been taught or apply that â€Å"lesson† we are trying to get across. References Bjork D.W. (1997) Allport: A Life in Washington D.C. American psychological association Fowler, R. D. (1990). Psychology: The core discipline. American Psychologist, 45, 1-6. Humanistic Psychology and Education. Don Closson 1991 Probe Ministries International Retrieved 4 April 2005 from http://www.probe.org/docs/psy-educ.html Educational Technology's Effect on Models of Instruction. Judith Conway. May, 1997 Retrieved 4 April 2005 from http://copland.udel.edu/~jconway/EDST666.htm Saul Kassin, B.S., M.A., PhD, "Psychology," Microsoft ® Encarta ® Online Encyclopedia 2005 Retrieved 4 April 2005 from http://encarta.msn.com Davis, Stephen F., Palladino, Joseph J. (2005) Psychology, Research and You, Psychology Chapter 1. Upper Saddle River, New Jersey: Pearson Custom Publishing