The Controversy of Clinical Versus Actuarial Prediction Essay Example

The Controversy of Clinical Versus Actuarial Prediction Paper In clinical prediction, psychologists use their clinical experience to formulate a prediction based on interview impressions, history ATA and test scores (Melee, Clinical versus Statistical 4). The formula in the title refers to statistical or actuarial prediction. In actuarial prediction, clergies access a chart or table which gives the statistical frequencies of behaviors (Actuarial Prediction). Advocates of the clinical method say that clinical prediction Is dynamic, meaningful and sensitive but actuarial prediction Is mechanical, rigid and artificial (Melee, Clinical versus Statistical 4). On the other hand, advocates of the actuarial method claim that actuarial method Is empirical, precise and objective but alnico prediction Is unscientific, vague and subjective (Melee, Clinical versus Statistical 4). The controversy of clinical versus actuarial judgment is not limited to the field of psychology; it also affects education in terms of predicting school performance, criminal justice system in terms of parole board decisions and business in terms of personnel selection. Although this controversy can be traced back half a century ago, social scientists today are still asking: Which of the two methods works better? Can we view any prediction dichotomously as either clinical or actuarial? And, if actuarial predictions are more accurate, should we abandon clinical predictions all together? On one side of the controversy, some people feel that using mere numbers to determine whether students can enter graduate schools or whether prisoners should be released Is dehumidifying (Melee, Causes and Effects 374). We will write a custom essay sample on The Controversy of Clinical Versus Actuarial Prediction specifically for you for only $16.38 $13.9/page Order now We will write a custom essay sample on The Controversy of Clinical Versus Actuarial Prediction specifically for you FOR ONLY $16.38 $13.9/page Hire Writer We will write a custom essay sample on The Controversy of Clinical Versus Actuarial Prediction specifically for you FOR ONLY $16.38 $13.9/page Hire Writer In her book about social psychology, Thompson describes a young woman who complains that It Is horribly unfair that she has been rejected by the Psychology Department at university of California on the bases of mere numbers, without even n interview (88). When my psychology teacher surveyed our class on this issue, about 20 percent of students believe that it is unethical to make predictions based on mere numbers (Brenner). The crux of this ethical concern lies on the belief that each individual is so unique that rigid statistics or equations cannot make the correct prediction in every single case. Indeed, most psychologists agree that rigid statistics are not sensitive to special cases. Paul Mà ªlà ©es well-known broken-leg example Illustrates how the special powers of the clinician can predict behaviors ore accurately in some special cases: If a sociologist were predicting whether Professor X would go to the movies on a certain night, he might have an equation Involving age, academic specialty, and Introversion score. The equation might yield [a very high probability] that Professor X will go to the movie tonight. But if Professor X Ana Just Darken Nils leg Ana en Is In a nil cast Tanat wont NT In a denature seat, no sensible sociologist would stick with the equation. (Clinical versus Statistical 24-25) Essentially, it is very important for clinicians to detect the characteristics of each unique individual and make predictions accordingly because clinicians deal with individual cases; they make predictions for each unique individual, not for a group of people. Thus, it is the individual case that defines the clinician (Melee, Clinical versus Statistical 25). Because of the insensitivity of statistics to special cases and the importance of predicting individual cases, many psychologists argue that statistics simply cannot apply to individuals (Melee, Causes and Effects 374). They believe that clinicians can make predictions about individuals can transcend the predictions bout people in general (Melee, Causes and Effects 374). For example, Patriots emphasized in his research on personality inventory that: In [nonproductive] tests, the results of every individual examination can be interpreted only in terms of direct, descriptive, statistical data and, therefore, can never attain accuracy when applied to individuals. Statistics is a descriptive study of groups, not of individuals. (633) On the other side of controversy, advocates of the actuarial approach have questioned the logic behind the assumption that statistics do not apply to single individuals or events. Stanchion uses a very good analogy to illustrate the fallacy behind this assumption (179). He asks us whether we want our operation done by an experienced surgeon who has a low failure probability or an inexperienced surgeon who has a high failure probability (179). Of course, any rational man will choose the experienced surgeon. However, if we believe that probabilities do not apply to the single case, we should not mind to have our operation done by the inexperienced surgeon. This question brings us to think about the role of chance in making reductions. Stanchion noted: Reluctance to acknowledge the role of chance when trying to explain outcomes in the world can actually decrease our ability to predict real-world events Acknowledging that our predictions will be less than 100 percent accurate can actually help us to increase our overall predictive accuracy. (175) An experiment done by Fainting and Subsidiaries (58-63) demonstrates Stanchions last point that we must accept error in order to reduce error. In this experiment, the participant sits in front of a red light and a blue light and is asked to predict which eight will be flashed on each trial (60). The experimenter has programmed so that the red light will flash 70 percent of the time and the blue light 30 percent of the time (59). Participants quickly pick up the fact that the red light is flashing more, thus they predict the red light roughly 70 percent of the time and the blue light roughly 30 percent of the time (62). The problem is that they do not understand that if they give up on trying to predict correctly on every trial, they can actually be more accurate. We can demonstrate the logic of this situation through a calculation on 100 trials. In 70 of the 100 trials, the red light will come on and the participant will be correct on about 70 percent of those 70 trials. That means, in 49 of the 70 trials (70 times . 70), the participant will correctly predict that red light will flash. In the same way, we can calculation that approximately in 9 trials (30 times . 30), the participant will correctly predict that the blue light will flash. Therefore, the participant can only predict correctly 58 percent of the time (49 percent from the red light and 9 percent from the (B). However, IT ten participant simply gives up on getting every trial relent Ana just predicts the red light on every trial, he can predict correctly 70 percent of the time (because the red light will come on 70 percent of the time), which is 12 percent better than switching back and forth trying to get right on every trial. This is what Stanchion means by accepting error in order to reduce error. Research on this controversial issue has consistently indicated that actuarial prediction is more accurate than clinical prediction. In Paul Mà ªlà ©es classical book Clinical versus Statistical Prediction, he had reviewed 22 studies comparing clinical and actuarial prediction (83-126). Out of these 22 studies, twenty show that actuarial prediction is more accurate than clinical prediction. These twenty studies cover almost all the clinical prediction domain, including psychotherapy outcome, criminal recidivism, college graduation rates, parole behavior and length of psychiatric hospitalizing. A graduate student at JIBE had also done a study comparing clinical and actuarial prediction (Simmons 3). In this study, Simmons compared the predictions made by a regression equation and by two experienced counselors on the school performance of JIBE freshmen (Simmons 3). The results again indicate the actuarial prediction using the regression equation was more accurate (Simmons 64). In addition, a recent meta-analysis using 136 studies has also confirmed that actuarial prediction is better regardless of the Judgment task, type of Judges, or Judges amount of experience (Grove et al. 9). Researchers found that actuarial prediction substantially outperformed clinical prediction in 45 percent of the studies whereas clinical prediction was more accurate in only 10 percent of the studies (19). Regarding the research consistently showing that actuarial prediction is more accurate , Paul Melee said, There is no controversy in social science which shows such a large body of qualitatively diverse studies coming out so uniformly in the same direction as this one (373-374). Mà ªlà ©es actuarial stance is strongly challenged by Robert R. Holt, who is also a renowned clinical psychologist. Holt criticizes that the twenty studies Melee cited in his book only focus on the final step of the prediction-making process, which is making the prediction (339). Holt rejects the dichotomous classification of studies as clinical or statistical because in field settings, clinicians do not simply make a prediction by evaluating the given data (338). In field settings, before the clinician can make the prediction, he has to carefully identify the criterion he can predict and choose predictive variables he wants to use. (Holt 339-340). For example, if a counselor wants to predict the school performance of first year university dents, he first identifies the criterion he is able to predict; the criterion can be Gaps or average marks of the students, but it can also be the students lecture attendances. He also has to choose which predictive variables he should use; he may use the students entrance grades or their scores on an aptitude test or a combination of both. Then, finally, he can make the prediction using either an equation or his own Judgment. This example shows that even if the clinician uses actuarial approach in the final step of the prediction-making process, he still plays an important role in all the preceding steps. I agree with Holt that Melee has oversimplified the distinction between clinical and statistical prediction. I believe that we should view these two methods as falling on a continuum rather than make an all-or-none distinction. Some predictions that can be completely done on computers are more statistical toner protections, Tort wanly psychoanalysts need to collect Ana analyze data, are more clinical. I also agree with Holt that we should still value clinical judgment although it is not as accurate. Without clinical Judgment, scientists will to be able to form hypotheses and theories, and to analyze research results and data. Like Western and Weinberg said in their article reviewing this controversial issue, try as we might to eliminate subjectivity in science, we can never transcend the fact that the mind of scientists, clinicians or informants is the source of much of what we know (609). Nevertheless, when countless research findings point toward one direction, I think we should recognize that actuarial predictions are more accurate than clinical predictions (at least in the final step of the prediction-making recess). Some people think that using mere numbers to make predictions is dehumidifying. They feel that using an equation to forecast a persons action is treating the individual like a white rat or an inanimate object (Melee Causes and Effects 374). However, I argue that in certain cases, it is unethical to use clinical judgment when actuarial approach has shown to be accurate. For example, when a clinical psychologist makes a prediction about whether a student is going to commit suicide within a year, would it be more ethical to use the actuarial prediction that is here times more accurate than the clinical prediction (Brook et al. 03)? The answer to this question should be as obvious as the question about whether we want our operation done by an experienced or an inexperienced surgeon. By admitting that actuarial Judgment is more accurate, clinicians who engage in activities in the role of experts and imply that they have unique clinical knowledge of individual cases may lose prestige and income; however, the field of psychology, and society, will benefit if we underst and that accepting error is reducing error.

Film Analysis of Field of Dreams essays

Film Analysis of Field of Dreams essays Ray Kinsella is an ordinary man from Eastern Iowa who has an extraordinary event happen to him that will change the life for him and his family forever. The movie "Field of Dreams" was released in 1989 and stared Kevin Costner, James Earl Jones, Amy Madigan, and Burt Lancaster. The film was nominated for three academy awards including "Best Picture". The film begins with a narrative of the life of Ray's father. His father played baseball when he was younger but never made it professionally. Instead, he got married and had a son and worked at a factory his entire life to support his family. Ray played baseball early in his life and was forced to live out the dreams of his father. Ray's father wanted him to go on and play baseball professionally since he never got the chance too. However, Ray saw things differently and rebelled against his father's wishes. He went to college at the University of California- Berkeley. He attended Berkeley he majored in English but really majored in the youth movement of the 1960's "Peace, Love, and Dope" was among his favorite saying of the era. While attending Berkeley, he met the love of his life Annie. They were married and after college moved, to Iowa near her parents bought some land and had a girl (Katie). Ray was now a farmer who loved his family, the 60s, and baseball. He is an ordinary man from a small farming community in Iowa. Life was all too normal for Ray until the day he heard a voice from the cornfield. "If you build it he will come". Ray at first does not know what the voice means by the statement "id you build he will come". He eventually ties the message from the voice to his Dad's baseball hero Shoeless Joe Jackson. Jackson was a Chicago White Sox baseball player that (along with his teammates) was kicked out of baseball for throwing games. Ray believes that if he builds a baseball filed that Shoeless Joe Jackson will come. Despite the financial concerns Ray supported by his wife...

Lockheed U-2 Spy Plane

Lockheed U-2 Spy Plane In the years immediately after World War II the US military relied on a variety of converted bombers and similar aircraft to collect strategic reconnaissance. With the rise of the Cold War, it was recognized that these aircraft were extremely vulnerable to Soviet air defense assets and as a result would be of limited use in determining Warsaw Pact intentions. As a result, it was determined that an aircraft capable of flying at 70,000 feet was needed as existing Soviet fighters and surface-to-air missiles were incapable to reaching that altitude. Proceeding under the codename Aquatone, the US Air Force issued contracts to Bell Aircraft, Fairchild, and Martin Aircraft to design a new reconnaissance aircraft capable of meeting their requirements. Learning of this, Lockheed turned to star engineer Clarence Kelly Johnson and asked his team to create a design of their own. Working in their own unit, known as the Skunk Works, Johnsons team produced a design known as the CL-282. This essentially married the fuselage of an earlier design, the F-104 Starfighter, with a large set of sailplane-like wings. Presenting the CL-282 to the USAF, Johnsons design was rejected. Despite this initial failure, the design soon received a reprieve from President Dwight D. Eisenhowers Technological Capabilities Panel. Overseen by James Killian of the Massachusetts Institute of Technology and including Edwin Land from Polaroid, this committee was tasked with exploring new intelligence weapons to protect the US from attack. While they initially concluded that satellites were the ideal approach for gathering intelligence, the necessary technology was still several years away. As a result, they decided that new spy plane was needed for the near future. Enlisting the aid of Robert Amory from the Central Intelligence Agency, they visited Lockheed to discuss the design of such an aircraft. Upon meeting with Johnson they were told that such design already existed and had been rejected by the USAF. Shown the CL-282, the group was impressed and recommended to CIA head Allen Dulles that the agency should fund the aircraft. After consulting with Eisenhower, the project moved forward and Lockheed was issued a $22.5 million contract for the aircraft. Design of the U-2 As the project moved forward, the design was re-designated U-2 with the U standing for the deliberately vague utility. Powered by the Pratt Whitney J57 turbojet engine, the U-2 was designed to achieve high altitude flight with a long range. As a result, the airframe was created to be extremely light. This, along with its glider-like characteristics, makes the U-2 a difficult aircraft to fly and one with a high stall speed relative to its maximum speed. Due these issues, the U-2 is difficult to land and requires chase car with another U-2 pilot to help talk the aircraft down. In effort to save weight, Johnson originally designed the U-2 to take off from a dolly and land on a skid. This approach was later dropped in favor of landing gear in a bicycle configuration with wheels located behind the cockpit and engine. To maintain balance during takeoff, auxiliary wheels known as pogos are installed under each wing. These drop away as the aircraft leaves the runway. Due to the U-2s operational altitude, pilots wear the equivalent of a spacesuit to maintain proper oxygen and pressure levels. Early U-2s carried a variety of sensors in the nose as well as cameras in a bay aft of the cockpit. U-2: Operation History The U-2 first flew on August 1, 1955 with Lockheed test pilot Tony LeVier at the controls. Testing continued and by spring 1956 the aircraft was ready for service. Reserving authorization for overflights of the Soviet Union, Eisenhower worked to reach an agreement with Nikita Khrushchev regarding aerial inspections. When this failed, he authorized the first U-2 missions that summer. Largely flying from Adana Air Base (renamed Incirlik AB on 28 February 1958) in Turkey, U-2s flown by CIA pilots entered Soviet airspace and collected invaluable intelligence. Though Soviet radar was able to track the overflights, neither their interceptors nor missiles could reach the U-2 at 70,000 ft. The success of the U-2 led the CIA and US military to press the White House for additional missions. Though Khrushchev protested the flights, he was unable to prove that the aircraft were American. Proceeding in complete secrecy, flights continued from Incirlik and forward bases in Pakistan for the next four years. On May 1, 1960, the U-2 was thrust into the public spotlight when one flown by Francis Gary Powers was shot down over Sverdlovsk by a surface-to-air missile. Captured, Powers became the center of the resulting U-2 Incident which embarrassed Eisenhower and effectively ended a summit meeting in Paris. The incident led to an acceleration of spy satellite technology. Remaining a key strategic asset, U-2 overflights of Cuba in 1962 provided the photographic evidence that precipitated the Cuban Missile Crisis. During the crisis, a U-2 flown by Major Rudolf Anderson, Jr. was shot down by Cuban air defenses. As surface-to-air missile technology improved, efforts were made to improve the aircraft and reduce its radar cross-section. This proved unsuccessful and work began on a new aircraft for conducting overflights of the Soviet Union. In the early 1960s, engineers also worked to develop aircraft carrier-capable variants (U-2G) to extend its range and flexibility. During the Vietnam War, U-2s were used for high-altitude reconnaissance missions over North Vietnam and flew from bases in South Vietnam and Thailand. In 1967, the aircraft was dramatically improved with the introduction of the U-2R. Approximately 40% larger than the original, the U-2R featured underwing pods and an improved range. This was joined in 1981 by a tactical reconnaissance version designated TR-1A. The introduction of this model re-started production of the aircraft to meet the USAFs needs. In the early 1990s, the U-2R fleet was upgraded to the U-2S standard which included improved engines. The U-2 has also seen service in a non-military role with NASA as the ER-2 research aircraft. Despite its advanced age, the U-2 remains in service due to its ability to perform direct flights to reconnaissance targets on short notice. Though there were efforts to retire the aircraft in 2006, it avoided this fate due to the lack of an aircraft with similar capabilities. In 2009, the USAF announced that it intended to retain the U-2 through 2014 while working to develop the unmanned RQ-4 Global Hawk as a replacement. Lockheed U-2S General Specifications Length:  63 ft.Wingspan:  103 ft.Height:  16 ft.Wing Area:  1,000 sq. ft.Empty Weight:  14,300 lbs.Loaded Weight:  40,000 lbs.Crew:  1 Lockheed U-2S Performance Specifications Power Plant:  1 Ãâ€" General Electric F118-101 turbofanRange:  6,405 milesMax Speed:  500 mphCeiling:  70,000 ft. Selected Sources FAS: U-2The CIA the U-2 Program: 1954-1974

What Should government do to protesct society from mass shootings Research Paper

What Should government do to protesct society from mass shootings - Research Paper Example The debate rages on. In recent years, the debate has become increasingly vocal, as mass shootings have begun to invade the American landscape. Some argue that such shootings are the very reason why the Constitution guarantees citizens the right to bear arms. Others, however, argue that society has changed in the past 300 years and the time for strict gun control has come. There are valid points to both sides and this paper will highlight some major positions, while arriving at the conclusion that the right to own and maintain a gun must remain a part of the American fabric for now and the foreseeable future. The Argument for Gun Control Individual freedom and liberty is a cornerstone birthright that comes with being an American citizen. There are certain rights that are written into the Constitution in an effort to prevent any future government from taking that liberty away. As time goes on, however, and society develops, the language written into the Constitution can become muddled and filled with doubt and uncertainty. There are some, for example, that claim the right to own a gun is not actually a fundamental right guaranteed under the second amendment. Much of this opinion involves cause and effect, and examining that actual reasoning behind the second amendment. There are multiple reasons a person might own a gun. Some may own a gun to hunt wild game, while others will maintain a functioning weapon for purposes of self-defense. Still others might have a gun due to military or police service, and some might own a gun to commit a crime such as robbing a bank. The modern day argument in support of gun control, then, largely centers on this issue. Since the Constitution does not possibly permit the right of a gun owner to use such a weapon in the commission of a crime, then it certainly does not permit the right of every individual in the country to own a gun. Guns are permitted under the second amendment for purposes of military service. Few would argue that point. Many would argue, however, that the Constitution does not inherently protect the right of gun ownership for other reasons (Stevens para. 4). The center of this debate is on the language in the Second Amendment. While it seems so clear to some, it is far from it to others. While the courts have generally upheld the principle that Americans have the right to gun ownership, there is a growing movement in government circles to have the courts take another look at the language and to issue new rulings. On this side of the issue, the opinion is that gun ownership is a right for some, but not for others. The distinction comes in the language used to write this part of the Constitution. The actual purpose governing the inclusion of the Second Amendment into the Constitution was to allow citizens to protect themselves from a well-regulated militia. In other words, if the government took away the rights of the people, the people had a right to fight back, or to defend themselves. In th is vein, people have argued for gun control on the basis that gun control, and the limiting of gun ownership, is permissible under these guidelines (Faria 133). In recent years, there has been an unfortunate rise in violence on school campuses, particularly colleges and universities. Some have used this as an argument for gun ownership and the permissibility of students to be able carry guns on campus in order to better protect themselves against threats, such as mass shootings. Others, however, have argued that this is the very reason we should have gun control. By taking guns out of the hands of all individual citizens, they claim

Bipolar disorder Term Paper Example | Topics and Well Written Essays - 1000 words

Bipolar disorder - Term Paper Example Bipolar disorder falls among the oldest illnesses, which are known. The recognition of the disorder was during the second century and the discovery was in a Turkey’s city. The findings were not noticed and neither were they substantiated up to the year 1650, when Richard Burton, a scientist wrote his book called The Anatomy of Melancholia. The book majorly laid much emphasis on depression. The findings of the scientist are still used today even by fields related to mental health (Brent and Pan, 2008). In the year 1952, a journal article was written that critically analyzed the disorder’s heredity. The article showed that manic depression is capable of being passe own in families that already have patients with the disorder. In 1960’s, several people with bipolar disorder were placed at a given institution and provided with little financial help since the Congress refused to acknowledge that manic depression is a legitimate illness. However, during the 1970â€℠¢s, laws were enacted and besides, standards were put into place to aid the afflicted individuals. Similarly, in the year 1979, National Association of Mental Health was established (Reich, Clayton and Winokur, 1969). During the 1980’s, research was finally capable of distinguishing between childhood as well as adult bipolar disorder. Presently, a number of studies are still needed to unravel the possible causes as well as the probable means of treating the illness (Baloch & Soares, 2010). Generally, bipolar disorder develops when an individual is approaching his late teens although it also develops when individuals approaches their adulthood. However, there are a number of cases commences before the age of 25 (Kessler et al, 2005). In a number of individuals, first symptoms occur during their childhood, while in others, symptoms may develop very late in their lives. Diagnosis of bipolar disorder is done after individuals report their experiences; however, it may also be done after friends, family members and co-workers detect an abnormality. Secondary signs of the illness may be detected by clinical psychologist, social workers, psychiatrist, nurses, and also through clinical evaluation. However, the diagnosis of the condition is dependent on the presence as well as the duration of specific signs as well as symptoms (Sadock & Sadock, 2007). For an individual having bipolar disorder to be diagnosed correctly, it takes roughly 20 years. In approximately 37% of patients, bipolar disorder is usually diagnosed erroneously since it is always mistaken for unipolar depression. Surveys also prove that about 50% of individuals suffering from the disorder fail to take the medications that are prescribed (Brent & Pan, 2008). In general, the problem is not caused by the patient, though impaired judgment offer powerful incentives for skipping the medication. In order to control the disorder, drugs should be used. However, the drugs have side effects, which include g aining of weight as well as cognitive dulling (Young et al., 1978). In about 90% of marriages, that involves partners with bipolar disorder result into divorce due to the diseases adverse effects. Moreover, researchers have made estimation that about 40 percent of individuals having the disorder abuse drugs. Researchers also state that approximately 15 to 25% of individuals ha

Advanced Glycation End Products (AGE) for Diabetes

Advanced Glycation End Products (AGE) for Diabetes Diabetes mellitus is a syndrome which defined as a group of metabolic diseases characterized by hyperglycemia, that result from insufficient production of insulin, or body cells poorly respond to the insulin that is produced, or both. Insulin is a hormone produced in the pancreas and secreted in the blood to maintain blood glucose in the body through enables body cells to absorb glucose, to turn into energy. If the body cells enable to absorb the glucose, the glucose will accumulates in the blood (hyperglycemia), leading to many and different potential medical complications (Harmel Mathur, 2004). Diabetes have several categories but the majority of cases fall into two categories which are type 1 diabetes mellitus and type 2 diabetes mellitus. These two types are powerful and highly independent risk factors causing coronary artery disease, stroke, peripheral arterial disease and organ damage and dysfunction including eyes and nerves (Harmel Mathur, 2004). Type 1 Diabetes Mellitus: Type 1 diabetes mellitus resulting from pancreas failure to produce insulin hormone. Person at risk of developing type 1 can be identified by doing serologic test markers that showing evidence of autoimmune destruction of beta cells (islet cells) of the pancreas which is responsible for insulin production. Type 1 diabetes is manifested in childhood and early adulthood, but can patient present at any age (Goroll Mulley, 2009). Type 2 diabetes mellitus: Patients with type 2 diabetes mellitus are prone with wide range of series complications. Type 2 is characterized by high blood glucose due to insulin resistance and relative insulin deficiency. There are 20.8 million people in United State with type 2 diabetes mellitus. Type 2 diabetes traditionally is seen in elderly people. However it is diagnosed in obese children. Many studies shows that type 2 diabetes mellitus are associated with high calorie diet, physical inactivity and life style (Feinglos Bethel, 2008). Other Types of Diabetes: There are other types of diabetes but they are less common but patients who are underlying defect or disease process can be identified in a relatively specific manner. These types are Genetic defects of beta-cell function, Diseases of the exocrine pancreas e.g Fibrocalculous pancreatopathy, Endocrinopathies and cystic fibrosis and Uncommon forms of immune-mediated diabetes. Diabetes mellitus complications: Diabetic complications can be grouped into macrovascular and microvascular disease. Macrovascular diseases are result from atherosclerosis which develops in earlier age in patient with diabetes. There are several factors contribute to atherosclerosis such as lipidemia, hypertension, increased platelets adhesion and aggregation, elevated factor V, factor VII and fibrinogen concentration. Macrovascular diseases are seen in both type one and two of diabetes mellitus and they include coronary heart disease, Ischemic stroke and peripheral vascular disease (which can lead to ulcers, gangrene and amputation) (Winter Signorino, 2002). Whereas, Microvascular complications is seen in type one diabetes mellitus. Hyperglycemia damages the basement membrane of capillaries in the retina and glomerulars which leads to retinopathy and neuropathy. Microvascular diseases include neuropathy (nerve damage), nephropathy (kidney disease) and vision disorders (eg retinopathy, glaucoma, cataract and corneal disease). Furthermore there are other complications of diabetes include infections, metabolic difficulties, dental disease, autonomic neuropathy and pregnancy problems (Winter Signorino, 2002). Several clinical research show a strong relationship between hyperglacemia and diabetic microvascular complications in both type 1 and type 2 diabetes. High glucose and insulin resistance play important roles in the pathogenesis of macrovascular complications due to atherosclerosis. Diabetes-specific microvascular disease in the retina, glomerulus and vasa nervorum has same pathophysiological features. Intracellular hyperglycaemia causes abnormalities in blood flow and increased vascular permeability which leads to decreased activity of vasodilators such as nitric oxide, increased activity of vasoconstrictors such as angiotensin II and endothelin-1, and elaboration of permeability factors such as vascular endothelial growth factor (VEGF) (Brownlee, 2001). There are several factors which contribute the formation of inflammation, atherosclerosis and diabetes mellitus complication. These factors are hyperglycemia, accumulation of advanced glycation endproducts, dyslipidemia and oxidative stress which lead to endothelial dysfunction resulting in thrombotic complications and cardiovascular (Altman, 2003). In type 1 diabetes mellitus, high blood glucose is usually as result of low level of insulin secretion whereas in type2 hyperglycemia is caused by resistance of insulin at the cellular level. Low insulin levels or insulin resistance enable the body to convert glucose into glycogen (a starch-as source of energy which stored in the liver). In type 1 diabetes, pancreatic beta cells are attacked by auto-immune which cause infiltration of inflammatory cells and increased expression and secretion of S100-calcium binding protein and high-mobility group protein 1 (HMGP1) through inflammatory cells which consequently lead to islet damage and increased blood glucose level, subsequent accumulation of AGE (Bierhaus Nawroth, 2009). Comparing to T1D, in type 2 diabetes mellitus, different metabolic disturbances stimulates inflammatory cells to secretes RAGE ligands, which cause low-grade inflammation and increased oxidative and carbonly stress, all these play roles in promoting AGE formation and RAGE expression in respective organs (Bierhaus Nawroth, 2009). Insulin resistance and Inflammation: In diabetic patients with hyperglycemia, cause by 1) impaired insulin secretion by the pancreatic ß-cells, 2) muscle insulin resistance, and 3) hepatic insulin resistance all play central roles in the development and progression of glucose intolerance. As I mention before, type 2 diabetes mellitus (T2DM) is characterized by insulin resistance in liver and muscle and impaired insulin secretion. Also include deranged adipocyte metabolism and modified fat topography in the pathogenesis of glucose intolerance in T2DM. Fat cells are resistant to insulins antilipolytic effect, which result in increased plasma free fat acid levels. Long period of increasing plasma fat fee acid stimulates gluconeogenesis, promote hepatic and muscle insulin resistance, and impairs insulin secretion in genetically predisposed patients. These pathways of FFA-induced are known as lipotoxicity. Fat cells Dysfunction makes excessive amounts of insulin resistance-inducing, inflammatory, and atherosclerotic-provoking cytokines and fails to secrete normal level of insulin-sensitizing adipocytokines. Enlarged fat cells are insulin resistant and have minimized capacity to store fat. When storage capacity of adipocyte is exceeded, lipid overflows into muscle, liver, a nd perhaps ß-cells, resulting in muscle, hepatic insulin resistance and impaired insulin secretion. In type 2 diabetics, the ability of insulin to stop lipolysis and to decrease the plasma FFA levels is markedly impaired. It is clearly that chronic elevated levels of plasma free fat acid leads to insulin resistance in muscle and liver, and impair insulin secretion. In addition to FFA in plasma, increase stores of triglycerides in muscle and liver which correlate closely with the presence of insulin resistance in tissues. The triglycerides in liver and muscle are in a state of constant turnover, and the metabolites of intracellular triglyceride lipolysis impair action of insulin in liver and muscle (Bays et al, 2004). This pathway of events has been referred to as lipotoxicity . The accumulation of lipid in dipocytes leads to activate NADPH oxidase which increases the production of reactive oxygen species (ROS). The mechanisms increased production of cytokines including TNF-ÃŽ ±, IL-6 and monocyte chemoattractant protein-1 and reduce the production of adiponectin (Shoelson et al, 2006). Furthermore accumulation of lipid activates the protein response to increased ER stess in fat and liver. All these have accumulated to induce lipotoxicity as an important cause of ß-cell dysfunction (Bays et al, 2004). Receptor for advanced glycation end products (RAGE): RAGE is type I transmembrane receptor of the immunogloblin superfamily. It is a receptor for advanced glycation endproducts (AGE). It is about 45-KD a protein and it is consist of 403 amino acids in human, rate and mouse. Its extracellular region consists of one V-type (variable) immunoglobulin domina, which followed by two C-type (constant) immunoglobulin dominas (Basta, 2004). Its name drive from its ability to bind AGE and also it is known as AGER. It is located within the major histocompatibility complex (MHC) class III region on chromosome 6, which contains numbers of genes involved predominantly in inflammatory and immune responses and several components of complements. Beside AGE, RAGE is able to bind several ligands therefore is called a pattern-recognition receptor. These ligands are high-mobility group protein 1 (HMGP1), S100-calicum binding protein (S100b) which is family of pro-inflammatory cytokines and it can be found in any inflammatory lesion and vascular walls of diabetics patients, amyloid-ß-protein and macrophage-1 glycoprotein (CD11B/CD18). RAGE plays role in diabetes and other metabolic disease. The interaction of RAGE and its ligands cause pro-inflammatory activation. It is involved in several diseases such as innate immune response, mediating immune and inflammatory response, cancer promoting and progressing and microvascular and mi crovascular diseases (Bierhaus Nawroth, 2009). Moreover, RAGE expression is increased in the cells of the vascular walls, at the site where AGEs and S100/calgranulins are accumulated, including endothelium vascular smooth muscle cells, glomerular mesangial cells and mononuclear phagocytes. This destrbution of RAGE and its ligands leads to increased cellular activation, causing further raised expression of the receptor (Basta et al, 2004). Recently the studies have been proved that RAGE and its ligands accumulate in diabetes and contribute to its pathology. Serum levels of S100A8/9 and S100A12 increased in type 2 diabetic patients. Also, evidence was provided by raised serum levels HMGB1 were linked to coronary artery disease in type 2 diabetes. In addition the studies which have been done in streptozotocin-induced diabetic rats proved that diabetes increased amyloid-beta-peptide (1-40) levels in the brain. Furthermore, CML-modification of S100A8 and S100A9 are seen in inflammatory bowel disease and promote RAGE-mediated sustained inflammatory. Moreover, Carboxylated N-glycans on RAGE eases binding of HMGB and mediates ligation of S100A8/A9 to subpopulation of RAGE on colon cancer cells (Bierhaus Nawroth, 2009). Advanced Glycation End products (AGE) and its biochemical mechanism production: There are various pathways involved in stimulation of atherosclerosis in diabetes mellitus. However the most important one is formation and deposition of AGEs through nonenzymetic reaction between extracellular protein and glucose and it accumulates within cells of the vascular walls, in the extracellular space, kidney, nerves and retina (Basta et al, 2004). Possible mechanism of AGEs formation arise from intracellular auto-oxidation of glucose to glyoxal, decompounding of the Amadori product (glucose-derived 1-amino 1-deoxyfructose lysine adducts) to 3-deoxyglucosone and fragmentation of glyceraldehyde-3-phosphate and dihydroxyacetone phosphate to methylglyoxal. These reactive intracellular dicarbonyls (glyoxal, methylglyoxal and 3-deoxyglucosone) which can react with amino groups of intracellular and extracellular proteins to form AGEs (pyrraline, pentosidine, CML, crossline) (Balasubramanyam et al, 2002). Several experimental studies evidenced that advanced glycation end products can alter vascular wall homeostasis in atherogenic through different ways which are: AGEs and mononuclear phagocytes Interaction: The binding of AGEs with mononuclear phagocytes MPs induces the activation of platelet-derived growth factor, insulin-like growth factor-1, and pro-inflammatory cytokines, such as IL-1ß and TNF-ÃŽ ±. Furthermore the interaction of AGEs with its receptor (RAGE) in the mononuclear phagocytes promotes cell migration (chemotaxis) (Basta et al, 2004). AGEs and vascular smooth muscle cells Interaction: Interaction of AGE with smooth muscle cells (SMCs) exhibits the proliferative activity and production of fibronectin. SMC growth are indirectly mediate by cytokines or growth factors which induced by AGEs in the MPs. Transforming growth factor-ß (TGF-ß) act as an intermediate factor in AGE-induced fibronectin formation by SMC(Basta et al, 2004). AGEs with vascular endothelium Interactions: alterations of vascular permeability and of adhesive properties As result its unique position and numerous properties, the vascular endothelium has important role in the regulation of extracellular permeability, the maintenance of blood fluidity, metabolism of hormones and vasoactive mediators and the regulation of vascular growth and tone. The endothelium is exposed to AGEs located on circulating proteins and cells (such as, diabetic RBCs), also those found in the underlying subendothelial matrix. Receptors for AGEs present on the endothelial cell surface, and mediate both the uptake and AGEs transcytosis, and the internal signal transduction. AGE-RAGE interaction leads to alteration of barrier function and an increased permeability of endothelial cells interact with AGEs and increased migrate of macromolecules through the endothelial monolayer. The increase in permeability is associated by alterations of the physical integrity of the endothelium, as shown by the destruction of structures and alterations of cellular morphology (Basta et al, 2004 ). Also, it has been proved that AGEs cause alterations of endothelial anti-hemostatic functions in vitro, through a reduction of thrombomodulin expression and accompanied with induction of tissue factor expression. The promoting of tissue factor and the decreasing in thrombomodulin activity change the dynamic endothelial features with regard to hemostasis from those of an anticoagulant to those of a procoagulant surface (Basta et al, 2004). Intraction of AGEs with endothelial RAGE also causes the depletion of cellular antioxidant defense mechanisms (such as glutathione, vitamin C) and the generation of reactive oxygen species. As a result of the increased cellular oxidative stress, NF-ÃŽ ºB activation occurs, thus inducing the expression of NF-ÃŽ ºB-regulated genes including, in addition to the procoagulant tissue factor, adhesion molecules, such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1); this past may prime diabetic vasculature towards enhanced interaction with circulating monocytes. Furthermore, the incubation of endothelial cells with EN-RAGE or S100B results in VCAM-1 induction, in a RAGE-dependent manner, as sustained by the inhibitory effect of anti-RAGE IgG or soluble RAGE (Basta et al, 2004). Alterations of endothelium-dependent vasodilatation AGEs linked to the vascular matrix may quench bioavailability of nitric oxide (NO), which is an important regulator of vascular tone inducing smooth muscle cell relaxation. Studies provided that, AGE inhibits NO activity, when it added to NO in vitro. Studies on animal exterminate induced diabetes show that an alteration of endothelium-dependent dilatation occurs in short period, within 2 months, from diabetes induction. A direct reaction between NO radical and other free radicals which are formed during the reactions of AGEs assumable leads to inactivation of NO. In parallel, advanced glyaction end products promote the expression of the potent vasoconstrictor endothelin-1 changing endothelial function towards vasoconstriction (Basta et al, 2004).   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  These four mechanisms promote and alter vascular wall homeostasis. When mononuclear phagocytes migrate to the site of immobilized AGEs in the tissue, their migrations allow them to interact with AGE -modified surface and become activated. This mechanism cause attracting and retaining MPs in tissue where AGEs deposit. Migration and activation of MPs and T cells (inflammatory cells) promote and cause chronic vascular inflammation through alter vessel wall (Basta et al, 2004). Promotion of atherogenesis pathways by AGEs: AGEs are most important factors in endothelial dysfunction in diabetic patients through binding its receptor (RAGE). Advanced Glycation Endproducts stimulate the expression of proinflammatory cells and molecules (Altman, 2003). AGEs can be seriously deleterious to the function of blood vessel walls in various ways. First it causes blood vessel dysfunction through cross bridges among vessel macromolecules. Secondly of damage is that accumulation of AGEs lead circulating blood cells to adhere to the vascular walls which promote atherosclerosis. Third way is through binding different receptors which have been recognized on various cell types such as macrophages, endothelial cells, and smooth muscle cells, renal and neuronal cells (Basta et al, 2004). Hyperglycaemia Mechanisms-caused damage: Hyperglycemia diverse microvascular and macrovascular complications in diabetic patients through several mechanisms such as increased formation and accumlation of advanced glycation end-product (AGE); activation of protein kinase C (PKC) isoforms; and increased generation of reactive oxygen species (Bonke et al,2008) Increased production advanced glycation end-products AGE promote atherogenesis pathway through accumulation of AGEs and AGEs ligation to RAGE on endothelial cells and macrophages induce inflammation through activating pro-inflammatory cytokines including TNF-ÃŽ ±, 1L-6 a L-1ß, induction of reactive oxygen species (ROS) and through increased oxidative stress which lead to degradation of IKBs (IKBs is normally bound to NF-KB to prevent translocation of NF-KB to nucleus). ROS activates NF-KB which results in translocation of NF-KB to nucleus. Activation of NF-KB cause pathological change of gene expression which is highly related to inflammation, immunity and atherosclerosis, increased expression of inflammatory mediators which lead to insulin resistance and increased RAGE expression as well (Basta et al, 2004). Mechanisms by which intracellular production of advanced glycation end-product (AGE) precursors damages vascular cells. Cellular functions are altered by dicarbonyl advanced glycation end products. Alteration of extracellular matrix proteins results in abnormal interactions with other matrix proteins and with integrins. Alteration of plasma proteins by AGE precursors generate ligands that bind to AGE receptors, inducing conversion of gene expression in endothelial cells, mesangial cells and macrophages. Activation of protein kinase C: The protein kinace C (PKC) family compromises at least eleven isoforms, nine are induced by the lipid second messenger diacylglycerol (DAG). Altered DAG-PKC pathway play an important role in diabetic complications. Intracellular hyperglycaemia raises the amount of DAG which activate PKC in cultured vascular cells and in the retina and renal glomeruli of diabetic animals. Hyperglycaemia may also activate PKC isoforms indirectly by AGEs bind receptors and increased activity of the polyol pathway, possibly through increased reactive oxygen species (ROS). AGE stimulated diacylglycerol (DAG) and activate protein kinase C (PKC) in VSMC. PKC is one of important signal transduction elements involved with multiple cell response. In early studies of diabetes, retinal and renal blood flow abnormalities are due to activation of PKC-ß isoforms perhaps through depressing nitric oxide production or increasing endothelin-1 activity. Abnormal activation of protein kinase C has several pathogenic c onsequences: It leads to decreased production of nitric oxide in smooth muscle cells and glomerular mesangial cells that is induced by hyperglycemia (Brownlee, 2001). Activation of PKC causes inhibition of insulin-stimulated expression of mRNA for endothelial nitric oxide synthase (eNOS) in cultured endothelial cells. Hyperglycaemia activates PKC to increased endothelin-1, permeability of endothelia cells and increased expression of the vascular permeability angiogenesis factor (VEGF) in smooth muscle cells (Brownlee, 2001). Increased generation of reactive oxygen species: Increased generation of reactive oxygen species (ROS) is another possible pathways of diabetes complications especially nephropathy complication. Production of Reactive oxygen species can be result from the activation of various enzymes, including NADPH oxidase, nitric oxide (NO) synthase, and myeloperoxidase, with arising evidence that NADPH oxidase is the major cytosolic source of ROS generation in diabetes. NADPH has homologues that are present within the kidney, namely nox-3, seen in fetal kidney, and nox-4, which is predominately expressed in the renal cortex. AGE bind RAGE induces signal transduction and activate NADPH oxidase in endothelial cells. The interaction between AGE-RAGE enhances production of the cytokine vascular endothelial growth factor (VEGF), which is directly induced by NADPH oxidase and is associated with the pathogenesis of albuminuria in diabetes (Bonke et al, 2008). Diabetes mellitus control and treatment: Both type 1 and 2 diabetes mellitus are characterized by elevated blood glucose level due to insufficiency of insulin level. Therefore, diabetes patients need to reduce blood glucose level through healthy diet, drugs such as (hypoglycemic tablets and anti-atherosclerosis drugs), insulin injection and regular physical exercise. Healthy Diet: In general, healthy diet for diabetes patients should include: limit fats (especially saturated fats and trans-fat acid), proteins and cholesterol. Also, patient should consume a lot of fiber and vegetables. Patients with insulin-producing or insulin synthesis treatment should monitor their blood glucose level to avoid hyperglycemia. For example, adults and teenager patients should maintain their blood glucose level between 80-120 mg/dl, and 100-200 mg/dl for children under 12 year old. Type 1 diabetes patients should test their blood glucose level four to more per day. However, in type 2 diabetes, patients recommend to measure blood glucose level 1 to 2 times daily, because glucose level in type 2 diabetes is more stable than in type 1. Such important tests are important during diet plans and treatment. For example, glycosylated hemoglobin test (HbA1 c) is an indicator for carbohydrate level. Micro and macroalbuminuria indicates of the proteinuria and renal function, for instance if the teat showed high level of proteinuria then the patient need to lowering protein intake (Flaws et al, 2002). Exercise: Physical exercise is important to manage diabetes complications. Regular exercise improves the status of both type 1 and 2 diabetes through transporting sugar to muscles, improving blood circulation, and increasing insulin receptors. Exercise has specific effects on diabetes patients include: reducing blood glucose level during and after exercise, increased insulin sensitivity, reduced triglyceride level and increased good cholesterol (HDL) (Flaws et al, 2002). However, diabetes patients may have several risks associated with exercise which include: hypoglycemia if patient under treatment with hyperglycemia agents, hyperglycemia and ketosis in insulin-deficient patients, and exacerbation of cardiovascular disease. Therefore, patients who are over 30 year old should be examined before doing physical exercise. These examinations include: cardiovascular exams such as blood pressure, blood lipid and ECG, and neurological evaluation such as eye exam (Flaws et al, 2002). Anti-inflammatory drugs Various drugs in recent clinical practice have been used as anti-inflammatory agents such as thiazolidinedione (TZD) class of PPARÃŽ ³ agonists and members of statin class of HMG CoA reductase inhibitors. Both of them have importane anti-inflammatory properities and both have action on glucose homeostasis and cholesterol redusing (Shoelson et al, 2006). TZDs are used to induced insulin sensivity and decresed hyperglicemia in patient with type 2 diabetes mellitus. TZDs drugs inculde pioglitazone, rosiglitazone and troglitazone. The role of TZDs is through binding and activiting PPARÃŽ ³ to induce a number of gene expression products in a dipocyte. TZDs action are attributed to fatty acid in the a dipose tissue. TZD decreases circulating free faty acid and keep faty acid out of musle and liver because accumalte of fatty acide in these tissue lead to insulin resistance. In addition, PPARÃŽ ³ is not only present in dipocyte but also in it is expressed in macrophages and other immune cells response, hepatocyte, endothelial cells and vascular smooth mucsle cells (VSMC). TZD play role in reduce the expression of targets gene for cytokines, growth factors, proliferation and migration of cells, and cell cycle progression (Shoelson et al, 2006). Rosigliatozone: Rosigliatozone decreses the inflammatory markers such as serum C-reactive protein, metalloproteinase-9, white blood cell, tumer necrosis factor-ÃŽ ± and serum amyloid-A in type two diabetes mellitus (Altman, 2003). Group of studies done on Diabetes Rodents: The recent research has demonstrated that rosiglitizone, a PPARÃŽ ³ agonist, attenuates diabetes associated atherosclorosis. The reaserch has studied the direct antiathersclosis effects of PPARÃŽ ³ afer long beriod of therapy in an experiment of insulin deficiency. This study show that rosiglitezone has no effect on glucose level in both control or diabetes mice. However, rosiglitizone , PPARÃŽ ³ (acting as insulin sinstiser) significally decresed plasma insulin level in control mice (Calkin et al, 2005). In addition to Calkin study and his collegous, another study shows that rosiglitazone increase the insulin content and iselt cells number and total mass of pancreas in diabetes rats. However, it is unknown if this is adirect effect of rsiglitazone by activation of PPARÃŽ ³ mediated pathway in islets or indirect effect of normalizing the hyperglicemia (Sanchez et al, 2002). Increaesd secration rate of proinsulin relative to insulin is one oa acommon feature in type 2 diabetes mellitus. The normal range of proinsulin in normal subjects is about 2 to 4% of the total amount of insulin and in type 2 diabetes proinsulin rate is about 15%. Curently the studies has been demonstrated that rosiglitazone in type 2 diabetes decrease proinsulin secretion. Proinsulin has been associated with activity of carboxypeptidase E. Fricker and collegous have evidenced that carboxypeptidase are present in secretory pathway and participate in peptide processing. CarboxypeptidaseB has similler feature as carboxypeptidaseE but the precursor sequence of carboxypeptidaseB has been seen in an adult mouse islet cells. Thus suggest that rosiglitazone may has primery effect on increasing the expression of carboxypeptidaseB precursor protein resulting in increse proinsulin to insulin conversion (Sanchez et al, 2002). Further more, rosiglitizone did not affect fasting insluin level in diabetic mice due to streptozotocin which induce insulin insufficency. Also, another group of study has curently demonstrated that short period of treatment with rosiglitizone decreased plaque area in diabetic mice but had no determination if effects seen were linked to insulin sensitization (Calkin et al, 2005). More current sutdies have evedanced that rosiglitezone treatment in diabetes mice reduce gene expression of the NF-KB subunit p65. Further study has shown that rosiglitizone has no direct effect o glucose-induce upregulation of oxidative stress. Same study had investigated RAGE expression acording to preveious finding that first of all, RAGE expression increse oxidative stress and secondly rosiglitezone which used in culture media alter RAGE expression. The study had shown, the expression of RAGE gene wasnt altered by rosiglitizone (Calkin et al, 2005). Some study showed no significant alteretion in gene expression after TZDs treatment. This is because of almost studies were not preformed in human adipose tissue in vivo but they used adipose tissue of rodents and adipocyte cell line. Actually under such study we should consider about some facts that, for example rosiglitazone dose which used in rodents study (10 mg/kg) is higher than human dose about 100-fold. furthermore, TZD may has an action on gene expressed in rodents but it is not necessarily to has same action on human gene. For example carbonic anhydrase 3 protein raised 2-fold after treated the mice with rosiglitazone, however there was no increasing in carbonic anhydrase 3 mRNA in human adipocyte. Although there were similarities in the action of TZD-induced insulin sensitivity, there may be TZD action has different mechanisms on experimental models and human (Kolak et al,2007). Therfore, Im going to discuss about the studies which have been done on human adipose tissue and there findings. Group of studies done in human patient with type 2 diabetes: Overactivity of ubiquitin-proteasome system is associated with the inflammation and atherosclerotic plaques in type 2 diabetes. Study by Marfella and his colegous on human diabetes patients has been shown that the PPAR-ÃŽ ³ agonist rosiglitazone reduce ubiquitin-proteasome activity and thuss prevent plaque progression to unstable phenotype in diabetes individulas (Marfella et al, 2006). Also, same study shows, the production of O2- by monocytes is reduced after rosiglitazone treatment. Thus proteasome reduction is induced by inhibition of oxidative stress and polyubiquitination. As oxidative stress induce insulin resistence through NF-kB activation, rosiglitazone enhance insulin sensivity and plaque stability in diabetes patien through reducing oxidative stress and ubiquitin-proteasome activity. Further possibility that, NF-KB activation is inhibited by rosiglitazone through a PPAR-ÃŽ ³ independent pathway. PPAR-ÃŽ ³ agonist inhibits NF-KB translocation and subsequent DNA binding through inhibits immune response which induce degradation of IKBs (Marfella et al, 2006). Rosiglitazone have significant effects on metabolism of faty acid and lowering circuliting non-esterified fatty acid. Therfore rosiglitazone prevent islet cells through reducing fatty acid exposure (Sanchez et al, 2002) Kolak and his colleagues investigated the gene of expression in human adipose tissue in vivo in type two diabetes mellitus, befor and after tratment with rosigliatozone and metformin. Reosigliatozone modulates expression of gene which involved in free faty acid synthesis and storage, protein strcture, inflammatory cells inculde macrophage and gene associated in glucose transport and insulin sensivity. Whereas metformin has no effect on these gene (Kolak et al, 2007). TZD decrease the expression of RAGE endothelial protien. From preveious finding, TNF-ÃŽ ± increase the expression of RAGE on endothelial cells, so

Benjamin Franklin

Preview Main Ideas: My speech is going to consist of some of his background which lead him to become the person he was, the role he played in U. S history, and some of his inventions that helped us come a long way. Body l. Main Idea: Benjamin Franklin was born on January 17, of 1706 and was one of seventeen children. Although Benjamin did not get much schooling, he enjoyed to read and write. He would them become an apprentice to his older brother James, who was a printer, composing pamphlets and selling them to the people. When Ben as only 15, his older brother had his own newspaper but wouldn't allow Ben to write for it.He was only an apprentice. The only way to get on that paper was to make up a name, which was â€Å"Silence Dogood†, and send his letters at night so he remained unknown. After some letters he finally admitted to being the owner of those letters which got James angry and Jealous. Once Benjamin could no longer take his brothers harassment he ran away to Philade lphia in 1723. In Philadelphia Ben found Jobs as a helper for many printers until he finally opened his own business. Once his business icked up and was able to retire, he then focused on science, experiments, and inventions which brings me to my next point.II. Main Idea: Franklin invented many things like bifocals, â€Å"the Franklin stove†, a flexible catheter, an odometer, a lightning rod and many more. He also had important concepts in meteorology and refrigeration. We do not take into consideration that many of these things have influenced other innovations that we have today therefore you must think of these inventions as roots. Many people use glasses to enhance their vision and you can thank Mr. Benjamin Franklin. I'm sure todays stoves and ovens are an evolution of his for all you cooks and bakers out there.People who suffer from kidney stones have to deal with a tremendous amount of pain, and back then the catheters were rigid, but again thanks to Ben with his flexi ble catheter it has eased some pain. Franklin did not necessarily invent the odometer as it dates back to the ancient times but he tweaked it to his own version and attached it by the wheel and rigged it to give him his this invention was placed on top of houses and building so that when lighting hits it oes down the rod connected to wires into the ground making the lighting harmless.And lastly Benjamin Franklin is an important man in political American history Ill. Main Idea: As he got older, politics became an interest to him. Franklin was a colonial representative for Pennsylvania, New Jersey, Georgia, and Massachusetts. He soon became a great leader in the American Revolution and started making his way to independence with many other breaking away from Great Britain. Franklin was elected to the Second Continental Congress and worked on a committee of five that elped to draft the Declaration of Independence. Although most of the writing of the Declaration of Independence is Thoma s Jefferson much of the contribution is Franklins. † As said in History. org Benjamin Franklin also helped write the Constitution of the United States which were laws for the new country. He went through a lot along with many other famous American figures to get us to where we are at, in a nation of freedom. Conclusion l. Summary/Recap Main Ideas : I have told you about Franklins a little about Franklins ackground, his inventions, and what he has done to make the country what it is today. Benjamin Franklin At the age of ten, his formal cooling had ended and his new life of self- taught knowledge began. He left Boston and devoted his time to books, becoming his older brother's apprentice In a Philadelphia printing store. By this time outrage against the British control was on an upswing and revolutionary liberal thought was in the air. This atmosphere created a space for innovative and forward thinkers Just like Franklin. Leaders emerged from the rough not because they climbed the verbal ladder to success but because it was necessary to fill the empty rolls of leadership In the new American society.America was calling for a new wave of forward thinkers and untapped potential In the new world's best leaders. Benjamin Franklins life story is a testament to this. His inept potential was arguably not uncommon but the situation and life he was apart of facilitated his rise from humble beginnings to one of the most historically significant American dreamers to date. His autobiography gives in sight to his life. An â€Å"important aspect of the American Dream theme in the Autobiography is the rise from Impotence to importance, from dependence to Independence, from helplessness to power. † O_ A.Leo Lemma 351) Though Benjamin Franklin Is the face of American innovation had he not the support of powerful individuals and progressiveness of the world in which he lived the innovative American environment would have produced another progressive thinker to fuel the flame of progression through innovation equally as renowned to his historical stature. (American Environment at the time provided all supplies needed for a man Like BE to become a legend. ) (America made BE, BE didn't make America. ) Environment- Ben Franklin was a leader not unorthodox to have untraditional educationLife of the normal 18th century colonist was fraught with an uneven match of control from Britain such as the Stamp Act and Tea tax that citizens of the new world were In complete support of break i n relationship from control of Britain. Free market systems were heavily encouraged In the U. S. During this time. The general education of the population of this time was minimal. Young Benjamin was brought up by a humble household who had the goal and aspirations of sending their youngest son to Harvard for the goal of going into the ministry.This fell flat due to finical reasons, UT during this time a formal education was not commonplace. Real ‘higher level' education was just being developed under the new government in the U. S. During the sass's, literacy rates were as high as ever being at 75% of all males and 65% for very uncommon due to modern day rules and regulations but this was definitely not the case in the early sass's. Benjamin Franklin is a great example of the fact that one does not need a formal education to succeed, and also another influential person whom Benjamin Franklin knew during this time also did not have a formal education as Thomas Edison.He ended up being home-schooled primarily and then eventually Joined the railroad at the age of 12, so during this time a formal education was not something that was absolutely necessary. Relationships w/ innovators- flourishing in environment through relationships he was supplied w/ money and power, giving him a sense of worth and importance that allowed him to bring his innovations into fruition. During this time of progression Benjamin Franklin was not alone in his felt of changing traditional thought.Throughout his life he made it a point to seek out other individuals of importance and power to allow him to be among men that will create change in traditional thought. Among these men were John Adams, Thomas Jefferson, George Washington, and James Madison who will later be called the forefathers of America. Provided these relationships that Franklin created it gave him the support that was necessary for his innovations to be known (celebrity). He carefully and deliberately became friends w ith wealthy and powerful people to elevate his social status. Quote) Counterargument- BE as a person- Proportioning self-improvement set him apart from nee Americans. Even in today's society he was revered for his scientific studies + forward thinking. He wasn't exceptional Just for his name. Conclusion- People born into poverty, given everything but can't follow through opportunity to shine/ creatively suppressed, not supported be of way of the world is in a dif environment. Restate thesis Throughout Benjamin Franklins life one can see a constant feeling or urge to better himself.He was brought up in a time when there were many new ideas and free-thinking liberties to be had, and Benjamin took full advantage of them. From his mumble beginnings, Franklin created wealth and prosperity for himself. An important aspect of the American Dream theme in the Autobiography is the rise from impotence to importance, from dependence to independence, from helplessness to power. † 0. A. Leo Lemma 351) Americans revere Benjamin Franklin as one of the most prolific minds of the modern age. But he came from a very meager family.He was born the 1 lath son of the family to a chandler and a housewife. He was pushed very much to become a priest and go to Harvard which would prepare him for the ministry, but his mother and father loud not financially afford for him to attend. He also had his own skepticism about his faith which clouted his ambitions. He reconsidered and decided at the age of 12 to attend another school for basic reading and writing. Around this time Benjamin showed a great interest in books and he ended being arranged as an apprentice under his brother at a printer.His life was created by these books and printing were Just the beginning. Throughout his childhood he became very much interested in learning new things picking up the violin, the guitar and other instruments. He taught himself German, French, and Latin. Through his work-ethic he advised more and m ore Franklins young life: Franklin as starting out on his own: Becoming more influential: thinking. The â€Å"New World† was being created as Benjamin grew, and with that, offered many incredible opportunities to him or to anyone who was bold enough to grasp them.Franklin was no ordinary man. Throughout his life he focused all of his efforts on becoming the best person he could be. Growing up the son of a poor chandler and soap maker he committed himself to becoming a wise learned mind, focusing mentally, physically, and philosophically. Granted, through his time and effort described in his autobiography he created many great situations for himself to develop into one of the wisest minds of the modern thought, but he tended to fall into many situations where he seemed to be in the right place at the right time.During this period of progression the leaders of this new world were being brought out to the fore-front, even if they seems not to be deserving of the role. Benjamin F ranklin poses the essence of the â€Å"self-made† man. Throughout his autobiography he shows us that it isn't always the position that you were born in that creates who we re, but instead, it is our outright curiosity and work-ethic that helps us travel through life and will potentially/eventually lead us to power/wealth/happiness/life satisfaction.An â€Å"important aspect of the American dream theme in the Autobiography is the rise from impotence to importance, from dependence to independence, from helplessness to power. † 0. A. Leo Lemma) Ben Franklin was not completely unaided in his endeavors. He worked incredibly hard for self- improvement and to better himself, but he Just seemed to continually be in the right place at the right time. Benjamin Franklin Benjamin Franklin made the proposition that his friends and himself consider pooling together their respective books in a common place to facilitate ease and convenience of use by all members. Franklin made this suggestion at a meeting that his Book Club was having at Mr. Grace’s house. In explaining the rationale behind his proposal, Franklin added that by placing the books at a single central location, all the members would have the opportunity of having access to every other book that is owned by their colleagues.After considering this suggestion, Franklins’ Book Club members agreed to it. Consequently, each member brought their books until an entire room was completely filled up with various books. Afterwards, following the apparent halting of the aforementioned book pooling arrangement, Franklin began organizing for the setting up of a subscription library. This entity was soon registered in the name of North American subscription libraries, thus marking the genesi s if the library. The following quote illustrates this process.‘About this time, our club meeting, not at a tavern, but in a little room of Mr. Grace's, set apart for that purpose, a proposition was made by me, that, since our books were often referr'd to in our disquisitions upon the queries, it might be convenient to us to have them altogether where we met, that upon occasion they might be consulted; and by thus clubbing our books to a common library, we should, while we lik'd to keep them together, have each of us the advantage of using the books of all the other members, which would be nearly as beneficial as if each owned the whole.It was lik'd and agreed to, and we fill'd one end of the room with such books as we could best spare’ (Franklin, 2006). Following the establishment of the library, Franklin as well as his society was able to engage each other on a more informed level. This is because as members read their colleagues’ books, they developed relevant questions that were presented to those colleagues, thus enhancing academic discourse. Explain Franklin's quest for moral perfection. What process did he use?How successful was he? Which virtues did he find the most challenging to maintain? What was meant by his saying, â€Å"a speckled ax is best? By the term ‘moral perfection,’ Franklin meant the quality of always being able to avoid being engaged in evil things. In addition, the phrase has to do with the humanly habit of always doing what is good or righteous. The succeeding statement illustrates this concept. ‘It was about this time I conceiv'd the bold and arduous project of arriving at moral perfection.I wish'd to live without committing any fault at any time; I would conquer all that either natural inclination, custom, or company might lead me into’ (Icon Reference, 2006). Considering the arduous process through which Franklin went as he pursued ‘moral perfection,’ I should say that he recorded considerable success in his quest. For instance, he noted that authors and commentators had lumped together numerous words to describe various virtues, thus making the virtues’ meanings blurred. He thus simplified the virtues by having succinct explanations for each.It is thus evident that Franklin was significantly successful in this endeavor. Franklin found maintaining the virtue of temperance very demanding sine eternal vigilance was required in order to ward off the numerous temptations that keep occurring. By the ‘a speckled ax is best’ phrase, Franklin meant that it is better for someone to be seen to be trying to observe morality despite the many impediments than for one to completely give in to evil inclinations. By struggling against evil, a person will have both bad and good faces, a situation that Franklin lauded.Was Franklin a religious man? Why, or why not? Provide specific evidence to support your conclusions. Based on his discourse as it i s presented through his autobiography, Franklin was a man who valued and respected religious ideas. For example, as he describes his experiences while in England, Franklin mentions a certain traveling doctor who maliciously distorted the Bible’s message. Considering the bad character that Franklin attributes to this doctor, it is evident that Franklin was a spiritual man.To illustrate, Franklin terms the doctor as ‘an unbeliever’ and a ‘wicked’ man. Such negative terms show that Franklin was unenthusiastic towards this malicious doctor primarily based on what the doctor did to the Bible. This viewpoint, through which Franklin explains his displeasure with the doctor’s action, shows that Franklin had religious roots. The succeeding phrase explains this idea. I imagine, an itinerant doctor, for there was no town in England, or country in Europe, of which he could not give a very particular account.He had some letters, and was ingenious, but much of an unbeliever, and wickedly undertook, some years after, to travestie the Bible in doggrel verse, as Cotton had done Vir gil. By this means he set many of the facts in a very ridiculous light, and might have hurt weak minds if his work had been published; but it never was (Bigelow, 2009). Further, Franklin mentions that he observed the Christian Lent ritual, thus showing that he had religious foundations. This concept is evident from the fact that Lent is usually celebrated by Christians, especially the Roman Catholic believers.The ‘I have since kept several Lents most strictly, leaving the common diet for that, and that for the common, abruptly, without the least inconvenience’ illustrates this religious inclination (Franklin, 2006). References Bigelow, J. (2009). The autobiography of Benjamin Franklin. Charleston, SC: BiblioBazaar, LLC. Franklin B. (2006). The autobiography of Ben Franklin. Sioux Falls, SD: NuVision Publications, LLC. Icon Reference. (2006). The a utobiography of Benjamin Franklin (Webster's Spanish Thesaurus Edition). San Diego, CA: ICON Group International, Incorporated.