Napoleon A Child and Destroyer of the Revolution

Free Essays on Nosferatu

Cinematics of Nosferatu In Nosferatu, the first thing I noticed was that the camera doesn’t move. Except for a few brief pans to show the setting or the landscape. When one scene ends, it blacks out to the next scene, or just jump cuts in a few places to a totally different theme. I think it was because of the old technology everyone moved really fast. An example of this is when the horse and buggy come down the long and winding road from the castle of Nosferatu. This made it seem more humorous than believable. There were places where the movie skipped too. I guess that is just because it was so old. The lack of lighting made it difficult to tell sometimes when it was supposed to be daytime or nighttime. I know from the story that vampires only come out at night, but the scenes that took place at midnight are lighted the same as during the day. That was a little confusing. The only time I was absolutely sure was when the guy lit the lantern and it was brighter than the already bright background. But it made little effect to the actual feel of the movie like good lighting can do in a modern film. Like a dark scene didn’t necessarily foreshadow evil. Even though this film was silent, it wasn’t hard to watch. The actors portrayed what was going on well without using dialog. The parts we had to read weren’t too long either. Each character sort of had their theme music. For the most part the music followed what was going on pretty well. When things moved fast, the tempo of the music increased, and there was increased dissonance for suspense. I only heard three sound effects in the whole film. One was when the clock struck midnight, the others were the cock crowing at dawn, and the drummer out in the streets announcing the plague had arrived. Or at least I think that’s what he was doing. But that’s a pretty lousy job. When they wanted to emphasize something they would either zoom in on it like the book o... Free Essays on Nosferatu Free Essays on Nosferatu Cinematics of Nosferatu In Nosferatu, the first thing I noticed was that the camera doesn’t move. Except for a few brief pans to show the setting or the landscape. When one scene ends, it blacks out to the next scene, or just jump cuts in a few places to a totally different theme. I think it was because of the old technology everyone moved really fast. An example of this is when the horse and buggy come down the long and winding road from the castle of Nosferatu. This made it seem more humorous than believable. There were places where the movie skipped too. I guess that is just because it was so old. The lack of lighting made it difficult to tell sometimes when it was supposed to be daytime or nighttime. I know from the story that vampires only come out at night, but the scenes that took place at midnight are lighted the same as during the day. That was a little confusing. The only time I was absolutely sure was when the guy lit the lantern and it was brighter than the already bright background. But it made little effect to the actual feel of the movie like good lighting can do in a modern film. Like a dark scene didn’t necessarily foreshadow evil. Even though this film was silent, it wasn’t hard to watch. The actors portrayed what was going on well without using dialog. The parts we had to read weren’t too long either. Each character sort of had their theme music. For the most part the music followed what was going on pretty well. When things moved fast, the tempo of the music increased, and there was increased dissonance for suspense. I only heard three sound effects in the whole film. One was when the clock struck midnight, the others were the cock crowing at dawn, and the drummer out in the streets announcing the plague had arrived. Or at least I think that’s what he was doing. But that’s a pretty lousy job. When they wanted to emphasize something they would either zoom in on it like the book o...

Compare and contrast the concepts of Leadership and Power. Draw Essay

Compare and contrast the concepts of Leadership and Power. Draw comparisons between French and Ravens (1959) Bases of Power, expansions of the bases, and a - Essay Example The capacity for individual and organizational transformation must be accompanied by moral responsibility, for transformational leaders shape powerful social and institutional cultures, which may either, be liberating or oppressive. Sources of Interpersonal Power may be 1) Expert -- based on knowledge and expertise, 2) Referent -- extent to which subordinate likes or identifies with supervisor, 3) Legitimate -- job title, 4) Reward -- ability to reward subordinates and 5) Coercive -- ability to punish subordinates.5 While Sources of Political Power (Yukl, 1989)6, Control over decision processes, 2) Forming coalitions, 3) Co-optation, and 4) Gaining influence in large organizations likely to be more a matter of political power than individual power. While t leader-member relations, task structure, and position power to deal with situation, determines the best kind of leader.

Easy A Essay Example | Topics and Well Written Essays - 500 words

Easy A - Essay Example The next Monday, the two goes to the bathroom, and Rhiannon asks about Olive’s encounter with the college student. Olive lies that she lost her virginity with the fictitious boyfriend on the same weekend. Marianne (Amanda Bynes) overheard the conversation. She then proceeded to spread the rumor about Olive’s promiscuity (Devine, Easy A). Marianne, the religious fanatic, and the school’s chastity queen, blames Olive unexpectedly about her promiscuity. Olive wears a cloth of a notorious student. During the English class, she identifies herself as Hester Prynne, the woman condemned by her neighbors in the novel by Nathaniel Hawthorne (Devine, Easy A). Olive confides the truth to her bullied gay friend, Brandon, suggesting to her to lie that he had slept with a girl. Brandon asks for help from Olive, and the two pretends to have had sex in a party. Olive’s reputation degrades. Outcast boys offer to pay Olive so as to improve their image too (Devine, Easy A). Her new power even worked for adults. The teacher Mr. Griffith, and his estranged wife, the guidance counselor who ends up entangled in embarrassments. She finally lost control of the situation and had to take an attitude to revert it. The main female character is Olive Penderghast. The real name of the actor is Emma Stones. In the film, she makes an innocent lie to avoid camping with her best friend, Rhiannon, together with her weird parents. She claims she had gone on a date while she had spent the weekend doing tedious things like singing alone in the room, painting her nails and the nails of her dog (Devine, Easy A). Another female character is Marianne, Amanda Bynes. She is the righteous religious girl in the film. She lights the fuse on olive’s lie and goes ahead in spreading it. Rhiannon, Aly Michalka, is also a female character in the film. She sets peak in the play (Devine, Easy A). Olive Penderghast, the virgin high school girl, never wanted to

Researching Media,Communication and Culture Essay

Researching Media,Communication and Culture - Essay Example Additionally, the story that received the most user comments for the day will be analyzed in terms of these comments. The study limitations are recognized as the challenge of making broad assumptions regarding these findings. TABLE OF CONTENTS I. Introduction and Theoretical Framework†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦...†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦4 II. Purpose of the Study†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦.†¦Ã¢â‚¬ ¦5 III. Review of the Literature†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦...5 IV. Questions†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..†¦7 V. The Design – Methods and Procedures†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦...†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦7 VI. Limitations and Delimitations†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦..†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦10 VII. Significance of the Study†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦.†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦10 I. Introduction and Theoretical Framework The Hollywood entertainment industry emerged as a major cultural force in the early 20th century. While films were the driving-engine of growth, even in the early eras of Hollywood, celebrity fandom emerged as a major occurrence. It was not long before an entire star system emerged, where actors and actresses under contract with specific studios had projects tailored to them. This process continues throu gh the present day as movie stars receive multi-million dollar contracts for a single film. While such prices seem exorbitant to some they are justified because of the significant fans these stars can bring into the theatres. Hollywood hasn’t been the only one to capitalize on such fandom; one considers that today the connection between celebrities and fans extends into a realm of not just appreciation, but also gossip and human interest. Indeed, there are a number of highly popular websites, such as TMZ and Perez Hilton where fans not only view pictures of celebrities but also gain intimate knowledge of the details of their lives. Perhaps a foundational theoretical consideration in terms of the topic is the recognition that the very linguistic origins of the term celebrity share roots with such terms as ‘fame’ and ‘being thronged;’ the French ‘celebre’ means well-known in public (Marshall 1997). With such a fundamental link between cele brity and the public, it is little stretch to consider the important role fandom plays in the equation. While fandom is a regularly occurring aspect of our daily lives, with some individuals exhibiting varying degrees of fanaticism, perhaps the more fundamental question is the underlining significance of this. With the recognition of these understandings in mind this research sets about investigating the motivating influences of fandom. II. Purpose of the Study The study seeks to identify the primary reasons individuals are interested in celebrity gossip. Additionally, it recognizes that there may be underlining issues the individuals are not aware of or external conditions that motivate their interest; as such the study is exploratory in that attempts to unearth and articulate cursory concerns as reflective or conflicting with past research paradigms. III. Review of the Literature There have been a number of research perspectives on the nature of fandom. It’s been argued tha t, â€Å"the emergence of celebrity as a public preoccupation is the result of three major interrelation

Anatomy and Pathophysiology of Gout and Lupus

Anatomy and Pathophysiology of Gout and Lupus Introduction Gout is an acute inflammatory arthritis with the potency to fully destroy the integrity of the joint leading to severe disability. It is termed as a true crystal deposition disease caused by formation of monosodium urate crystals in joints and other tissues. It is the common cause of inflammatory arthritis that has increased in prevalence in recent decades (Roddy and Doherty 2010). Gout normally results from the interaction of genetic, constitutional and environmental risk factors. It is more common in men and strongly age related. Both acute arthritis and chronic arthropathy (tophaceous gout) are considered under the rubric of gout (Mikuls and Saag 2006; Roddy et al. 2007). In a broader term, it can be defined as combination of events involving an increase in the serum urate concentration, acute arthritic attacks with monosodium urate monohydrate crystals demonstrable in synovial fluid leukocytes, and tophi which usually occurs in and around joints of the extremities. These physio-c hemical changes either occur separately or in combination (Terkeltaub 2003; Shai et al. 2010). Gouty arthritis accounts for millions of outpatient visits annually and the prevalence is rising. It affects 1-2% of adults in developed countries, where it is the most common inflammatory arthritis in men. Epidemiological data are consistent with a rise in prevalence of gout. Rates of gout have approximately doubled between 1990 and 2010. A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2% (Eggebeen 2007). Anatomy and Pathophysiology Gouty arthritis is one of the most painful rheumatic diseases and its incidence increases promptly with advancing age. In 75% of the patients, gouty arthritis initially strikes a single joint which is most commonly the big toe. In women gout develop in increasing numbers after menopause eventually at an incidence rate equal to that of men (Hootman and Helmick 2006). In elderly patients, an occurrence of gout is usually less spectacular than in middle age and often implies an upper extremity poly or mono articular presentation rather than the classic mono articular lower extremity picture commonly displayed by middle-aged men. In older patients, gout can be more likely the clinical picture of osteoarthritis or rheumatoid arthritis (Cassetta and Gorevic 2004). Gouty arthritis can be classified into four stages depending upon level of severity namely; (i) Asymptomatic Hyperuricemia: In this stage, a person has elevated blood uric acid levels but no other symptoms and therefore requires no treatment. (ii) Acute Gouty Arthritis: In this stage, hyperuricemia leads to deposition of uric acid crystals in joint spaces, leading to gouty attacks (iii) Interval / Intercritical: This is the stage between acute gouty attacks with no symptoms and (iv) Chronic Tophaceous Gout: where the disease leads to permanent damage (Bhansing et al. 2010). Pathogenesis of gouty arthritis is critically influenced by sodium urate crystals and inflammatory processes they induce (Wise and Agudelo 1996). An inefficient renal urate excretion which leads to the elevated levels of uric acid above the saturation point for urate crystal formation is a major determinant of the disease. Purine catabolism leads to the formation of metabolic by-product, uric acid. In most mammals like higher primates, many birds and some reptiles, the urate oxidase (uricase) enzyme converts uric acid (relatively insoluble) to allantoin (highly soluble), leading to very low serum uric acid levels. A series of parallel mutations in the genes of uricase in the Miocene period results in the production of the dysfunctional form of uricase that leads to accumulation of relatively higher level of insoluble uric acid and subsequently the development of gouty arthritis (Liote and Ea 2006; Eggebeen 2007). Degradation of purines results in the endogenous production of uric aci d that usually contributes about two-thirds of the body urate pool, the remainder being originated by dietry intake. Of the uric acid formed daily, about 70% is excreted through the kidney while the rest is eliminated into the biliary tract and then converted to allantoin by colonic bacterial uricase. Therefore, in the vast majority gouty patients, hyperuricaemia occurs from reduced efficiency of renal urate clearance (Laubscher et al. 2009; Terkeltaub 2010). Development of the acute and chronic inflammatory gout is facilitated with the deposition of monosodium urate (MSU) crystals in joints. while MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a danger signal released from dying cells, little is known about the molecular mechanisms underlying MSU-induced inflammation (Martinon et al. 2006). For crystal formation n occurrence of gout, the ionic product of sodium and uric acid must be at or above the saturation level at which MSU crystals can form. Uric acid is a weak acid of pKa 5.75 and, it exists mainly in the ionized form as urate at physiological pH of 7.40. MSU has limited solubility under physiological conditions and the saturation level in plasma at a pH of 7.40 is 6.8 mg/dl (408 ÂÂ µmol/l) and when the plasma concentration exceeds this level, crystals may form in the joints and tissues (Terkeltaub 2010). MSU crystals preferentially form within cartilage and fibrous tissues, where they are relatively safer from contact with inflammatory mediators and may dwell for years without causing any defects. However, if shed from these sites of origin into the joint space or bursa, they are highly phlogistic particles that are immediately phagocytosed by monocytes and macrophages, stimulating the NALP3 inflammasome, triggering the release of IL-1 and other cytokines and a subsequent infiltration of neutrophils. Here the white cells release a package of inflammatory mediator substances which, in addition to destroying the crystals, also damage the surrounding tissues (Martinon et al. 2006). This acute inflammation defines the symptoms of an acute flare such as pain, swelling and redness and is typically self-limiting. Continual deposition of large numbers of MSU crystals may also heading out the joint damage through mechanical effects on cartilage and bone (pressure erosion), and probably low-gr ade inflammation. However, these more chronic crystal-tissue interactions still remain elusive and in need of further investigations (VanItallie 2010). Systematic Lupus Erythematosus (SLE) Introduction Lupus is an autoimmune disease which leads to both acute and chronic inflammation of various tissues of the human body. Lupus can be classified into different form depending upon the target tissues and organ system. Defined as Type III hypersensitivity reaction, people with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas such as heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. When internal organs are involved, the condition is referred to as systemic lupus erythematosus (SLE). The disease may be mild or severe and life-threatening (Wallace 2010). The prevalence of lupus ranges from approximately 40 cases per 100,000 persons among Northern Europeans to more than 200 per 100,000 persons among blacks (Johnson et al. 1995). In the United States, the number of patients with lupus exceeds 250,000. The life expectancy of such patients has improved from an approximate 4-year survival rate of 50% in the 1950s to a 15-year survival rate of 80% today (Merrell and Shulman 1955; Abu-Shakra et al. 1995). Even so, a patient in whom lupus is diagnosed at 20 years of age still has a 1 in 6 chance of dying by 35 years of age, most often from lupus or infection. Later, myocardial infarction and stroke become important causes of death (Cervera et al. 2003). Anatomy and Pathophysiology SLE is an inflammatory and multi-systemic autoimmune disorder characterized by an uncontrolled auto-reactivity of B and T lymphocytes. This results in the production of auto antibodies (auto-Abs) against self-directed antigens and causes tissue destruction (Cuchacovich and Gedalia 2009). Pathogenesis of SLE is a multi-factorial event and the exact mechanism of disease development and progression is still unclear. Multiple factors are known to be associated with the development of the disease such as genetic, racial, hormonal, and environmental factors. Defects in apoptosis are one of the proposed mechanisms involved in patho-physiological events of SLE. Imbalance in apoptotic machinery leads to the production of auto-antibodies. These antibodies lack the ability to differentiate between pathogenic and normal host cells and cause increase cell death and abnormalities in immune tolerance (Andrade et al. 2000; Rahman and Isenberg 2008). It is believed that all the major components of immune system are involved in SLE progression at various levels. Mostly proteins present in cell nucleus are targeted by the immune system. The likely environmental triggers for SLE include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. It is observed that in patients suffering from SLE, there is increased cell death in monocytes and keratinocytes and hyper expression of Fas protein by B and T cells of the immune system. Tingibl e body macrophages (TBMs) are large phagocytic cells present in the germinal centers of secondary lymph nodes. They express CD68 protein. These cells normally engulf B cells which have undergone apoptosis after somatic hypermutation. In some patients with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells (Gaipl et al. 2006). Monocytes isolated from whole blood of SLE sufferers show reduced expression of CD44 surface molecules involved in the uptake of apoptotic cells. Most of the monocytes and tingible body macrophages (TBM), which are found in the germinal centres of lymph nodes, even show a definitely different morphology; they are smaller or scarce and die earlier. Serum components like complement factors, CRP, and some glycoproteins are, furthermore, decisively important for an efficiently operating phagocytosis. With SLE, these components are often missing, diminished, or inefficient. References Abu-Shakra M, Urowitz MB, Gladman DD, Gough J (1995) Mortality studies in systemic lupus erythematosus. Results from a single center. II. Predictor variables for mortality. J Rheumatol 22:1265-1270 Andrade F, Casciola-Rosen L, Rosen A (2000) Apoptosis in systemic lupus erythematosus. Clinical implications. Rheum Dis Clin North Am 26:215-227, v Bhansing KJ, van Bon L, Janssen M, Radstake TR (2010) Gout: a clinical syndrome illustrated and discussed. Neth J Med 68:352-359 Cassetta M, Gorevic PD (2004) Crystal arthritis. Gout and pseudogout in the geriatric patient. Geriatrics 59:25-30; quiz 31 Cervera R et al. (2003) Morbidity and mortality in systemic lupus erythematosus during a 10-year period: a comparison of early and late manifestations in a cohort of 1,000 patients. Medicine (Baltimore) 82:299-308 doi: 10.1097/01.md.0000091181.93122.55 Cuchacovich R, Gedalia A (2009) Pathophysiology and clinical spectrum of infections in systemic lupus erythematosus. Rheum Dis Clin North Am 35:75-93 doi: S0889-857X(09)00004-0 [pii] 10.1016/j.rdc.2009.03.003 Eggebeen AT (2007) Gout: an update. Am Fam Physician 76:801-808 Gaipl US et al. (2006) Clearance of apoptotic cells in human SLE. Curr Dir Autoimmun 9:173-187 doi: 10.1159/000090781 [pii]Â   10.1159/000090781 Hootman JM, Helmick CG (2006) Projections of US prevalence of arthritis and associated activity limitations. Arthritis Rheum 54:226-229 doi: 10.1002/art.21562 Johnson AE, Gordon C, Palmer RG, Bacon PA (1995) The prevalence and incidence of systemic lupus erythematosus in Birmingham, England. Relationship to ethnicity and country of birth. Arthritis Rheum 38:551-558 Laubscher T, Dumont Z, Regier L, Jensen B (2009) Taking the stress out of managing gout. Can Fam Physician 55:1209-1212 doi: 55/12/1209 [pii] Liote F, Ea HK (2006) Gout: update on some pathogenic and clinical aspects. Rheum Dis Clin North Am 32:295-311, vi doi: S0889-857X(06)00024-X [pii] 10.1016/j.rdc.2006.03.001 Martinon F, Petrilli V, Mayor A, Tardivel A, Tschopp J (2006) Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 440:237-241 doi: nature04516 [pii] 10.1038/nature04516 Merrell M, Shulman LE (1955) Determination of prognosis in chronic disease, illustrated by systemic lupus erythematosus. J Chronic Dis 1:12-32 Mikuls TR, Saag KG (2006) New insights into gout epidemiology. Curr Opin Rheumatol 18:199-203 doi: 10.1097/01.bor.0000209435.89720.7c 00002281-200603000-00014 [pii] Rahman A, Isenberg DA (2008) Systemic lupus erythematosus. N Engl J Med 358:929-939 doi: 358/9/929 [pii] 10.1056/NEJMra071297 Roddy E, Doherty M (2010) Gout. Epidemiology of gout. Arthritis Res Ther 12:223 doi: ar3199 [pii] 10.1186/ar3199 Roddy E, Zhang W, Doherty M (2007) The changing epidemiology of gout. Nat Clin Pract Rheumatol 3:443-449 doi: ncprheum0556 [pii] 10.1038/ncprheum0556 Shai A, Rimar D, Rozenbaum M, Wolfovitz E, Rosner I (2010) Gout in young migrant Filipino women in Israel: a changing epidemiology. Case reports and review of the literature. Rheumatol Int 30:1685-1687 doi: 10.1007/s00296-009-1198-7 Terkeltaub R (2010) Update on gout: new therapeutic strategies and options. Nat Rev Rheumatol 6:30-38 doi: nrrheum.2009.236 [pii] 10.1038/nrrheum.2009.236 Terkeltaub RA (2003) Gout. New England Journal of Medicine 349:1647-1655 doi: doi:10.1056/NEJMcp030733 VanItallie TB (2010) Gout: epitome of painful arthritis. Metabolism 59 Suppl 1:S32-36 doi: S0026-0495(10)00229-5 [pii] 10.1016/j.metabol.2010.07.009 Wallace DJ (2010) Advances in drug therapy for systemic lupus erythematosus. BMC Med 8:77 doi: 1741-7015-8-77 [pii] 10.1186/1741-7015-8-77 Wise CM, Agudelo CA (1996) Gouty arthritis and uric acid metabolism. Curr Opin Rheumatol 8:248-254

Leukemia Essay -- Health Medical Cancer

Leukemia Leukemia is a disease that affects blood-forming tissues, mainly bone marrow. Leukemia also affects the lymph glands and spleen. Leukemia causes the body to produce an extreme amount of abnormal white blood cells. This causes infections because the abnormal cells cannot stop infections like the normal cells do. Leukemia also causes anemia. Anemia is a disease in which the body makes less blood cells. This happens because the leukemic cells crowd the system. Leukemia also causes excessive bleeding. This happens because the amount of platelets will decrease and clotting will not occur, Researchers think a change in genetic structure causes leukemia. Changes in gene structure could be caused by environmental problems. Some of these problems could be: birth defects, radiation, viruses, and chemicals. Leukemia is not inherited and is not contagious. There are two major types of Leukemia, Lymphocytic and Granulocytic. In Lymphocytic Leukemia white blood cells known as Lymphocytes, which are made in the Lymph glands and bone marrow are abnormal or immature. In Granulocytic Leukemia this causes an increase in white blood cells known as granulocytes. Granulocytes are made in the bone marrow, and other tissue. Granulocytes that are affected by leukemia cannot fight of infections. There are two ways in which leukemia can occur. One is acute, and the other is chronic. Acute leukemia is found most in children. It progresses r...