Essay Uncle Toms Cabin as written by Harriet Beecher Stowe

Uncle Toms Cabin as written by Harriet Beecher Stowe The novel Uncle Tom’s Cabin as written by Harriet Beecher Stowe and published in the United States in 1852. The novel depicted slavery as a moral evil and was the cause of much controversy at the time long after. Uncle Tom’s Cabin had impact on various groups publics. It caused outrage in the South and received praise in the North. It is in opinions and historical movements that the impact of this novel can be justified and shows how its publication was a turning point which helped bring about the Civil War. When Abraham Lincoln met Harriet Beecher Stowe in 1852 after the beginning of the American Civil War, he supposedly said to her, â€Å" So you’re the little woman that†¦show more content†¦Stowe convinced readers that the institution of slavery itself was evil, because it supported people like Legree and enslaved people like Uncle Tom. Because of her work, thousands rallied to the anti-slavery cause. Due to popular demand Stowe’s work was p ublished in book form as Uncle Tom’s Cabin on March 20th, 1852. It was not the first anti-slavery novel, but it was by far the most successful. The novel sold 10,000 copies in the first week and 30,000by the end of the first year. Within two years Uncle Tom’s Cabin had sold 2,000,000 copies worldwide. Performances of a play based on the novel drew audiences numbering in the hundreds of thousands. For many Northerners who had no experience with slavery, the novel personalised the evils of slavery. Some Northerners, however, criticised the book, some because they believed it exaggerated slavery’s cruelty but some abolitionists because they thought it downplayed slavery’s cruelty. Although it created some divisions in Northern society, the boundary lines between North South were clearer than ever. Abolitionists especially, loved the novel and the way in which it had impact on the North and South. Northern and Southern authors wrote at least 25 proslavery an d â€Å"Anti-Tom† novels between 1852 and the beginning of the Civil War in 1861. Anti-slavery writings were significant in the abolitionists’ fight against slavery. Using books,Show MoreRelatedHarriet Beecher Stowe s Family897 Words   |  4 PagesHarriet Beecher Stowe was born on June 14, 1811 in a town in Connecticut called Litchfield. Her parents were Reverend Lyman Beecher and Roxanna Foote Beecher, who wanted their children to influence the world in some way. Harriet Beecher Stowe’s family based their philosophies on social justice. Some of the Beecher’s children were ministers, teachers in education for women, the youngest daughter was founder of the National Women’s Suffrage Association, and Harriet was the writer of the family (HarrietRead MoreHarriet Beecher Stowe and the Civil War862 Words   |  4 Pagesonce told Harriet Beecher Stowe,†So you’re the little lady who wrote the book that made this great war†(Hillstrom and Baker 431). Harriet Beecher Stowe, in a way, did start the Civil War, one of the bloodiest battles in American history. She tried her hardest to abolish slavery and never gave up on the slaves no matter what obstacles there were along the road. Stowe wrote Uncle Tom’s Cabin, helped release slaves during the Civil War, and also worked to abolish slavery in her life. Harriet BeecherRead MoreHarriet Beecher Stowes Uncle Toms Cabin Essay1314 Words   |  6 Pageshate. One of the greater uses of fiction’s power is Uncle Tom’s Cabin. Uncle Tom’s Cabin in the era leading up to the American Civil War, which made a lasting impact for years to come, and hit many different characteristics of nineteenth century American beliefs. Harriet Beecher Stowe released her novel Uncle Tom’s Cabin in 1852 and it was immediately controversial. When the book reached southern readers, they were irate. Stowe’s novel was written to confront the basis of the southern way of life andRead MoreFiction in Uncle Toms Cabin by Harriet Beecher Stowe1477 Words   |  6 Pageshate. One of the greater uses of fiction’s power is Uncle Tom’s Cabin. Uncle Tom’s Cabin in the era leading up to the American Civil War, which made a lasting impact for years to come, and hit many different characteristics of nineteenth century American beliefs. Harriet Beecher Stowe released her novel Uncle Tom’s Cabin in 1852 and it was immediately controversial. When the book reached southern readers, they were irate. Stowe’s novel was written to confront the basis of the southern way of life andRead MoreUncle Tom s Cabin By Harriet Beecher Stowe1522 Words   |  7 PagesLincoln is quoted as saying, â€Å"So you’re the little woman who wrote the book that started this great war.† upon meeting Harriet Beecher Stowe for the first time. The book that the former president is referring to is Uncle Tom’s Cabin, a 1850s book about the moral wrongs of slavery. It has been said to be the most influential anti-slavery book that has ever been written. Harriet Beecher Stowe is an effective author. She uses numerous literary devices such as facile characters, character foils, and symbolismRead MoreUncle Tom s Cabin By Harriet Beecher Stowe1037 Words   |  5 PagesHarriet Elisabeth Beecher Stowe was a famous author and abolitionist from America that wrote the famous novel Uncle Tom’s Cabin. This book supposedly depicted the life of an average African-American slave from the southern states of America. It was very popular during the 1800s and reached a wide audience as a play and a novel in the United Kingdom and the United States of America. This novel angered many of the Southerner’s because she wrote Uncle Tom’s Cabin without the proper knowledge of slaveryRead MoreSource Evaluation of Uncle Toms Cabin, by Harriet Beecher Stowe1263 Words   |  6 Pagessurrounding the novel? Whatever the criterion for a good novel is Uncle Tom’s Cabin by Harriet Beecher Stowe may well be one of the critical controversial novel of its time. Regarding Uncle Tom’s Cabin, I collected sources about the critical controversy about the novel. In my findings, there is Norton Critical Edition, A Routledge Literary Sourcebook on the novel, Uncle Tom’s Cabin by Harriet B. Stowe, lastly â€Å"The Little Cabin of Uncle Tom† by Egbert Oliver. I classified each source from best to worseRead MoreAnalysis Of The Novel Uncle Tom s Cabin 1345 Words   |  6 Pagesnovel has been more harshly treated than works written by men which are just as dated and offensive in their treatment of race, notably, Huckleberry Finn.† (Annette Gordon-Reed). I believe that Stowe’s novel was taken seriously as a woman’s novel. Uncle Tom’s Cabin was very influential in that time period, and still is today. The novel is commonly noted as a big influence that began the Civil War, and people still refer to it today. Uncle Tom’s Cabin is used very commonly today as a reference to slaveryRead MoreHarriet Bee cher Stowe: The Eyes Behind Slavery1640 Words   |  7 PagesHarriet Beecher Stowe: The Eyes Behind Slavery Harriet Beecher Stowe became one of the most famous writers, reformers, and abolitionist women of the 1800s in large part due to her most effective selling fictional book, Uncle Toms Cabin. The image of brutal whippings, rape, and the splitting of families broke down the hearts of people in the eighteenth century. Her writing influenced thousands to become a great phenomenon, take a stand, and change the world. Harriet Beecher Stowe lived much ofRead MoreTerm Paper1494 Words   |  6 Pagesbecause Matthiessen did not appreciate women writers of the nineteenth century does not mean that others have to follow in his footsteps; which is why this is an appreciation essay to two nineteenth century female writers: Catherine Sedgwick and Harriet Beecher Stowe. Catharine Maria Sedgwick was born December 28, 1789 in Stockbridge, Massachusetts. In childhood, Sedgwick was cared for by a former slave and as a young woman, Sedgwick attended a private school where girls are prepared for entry into fashionable

Enzyme Structure and Functions Free Essays

ENZYME STRUCTURE AND FUNCTIONS: Enzymes are biological catalysts. They increase the rate of reactions by a factor of between 106 to 1012 times, allowing the chemical reactions that make life possible to take place at normal temperatures Definition of enzyme: A protein with catalytic properties due to its power of specific activation is defined as an enzyme. STRUCTURE Enzymes are proteins their function depends on its complexity. We will write a custom essay sample on Enzyme Structure and Functions: or any similar topic only for you Order Now The reaction takes place in a small part of the enzyme called the active site, while the rest of the protein acts as â€Å"scaffolding†. The shape and the chemical environment inside the active site permits a chemical reaction to proceed more easily Many enzymes need cofactors (or coenzymes) to work properly. Tightly bound cofactors are called prosthetic groups Cofactors that are bound and released easily are called coenzymes These can be metal ions (such as Fe2+, Mg2+, Cu2+) or organic molecules (such as haem, biotin, FAD, NAD or coenzyme A). Many of these are derived from dietary vitamins, which is why they are so important. The complete active enzyme with its cofactor is called a holoenzyme, while just the protein part without its cofactor is called the apoenzyme. HW DOES AN ENZYME WORK? 1) REACTION MECHANISM 2) MOLECULAR GEOMETRY REACTION MECHANISM: In any chemical reaction, a substrate (S) is converted into a product (P) In an enzyme-catalysed reaction, the substrate first binds to the active site of the enzyme to form an enzyme-substrate (ES) complex, then the substrate is converted into product whilst attached to the enzyme, and finally the product is released, thus allowing the enzyme to start all over again An example is the action of the enzyme sucrase hydrolysing sucrose into glucose and fructose. MOLECULAR GEOMETRY The substrate molecule is complementary in shape to that of the active site. It was thought that the substrate exactly fitted into the active site of the enzyme molecule like a key fitting into a lock (the now discredited ‘lock and key’ theory). This explains enzyme specificity This explains the loss of activity when enzymes denature The Induced Fit Hypothesis  : * Some proteins can change their shape (conformation) When a substrate combines with an enzyme, it induces a change in the enzyme’s conformation * The active site is then moulded into a precise conformation * Making the chemical environment suitable for the reaction * The bonds of the substrate are stretched to make the reaction easier (lowers activation energy) ENERGY CHANGES  : Energy needed for initial reaction is known as ACTIVATION ENERGY. The larger the activation energy is, the slower the reaction will be. This is because only a few substrate molecules will have sufficient energy to overcome the activation energy barrier. Enzymes reduce the activation energy of a reaction so that the kinetic energy of most molecules exceeds the activation energy required and so they can react. Factors affecting Enzymes substrate concentration pH temperature enzyme concentration inhibitors SUBSTARTE CONCENTRATION The rate of an enzyme-catalysed reaction is also affected by substrate concentration. As the substrate concentration increases, the rate increases because more substrate molecules can collide with active sites, so more enzyme-substrate complexes form. At higher concentrations the enzyme molecules become saturated with substrate, and there are few free active sites, so adding more substrate doesn’t make much difference The maximum rate at infinite substrate concentration is called vmax, and the substrate concentration that gives a rate of half vmax is called KM. These quantities are useful for characterising an enzyme. A good enzyme has a high vmax and a low KM. pH Enzymes have an optimum pH at which they work fastest. For most enzymes this is about pH 7-8 (normal body pH), but a few enzymes can work at extreme pH. The pH affects the charge of the amino acids at the active site, so the properties of the active site change and the substrate can no longer bind. TEMPERATURE: Enzymes have an optimum temperature at which they work fastest. For mammalian enzymes this is about 40 °C. Up to the optimum temperature the rate increases geometrically with temperature. Above the optimum temperature the rate decreases as more of the enzyme molecules denature. The thermal energy breaks the hydrogen bonds holding the secondary and tertiary structure of the enzyme together, so the enzyme loses its shape Q10 (the temperature coefficient) = the increase in reaction rate with a 10 °C rise in temperature. ENZYME CONCENTRATION As the enzyme concentration increases the rate of the reaction also increases, because there are more enzyme molecules (and so more active sites), available to catalyse the reaction therefore more enzyme-substrate complexes form INHIBITORS Inhibitors inhibit the activity of enzymes, reducing the rate of their reactions. 2 TYPES: Competitive and non competitive COMPETITIVE: A competitive inhibitor molecule has a similar structure to the substrate molecule, and so it can fit into the active site of the enzyme. It therefore competes with the substrate for the active site, so the reaction is slower. Increasing the concentration of substrate restores the reaction rate and the inhibition is usually temporary and reversible. NON COMPETITIVE: A non-competitive inhibitor molecule is quite different in structure from the substrate and does not fit into the active site. It binds to another part of the enzyme molecule, changing the shape of the whole enzyme, including the active site, so that it can no longer bind substrate molecules. Non-competitive inhibitors therefore simply reduce the amount of active enzyme. How to cite Enzyme Structure and Functions:, Essay examples

Leadership for Sustainability of the Health System- myassignmenthelp

Question: Discuss about theLeadership for Sustainability of the Health System. Answer: Leadership exists at the governance, management and clinical care levels of healthcare. Various researches show that the quality of leadership is a major factor affecting individuals. Key considerations include contentment, trust, commitment, efficacy, values and the internal climate of an organization. (Bell et al. 2004; Burke et al.2006; DeGroot, Kiker Cross 2000; Dirks Ferrin 2002; Gerstner Day 1997; Kouzes Posner 2007). The critical role is in the steering of an objective to completion (Avolio, Wlaumba Weber 2009; Kouzes Posner 2007). A study was done on 1300 hospitals based in Europe and the United States and t was indicated that leadership is pivotal. The health outcome is dependent on good management and clinically competent leadership (Dorgan et al. 2010). In the United Kingdom, the health workforce is anchored on leadership especially on higher managerial ranks. Patients complaints also reduce with good performance indices (CQC 2011). Clinicians take the pole positon in leadership rather than flooding the helm of clinical management with clinicians. Clinical governance is seen in management, decision making and encouraging of the peers by steering innovation and upholding relevant trends that favor results. The course of this can be achieved through embedding developmental leadership in upgrading quality, security or a vibrant healthcare training. Participation of clinicians in the substance of leadership and management is critical in order to save costs and solving of clinical problems. Errs in decision making and control of the clinical structure occur from bogus management that is resource management and budgeting is left to senior clinicians while very senior colleagues have limited leadership capability. Effective leadership greatly improves nurse retention rates and does reduce the nursing turnover. Practice involves loads of work and increased propensity to burnout and truancy for which the managerial team employs staffing to manage (Duffield et al., 2008). The nursing workplace reports productivity in a well set leadership system with proper protocols to conflict resolution, performance appraisal, collective motivation and inspiration of nurses at all cadres (Duffield et al., 2008; Eddy et al., 2009; Frandsen, 2009). References Health Workforce Australia (2012). Leadership for the Sustainability of the Health System: Part 1-A Literature Review. Health Workforce Australia. Adelaide, Australia. Retrieved from;https://www.hwa.gov.au/sites/uploads/leadership-for-sustainability-of-health-sector-literaturereview-012012.pdf Health Workforce Australia (2012). Leadership for the Sustainability of the Health System: Part 1-A Literature Review. Health Workforce Australia. Adelaide, Australia. Retrieved from;https://www.hwa.gov.au/sites/uploads/leadership-for-sustainability-of-health-sector-keyinformant-012012.pdf Nelsey, L., Brownie, S. (2012). Effective leadership, teamwork and mentoring ssss Essential elements in promoting generational cohesion in the nursing workforce and retaining nurses. Collegian 19(4), 197-202

Battle Between Corruption And Stability Essays -

Battle Between Corruption and Stability Annonymous Nathaniel Hawthorne's background influenced him to write the bold novel The Scarlet Letter. One important influence on the story is money. Hawthorne had never made much money as an author and the birth of his first daughter added to the financial burden (Biographical Note VII). He received a job at the Salem Custom House only to lose it three years later and be forced to write again to support his family (IX). Consequently, The Scarlet Letter was published a year later (IX). It was only intended to be a long short story, but the extra money a novel would bring in was needed (Introduction XVI). Hawthorne then wrote an introduction section titled The Custom House to extend the length of the book and The Scarlet Letter became a full novel (XVI). In addition to financial worries, another influence on the story is Hawthorne's rejection of his ancestors. His forefathers were strict Puritans, and John Hathorne, his great-great-grandfather, was a judge presiding during the S! alem witch trials (Biographical Note VII). Hawthorne did not condone their acts and actually spent a great deal of his life renouncing the Puritans in general (VII). Similarly, The Scarlet Letter was a literal soapbox for Hawthorne to convey to the world that the majority of Puritans were strict and unfeeling. For example, before Hester emerges from the prison she is being scorned by a group of women who feel that she deserves a larger punishment than she actually receives. Instead of only being made to stand on the scaffold and wear the scarlet letter on her chest, they suggest that she have it branded on her forehead or even be put to death (Hawthorne 51). Perhaps the most important influence on the story is the author's interest in the dark side (Introduction VIII). Unlike the transcendentalists of the era, Hawthorne confronted reality, rather than evading it (VII). Likewise, The Scarlet Letter deals with adultery, a subject that caused much scandal when it w! as first published (XV). The book revolves around sin and punish ment, a far outcry from writers of the time, such as Emerson and Thoreau, who dwelt on optimistic themes (VII). This background, together with a believable plot, convincing characterization, and important literary devices enables Nathaniel Hawthorne in The Scarlet Letter to the develop the theme of the heart as a prison. The scaffold scenes are the most substantial situations in the story because they unify The Scarlet Letter in two influential ways. First of all, every scaffold scene reunites the main characters of the novel. In the first scene, everyone in the town is gathered in the market place because Hester is being questioned about the identity of the father of her child ( Hawthorne 52). In her arms is the product of her sin, Pearl, a three month old baby who is experiencing life outside the prison for the first time (53). Dimmesdale is standing beside the scaffold because he is Hester's pastor and it is his job to convince her to repent and reveal the father's name (65). A short time later, Chillingworth unexpectedly shows up within the crowd of people who are watching Hester after he is released from his two year captivity by the Indians (61). In the second scene, Dimmesdale is standing on top of the scaffold alone in the middle of the night (152). He sees Hester and Pearl wal! k through the market place on their way back from Governor Winthrop's bedside (157). When Dimmesdale recognizes them and tells them to join him, they walk up the steps to stand by his side (158). Chillingworth appears later standing beside the scaffold, staring at Dimmesdale, Hester, and Pearl. In the final scaffold scene, Dimmesdale walks to the steps of the scaffold in front of the whole town after his Election day sermon (263). He tells Hester and Pearl to join him yet again on the scaffold (264). Chillingworth then runs through the crowd and tries to stop Dimmesdale from reaching the top of the scaffold, the one place where he can't reach him (265). Another way in which the scenes are united is how each illustrates the immediate, delayed, and prolonged effects that the sin of adultery has on the main characters. The first scene shows Hester being publicly punished on the scaffold (52). She is being forced to stand on it for three hours straight and listen to peop! le talk about her as a disgrace and a shame to the community (55) . Dimmesdale's instantaneous response to the sin is to lie. He

Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma The WritePass Journal

Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma Introduction Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma IntroductionEpidemiology of Primary Infantile Glaucoma Signs, Symptoms and Consequences of Primary Infantile GlaucomaPathology, Pathogeneses and Causes of Primary Infantile GlaucomaOptic Cup Asymmetry in Primary Infantile Glaucoma Secondary infantile glaucomaReferencesRelated Introduction The incidence of glaucoma in the young population is incomparable to the incidence in the adult population, as it is very rare in infants, nevertheless it can significantly affect a child’s life, as vision is vital for a young child. Signs and symptoms of infantile glaucoma can commonly be overlooked and this can cause a delay to the treatment process. The underlying causes of infantile glaucoma have been agreed upon by most authors, however the exact mechanism by which the structures in the young eye are affected are debatable. As well as primary infantile glaucoma, young children can also be affected by secondary infantile glaucoma, which again can significantly impact a young child’s life. This paper looks at the classifications, epidemiology, signs, symptoms, aetiology and pathogenesis of primary infantile glaucoma, as well as touching upon the causes of secondary infantile glaucoma. ‘Glaucoma is an Optic neuropathy with characteristic appearances of the optic disc and specific pattern of visual field defects that is associated frequently but not variably with raised intra-ocular pressure (IOP)’ (Kanski, 2003). The ciliary processes of the eye produce aqueous humor; this is then drained by the trabecular meshwork; Figure 1. A balance of this production and drainage maintains a normal IOP. The aqueous humor produced flows into the posterior chamber, then through the pupil and into the anterior chamber. The trabecular meshwork drains the aqueous humor through Schlemm’s canal. Open angle glaucoma occurs when there is a decrease in the outflow of aqueous through the trabecular meshwork, and angle closure glaucoma occurs when the iris adheres to the lens leading to a build-up of aqueous humor in the posterior chamber   (Kanski, 2003). In addition to open and closed angle glaucoma there are other types of glaucoma which are classified in Figure 2. There are several classifications of congenital and infantile glaucomas, the most accepted and simplified version is presented in figure 3. Primary infantile glaucoma is defined as ‘the result of isolated abnormal development of the anterior chamber angle structures’ (Myron Yanoff, 2009) Secondary infantile glaucomas are ‘associated with a variety of ocular and systemic syndromes and with surgical aphakia’ (Myron Yanoff, 2009). Primary congenital glaucoma is present at birth however it is not always recognised at this stage and sometimes it is diagnosed later during infancy or in early childhood. To minimise problematic visual development, recognition of primary congenital glaucoma must be as early as possible followed by respective treatment or therapy, allowing the child to lead a ‘normal’ life (A.Armstrong, 2008). Glaucoma in infants and young children is relatively rare and in some cases asymptomatic (Kanski, 2003). And so, if an increase in IOP is not detected at an early stage then there is a greater risk of blindness (Robert N. Shaffer, 1970). Some cases of glaucoma in infants are only recognised and diagnosed after several months or years at which stage sometimes significant glaucomatous damage has already occurred (Robert N. Shaffer, 1970). Most cases will present bilaterally nevertheless this does not rule out the fact that it can sometimes present unilaterally   (Robert N. Shaffer, 1970). Epidemiology of Primary Infantile Glaucoma Primary infantile glaucoma is extremely rare and occurs in one out of 10,000 births (MillerSJ, 1966). It accounts for 0.01% to 0.04% of cases of total blindness (A.Armstrong, 2008) (Vincent P Deluise, 1983) In the Irish childhood population primary open angle glaucoma is the cause of blindness for 4% of the population. (Morin JD, 1974) The majority of cases in the US and Europe present with bilateral primary infantile glaucoma; 65%-80% (Moller, 1977). It is also well-known that it occurs greater in males compared to females with a ratio of 3:2 respectively (Vincent P Deluise, 1983). This is proven by a study with 125 infants from Westerlund, 76 of whom were male i.e. nearly 61% were males (Vincent P Deluise, 1983). On the other hand in Japan, this is no longer true and the ratio is actually reversed (Vincent P Deluise, 1983). In another study based in Japan out of 46 children with primary infantile glaucoma 63% were actually female (Vincent P Deluise, 1983). In the majority of cases the development of primary infantile glaucoma is found to sporadic, and so it is non-familial and nonhereditary, but approximately 10% of cases are familial, transmitted to the child via autosomal recessive inheritance (Vincent P Deluise, 1983). Signs, Symptoms and Consequences of Primary Infantile Glaucoma Children are commonly referred to the Ophthalmologist due to clinical evidence of corneal oedema. Primary infantile glaucoma is commonly misdiagnosed, hence causing a delay in the correct diagnosis, as it may initially show symptoms similar to conjunctivitis such as a ‘red eye’ (Becker B, 1965). There will also be evidence of the classic triage; epiphora, blepharospasm and photophobia. (Becker B, 1965). Further examination will reveal megalocornea (enlarged corneal diameter), buphthalmos (enlarged globe), Haab’s striae (breaks in Descemet’s membrane) and optic nerve head changes (Becker B, 1965). Buphthalmos; figure 4, or ocular enlargement, occurs in primary infantile glaucoma because the globe of neonates is still distensible (Vincent P Deluise, 1983). Collagen of the cornea and scleral have not hardened enough, so expansion of the fibrils occurs due to an increase in IOP (Vincent P Deluise, 1983). This therefore causes stretching to occur in several structures of the infant eye; such as the cornea, the anterior chamber angle, the sclera, the optic nerve, scleral canal and the lamina cribrosa (Becker B, 1965). This explains why ocular enlargement due to glaucoma does not occur in adults, as the globe is no longer distensible and collagen fibres of the cornea are sclera are hardened hence expansion doesn’t occur in adults. It is agreed that delayed therapy of infants with glaucoma, will result in a poor visual outcome for the infant, which could have been prevented or at least minimised. To understand why some infants had more advanced glaucoma than others; a study with 24 infants and children was conducted (David J. Seidman MD1, 3 March 1986). Their signs and symptoms were noted. The parents of the infant were asked to indicate whether they had noticed either epiphora or photophobia and only 32% said their infant had these symptoms. A small 21% of infants presented with only signs of glaucoma, noticed by the parents but no symptoms. And finally the majority of infants, 90%, actually did have signs when presenting to the physician. It has been noted that signs of infantile glaucoma are more difficult to notice when it is bilateral, as in all 3 cases where the physicians failed several times to refer the infant to an ophthalmologist the glaucoma was in fact bilateral   (David J. Seidman MD1, 3 March 1 986). A normal value for the corneal diameter of a neonate is approximately 10mm, an increase to 12mm or greater, along with expansion of the corneal-scleral junction, is usually due to increased IOP (Kwitko, 1973). Enlargement of the cornea due to an increase in IOP is most likely to occur up to the age of three (Scheie, 1955) after which the sclera may become deformed up to age ten (Mann, 1957). Breaks occur in the endothelium and Descemet’s membrane due to the increase in IOP which also causes stretching in these layers (Vincent P Deluise, 1983).   ‘Haab’s striae form as endothelial cells lay down new basements membrane (Descemet’s membrane) and hyaline ridges develop. Breaks in Descemet’s membrane from increased IOP rarely occur after age three’ (Vincent P Deluise, 1983).   Increased IOP also causes slow expansion of the sclera of the neonate. A ‘bluish’ scleral appearance is seen due to thinning of the sclera, causing the choro id to be more apparent (Vincent P Deluise, 1983). As the neonate becomes older and growth occurs the expansion of the sclera no longer occurs due to a build-up of extracellular connective tissue (Vincent P Deluise, 1983). Even if the IOP decreases back to a value within normal the globe does not usually return to normal size (Vincent P Deluise, 1983). Studies have shown that myopia and astigmatism are the consequence of an increase in the axial length of the globe, figure 5 (Robin AL, 1979). Robin et al also found that ‘In contrast to adult eyes, the scleral canal in children apparently enlarges with high IOP. Thus, disk cup size increase in children could occur from neural tissue loss, from scleral canal enlargement, or from a combination of the two processes’ (Robin AL, 1979). ‘Myopic astigmatism and anisometropia are particularly common in cases of unilateral or asymmetric primary infantile glaucoma’ (Vincent P Deluise, 1983).   A study carried out by Broughton and Parks found that all of their patients with unilateral primary infantile glaucoma had anisometropia; on the affected side an average difference of 4.93D of myopia was found (Broughton WL, 1981 May). Optic nerve changes which occur in adults with glaucoma are very different to the optic nerve changes which occur in children with glaucoma. At first Becker Shaffer initially thought that cupping in primary infantile glaucoma was a process which was gradual however it was soon discovered that optic nerve changes in primary infantile glaucoma could also occur early and rapidly (Becker B, 1965). In adults with optic nerve changes which occur due to an increase in IOP the change is very unlikely to be reversible, however in infants optic nerve cupping which occurs due to an increase in IOP can be reversed once the IOP is returned back to normal (Vincent P Deluise, 1983). The most accepted and most reasonable hypothesis which aims to explain why cupping is reversible in neonates is based on the fact that the connective tissue of the lamina cribrosa is not matured (Quigley, 1977 Sep). However there are cases when even though the pressure has decreased back to normal the Optic nerve head damage does not reverse, this is due to one of two reasons. Firstly it is possible that some of the stretching is permanent ‘with remoulding of the connective tissue’   (Vincent P Deluise, 1983). Secondly it could be due to ‘a loss of glial and axons’ (Vincent P Deluise, 1983).   ‘Adult optic nerve heads with their dense connective tissue investments are more resistant to remoulding, indicating that cupping is caused by permanent loss of glia and axons’ (Vincent P Deluise, 1983). Pathology, Pathogeneses and Causes of Primary Infantile Glaucoma The explanation for the increase in IOP in primary infantile glaucoma has been described using Barkan’s membrane theory. This theory is based on the fact that the anterior chamber angle is covered by a thin and imperforate membrane, which inhibits aqueous outflow, which in turn leads to raised IOP (Vincent P Deluise, 1983). According to the theory, this raised IOP is treated by goniotomy when the surface tissue of this membrane is detached, and so â€Å"the peripheral iris falls posteriorly,† subsequently there is aqueous outflow and a decrease in IOP (Vincent P Deluise, 1983). Worst also agreed with the Barkan membrane theory, â€Å"†¦in congenital glaucoma the chamber angle is filled with a band of persistent mesodermal tissue (persistent uveal meshwork or persistent pectinate ligament). This tissue completely covers the fetal corneoscleral system, but is not the cause of the obstruction to aqueous outflow in its own right. It is the presence of an imperforate surface layer on this persistent mesodermal tissue, which is the only cause of obstructed outflow. This surface membrane, Barkans membrane, is probably an endothelial surface, which normally breaks apart, but which persists in congenital glaucoma† (Worst, April 1968). There is no well supported histopathologic evidence to support Barkan’s membrane theory, despite this Worst still believes that the theory along with its concepts are valid, he says â€Å"though histopathologic proof of this structure is almost completely lacking†¦this has little influence on the probability th at this concept is valid† (Worst, April 1968). So if Barkan’s membrane theory has insufficient evidence to explain the cause of an increase in IOP in congenital glaucoma, then what is the alternative? There is some histopathologic evidence which aims to explain in detail the anterior chamber angle and its histopathology in infants with primary infantile glaucoma see Figure 6 (Vincent P Deluise, 1983). Anderson thoroughly researched the development of the trabecular meshwork in infantile glaucoma. He said that earlier thoughts were that â€Å"the anterior chamber recess deepens by atrophy of the rarified tissue that in the earlier stage separated the trabecular meshwork and ciliary body.† He then confirmed that later thoughts highlighted the function of cleavage into the loose tissue, as there was no proof of atrophy (D.R.Anderson, 1981). These views may have seemed correct at the time however, evidence has proven that cleavage or atrophy are not the only explanations of the process of development. Both cleavage and atrophy would cause the uveal tract to become fragmented from the shell of the cornea and sclera as well as the tissue of the trabeculae (Fig 7A) (D.R.Anderson, 1981). This would result in extension of the ciliary muscle to the peripheral iris and on the posterior surface of the peripheral iris would be the ciliary processes (D.R.Anderson, 1981). However this does not actually occur, in fact the ciliary muscle and the ciliary processes continue to adhere to the envelope of the cornea and sclera although compared to their earlier position they do become depressed (Fig 7B) (D.R.Anderson, 1981). Anderson found that there is an overlay of the ciliary muscle in particular the ciliary processes over the trabecular meshwork; however they are subsequently depressed behind the scleral spur (D.R.Anderson, 1981). He found that â€Å"This repositioning can be explained only by a posterior sliding of the uveal tissues in relation to the cornea and sclera, presumably due to a differential growth rate of the various tissue elements† (D.R.Anderson, 1981). He concluded that this course of repositioning was not simply due to the â€Å"sliding of the uveal tract along the inner side of the sclera. There is also a repositioning of the various layers within the uveal tract in relation to one another: initially the innermost muscle fibers have a position relatively more anterior than the outermost fibers† (D.R.Anderson, 1981) Anderson also found that compared to the ciliary muscle the ciliary processes are at first a lot more frontward, as time passes both become level behind the scleral spur and meshwork (D.R.Anderson, 1981). So, far it has been established that primary infantile glaucoma occurs because the anterior chamber does not develop normally. At what stage of development do these changes or lack of changes occur? It has been noted that at week twelve of development â€Å"a wedge shaped mass of mesenchyme can be identified at the anterior chamber angle i.e. at the junction of the papillary membrane and the lateral margins of the cornea. Within this wedge shaped portion of the tissue there is a row of small capillaries, which are lined with mesoderm-derived vascular endothelial cells† (A.Armstrong, 2008). At the beginning of the fifth month â€Å"early trabeculae are apparent separated by intervening spaces† (A.Armstrong, 2008) subsequently the capillaries fuse to form the canal of Schlemm, this is continuous with the collector channels as well as the scleral vessels (A.Armstrong, 2008). â€Å"The meshwork becomes specialised into inner uveal trabeculae, numerous intermediate layers of lamellar corneoscleral trabeculae, and a more loosely organised cribriform meshwork† (A.Armstrong, 2008). The inner surface of the meshwork is lined with cuboidal cells, perforations of these cells occur onwards from 15 weeks (A.Armstrong, 2008). Communication between the meshwork and the anterior chamber occur via these cuboidal cells (A.Armstrong, 2008). Between the sixth and ninth month development of the anterior chamber occurs (A.Armstrong, 2008). It presents â€Å"as a chink in the mesoderm between the iris root and the developing trabeculum. If the mesoderm does not entirely regres s in this region, an impervious layer may remain bridging the angle between the iris and the cornea and which impedes access of aqueous to the trabecular meshwork† (A.Armstrong, 2008). Figure 8: Comparision of optic cup asymmetry in normal infants with unilateral glaucoma infants. Taken from (Richardson, April 1968) Optic Cup Asymmetry in Primary Infantile Glaucoma It has been established that chronic open angle glaucoma is found to be bilateral and symmetrical to a certain extent, however some meticulous studies may find that there is somewhat of asymmetry in the cupping of the optic discs (Richardson, April 1968). Nevertheless the asymmetry of the discs can be used to diagnose early signs of glaucoma (Richardson, April 1968). Although optic disc cupping is assessed in infantile glaucoma it is not used as prominently compared to chronic open angle glaucoma (Richardson, April 1968). One of the reasons for this is due to the obvious fact that it is not as easy to conduct ophthalmoscopy in infants especially with added factors such as hazy corneas, miotic pupils (Richardson KT, 1966). It is also a common misconception that cupping in the optic nerve occurs at a very late stage and so it is no longer relevant to aid diagnosis (Richardson, April 1968). The opposite is actually true, as changes to the optic disc in infantile glaucoma occur relatively early on, hence valuable factor to aid prognosis (Shaffer.RN, 1967). To emphasise the importance of asymmetry of optic discs in infantile glaucoma compared to chronic glaucoma, the following study was conducted by Kenneth Richardson. Normal newborn infants, 96 hours old or less, were randomly chosen and their optic discs were assessed. Out of 468 it was found that only 11 infants had optic cup asymmetry, 2.3%; figure 8 (Richardson, April 1968). Similarly Snydacker found that out a random 500 adults only 15 had any sign of asymmetry, 3% (SyndackerD, 1964). Going back to the infants it was found that only 3 out of the 11 actually had marked asymmetry between their optic cups i.e. only 0.6%; figure 8 (Richardson, April 1968). A very different but much predicted result was found when Shaffer conducted a slightly different study (Shaffer.RN, 1967). 27 infants with unilateral glaucoma were assessed and it was found that 89% or 24 out of 27 had marked asymmetry; figure 8 (Shaffer.RN, 1967). In other infantile glaucoma studies Schaffer also found that 61% (52/85) patients had optic cups with a disc diameter greater than 1/3 in comparison to 2.6%(26/936) normal newborns who had optic cups with a disc diameter greater than 1/3 (Shaffer.RN, 1967). The above data provides vital evidence supporting the views that optic disc assessment in newborn infants is extremely important and any asymmetry in optic cupping is very significant as ‘normal’ infants are expected and likely to have symmetrical optic cups. Hence any asymmetry of cupping could be indicative of congenital glaucoma. Also it can be said that optic cupping assessment is of more importance in congenital glaucomas â€Å"since these cases are prone to follow a more asymmetrical course than adult glaucomas† (Richardson, April 1968). In order chronic glaucoma in order to be able to determine whether cupping is physiological or pathological the disc appearance must be tracked over many years. Whereas in newborns the cupping is expected to be symmetrical at birth therefore any asymmetry should be and can be picked up at birth (Richardson, April 1968). Secondary infantile glaucoma There are several causes of secondary infantile glaucoma, the most important is ocular trauma and this is due to the fact that ocular trauma is common in young infants. Blunt trauma to the eye causes compression of the globe which in turn leads to a temporary increase in IOP. When a blunt object hits the eye its cause indentation of the cornea, this then forces the aqueous humor â€Å"laterally against the anterior chambers angle structures and backwards against the iris and lens† (Robert N. Shaffer, 1970). Thereafter â€Å"in the anterior segment the iris sphincter ruptures† (Robert N. Shaffer, 1970) the ciliary body could become separated from the scleral spur or it may just be split or torn (Robert N. Shaffer, 1970). Likewise the trabecular meshwork may become ruptured, consequently leading to glaucoma (Robert N. Shaffer, 1970). Traumatic iritis is another cause of secondary glaucoma. Blunt ocular trauma can cause inflammatory cells and increase in proteins in the aqueous humor, in the early stages. These cells along with the protein molecules then cause obstruction of the trabecular meshwork. (Robert N. Shaffer, 1970) Oedema of the trabecular meshwork will also lead to resistance in the outflow of the aqueous. Even though there is an increase in the resistance of outflow, the IOP will remain within a normal range and in some cases it may actually be lower than normal because the blow will have caused depression of the ciliary body along with hyposecretion (Robert N. Shaffer, 1970). Anterior chamber haemorrhage (hyphema) occurs due to trauma or injury to the eye. Small haemorrhages are unlikely to clot, however large haemorrhages may fill the anterior chamber and cause compression of the meshwork which in turn leads to an acute increase in IOP (Robert N. Shaffer, 1970). Another cause of secondary glaucoma is recession of the anterior chamber angle. â€Å"A significant percentage of traumatic hyphemas results from a longitudinal cleavage of the ciliary body† (Robert N. Shaffer, 1970). A chain of damage reactions which occur to the trabecular meshwork following this will decrease the outflow and lead to glaucoma. Contusion cataract can be caused by blunt trauma. â€Å"If the cataract intumesces, a phacogenic pupillary block glaucoma may result. If the cataract becomes hypermature the lens cortex which is liquefied may leak into the anterior chamber†¦Ã¢â‚¬ , (Robert N. Shaffer, 1970) a macrophage response occurs and these cells then cause an increase in IOP as they block access of the aqueous to the trabecular meshwork. (Robert N. Shaffer, 1970) This is known as phacolytic glaucoma. Dislocation of the lens most likely occurs due to trauma, and if the lens after dislocation ends up in the anterior chamber then pupillary block glaucoma is l ikely (Robert N. Shaffer, 1970). Secondary glaucoma is usually the result of a laceration to the globe. A blunt blow, by a child’s fist, is often very serious as the smaller size of the fist does not allow the orbit to provide protection and the blow lands straight on the eye (Robert N. Shaffer, 1970). Intra-ocular foreign bodies can also cause glaucoma; particles which contain iron will oxidise and can be toxic to structures within the eye such as the trabecular meshwork (Robert N. Shaffer, 1970). Severe iritis can lead to glaucoma, and transient or chronic glaucoma can result from inflammation of the trabecular meshwork with increased resistance to outflow (Robert N. Shaffer, 1970).   Inflammation of the cornea can also cause secondary glaucoma, due to further inflammation of the meshwork leading to obstruction of the aqueous outflow (Robert N. Shaffer, 1970). It is well-known that glaucoma can be induced by steroids. An increase in IOP can be induced by prolonged use of topical steroids, in susceptible individuals. Ocular tumours uncommon in children, however if one is present it can sometimes lead to secondary glaucoma (Robert N. Shaffer, 1970). Retinoblastoma, a well-known and common tumour found in the young can also cause glaucoma. The tumour will invade the anterior chamber angle structures; iris and trabecular meshwork. There is a very strong link between prenatal rubella infection and glaucoma and it is now well agreed upon that prenatal rubella can in fact cause glaucoma. It is estimated that rubella infantile glaucoma occurs in 2-4% of children with congenital rubella syndrome (Robert N. Shaffer, 1970). It usually presents in the first six months of life and the symptoms are identical to those of primary congenital glaucoma; an enlarged oedematous cornea which is cloudy, a deep anterior chamber and the classic high IOP (Robert N. Shaffer, 1970). Clinically it is found to be almost impossible to distinguish rubella infantile glaucoma from primary congenital glaucoma (Robert N. Shaffer, 1970). In conclusion, it has been determined that although rare conditions both primary and secondary infantile glaucoma can significantly affect the life of a child. Hence examination of the optic discs at birth is vital to ensure that any asymmetry of optic cups is detected and the possibility of the newborn developing glaucoma is known immediately, as it has been proven that infants with glaucoma are significantly more likely to show asymmetry of optic cupping compared to ‘normal’ infants. If the glaucoma is not detected at birth it is vital that healthcare professionals are able to recognise the signs and symptoms of infantile glaucoma so it can be treated before any significant damage has occurred, as it has been proven that the majority of children present with all or some of the signs and symptoms of glaucoma yet they are either overlooked by the parents or misdiagnosed by clinicians. In relation to the pathogenesis of infantile glaucoma significant evidence or lack of has proven that Worst along with Barkan’s Membrane theory are no longer valid. Vital histopathologic evidence undermines the theory; in fact Anderson has provided substantial evidence to prove that repositioning, sliding, cleavage and atrophy play a significant role in the development of primary infantile glaucoma. Along with the histopathologic evidence it can be concluded that Anderson’s findings can be accepted. References A. Edward Maumenee, M. (1962). Further observations on the pathogenesis of congenital glaucoma. TR. AM. OPHTH J. SOC, VOl. 60, 140-162. A.Armstrong, R. (2008, December 12th). Congenital Glaucoma; The genetics of primary congenital glaucoma. Optometry Today, pp. 40-43. Becker B, S. R. (1965). Diagnosis and Therapy of the Glaucomas. St Louis: CV Mosby. Broughton WL, P. M. (1981 May). An analysis of treatment of congenital glaucoma by goniotomy. Am J Ophthalmol. , 91(5):566-72. Ching Lin Ho, F. a. (September/October 2004). Primary Congenital Glaucoma: 2004 Update. Journal of Pediatric Ophthalmology and Strabismus , Vol. 41:271-288. D.R.Anderson. (1981). The development of the trabecular meshwork and its abnormality in primary infantile glaucoma. Trans Am Ophthalmol Soc, 79:458-85. David J. Seidman MD1, L. B. (3 March 1986). Signs and Symptoms in the Presentation of Primary Infantile Glaucoma. PEDIATRICS , Vol. 77 No. pp. 399-404. Harley, R. D. (1983). Pediatric Ophthalmology. Saunders. John S Crawford, J. D. (1983). The Eye in Childhood. New York: Grune and Stratton. Kanski, J. J. (2003). Clinical Ophthalmology A Systematic Approach. Butterworth Heinemann. Kwitko, M. (1973). Glaucoma in Infants and Children (ed 2). New York: Appleton-Century-Crofts. Mann, I. (1957). Developmental Abnormalities of the Eye. Philadelphia: JB Lippincott. MillerSJ. (1966). Genetic aspects of glaucoma. Trans Ophthalmol Soc U K., 86:425-34. Moller, P. (1977). Goniotomy and congenital glaucoma. Acta Ophthal, pp. 55: 436-442. Morin JD, M. S. (1974). Primary congenital glaucoma: a survey. Can J Ophthal, pp. 9:17-28. Myron Yanoff, J. S. (2009). Ophthalmology. Mosby Elsevier. NEI. (1968-date). Glaucoma. Retrieved February 2011, from National Eye Institue: nei.nih.gov/health/glaucoma/glaucoma_facts.asp Quigley, H. (1977 Sep). The pathogenesis of reversible cupping in congenital glaucoma. Am J Ophthalmol., 84(3):358-70. Richardson KT, S. R. (1966). Optic nerve cupping in congenital glaucoma. Am J. Ophth., 62: 507. Richardson, K. T. (April 1968). Optic Cup symmetry in normal newborn infants. Investigative Ophthalmology, 137-140. Robert N. Shaffer, D. I. (1970). Congenital and Pediatric Glaucomas. USA: The C. V. Mosby Company. Robin AL, Q. H. (1979). An analysis of visual acuity, visual fields, and disk cupping in childhood glaucoma. Am J Ophthal , 88(5):847-58. Scheie, H. (1955). Symposiumon congenital glaucoma: Diagnosis, clinical course and treatment other than goniotomy (ed 2). Trans Am Acad Ophthalmol Otolaryngol 59, pp. 309–321. Shaffer.RN. (1967). New concepts in infantile glaucoma. Canad J. Ophth, 2: 243. SyndackerD. (1964). The normal optic disc. Ophthalmoscopic and photographic studies. Arch Ophthal, 58:958. Vincent P Deluise, D. R. (1983). Primary Infantile Glaucoma (Congenital Glaucoma). 28(1). Worst, J. G. (April 1968). Congenital glaucoma Remarks on the aspect of chamber angle: Ontogenic and pathogenic background and mode action of goniotomy. Investigative Ophthalmology, 7:127-134.

FM Essay Example | Topics and Well Written Essays - 1500 words

FM - Essay Example An increase in the scale of production could likely result in changes to both fixed and variable cost. Increasing the scale may lead to increased fixed cost. Additionally, buying more raw materials could result in a lower cost per unit. Furthermore, producing more of an item could lead to higher hourly rate for labour as overtime may be necessary. Overtime is normally charged at a higher rate of time and a half. Break even analysis, assumes that the quantity of Racey that is produced will be sold. It may not be possible for JxCorp to sell all the products produced. Profit is calculated on the quantity of goods sold and not the quantity of goods expected to be sold. Additionally, JxCorp may not be selling Racey to one customer. Other customers may demand a lower price per unit. Break-even analysis breaks down as it assumes there is only one market for the product and all units are sold at the same price. It does not take into consideration that JxCorp may have to sell Racey to different customers at different prices. It uses only one selling price to determine how changes in volume sold will affect profits. It is common practice to sell goods at different prices to different customers. The weighted cost of capital is the weighted average of the components of capital (Brigham and Ehrhardt 2005). In this case, the components are equity and debt. The calculation of the weighted cost of capital WACC is shown in Table 4 below. The calculations in Table 4 indicate that WACC is 11%. The weight of each component is 50% (0.5). The symbol Wd represents the weight of Debt and We the weight of equity. The symbol rd represents the interest rate on the debt which is 9% and re the return on equity which is 15%. The corporation tax rate, T is 22% or 0.22. The information in Table 5 indicates that capital allowances of  £100,000,  £75,000, and  £56,250 were charged in years 1, 2 and 3 respectively and balancing charge of  £168,750 in year 4. The

Edna Manley Essay Example | Topics and Well Written Essays - 1000 words

Edna Manley - Essay Example However, her later works were done in clay and cast. The sculptors she made were greatly influenced by the cultural changes taking place in Jamaica at the time. Her art was aimed at reflecting the Jamaican culture and the experiences Jamaicans were undergoing at the time. During the early 1920s, after she had returned to Jamaica from England, Edna realized that Jamaican middle class expected all women to be subjects of their husbands and operate in their shadows. However, she was a keen observer of the Jamaican way of life, and through this observation, she got inspiration for her work. Beadseller is the first bronze casting sculptor she created in 1923. The beadseller was a sharp and lean body depicting a person undergoing hardships. This piece personified the suffering and troubles many people in Jamaica went through. Through her work, Edna also attempted to elevate the status of women in the society. Unlike many other artists at the time, her style mainly centered on women, for instance, in 1928, she created the carving Eve from mahogany. This image had rounded and sensual body forms (Laduke, 37). This piece was recognized as one of Edna’s important works in which she acknowledges the mother of mankind. Through her art, she was able to recognize the role women had in the society. For instance, in her work The Message (1977), Edna shows two women sharing a secret. She claimed that she saw these two women in the market place and knew that it was a secret an older woman tells a younger one. Other works with the theme of older women include Man-Child (1974) and The Ancestor (1974) (Laduke, 37). She was a champion and advocate of the Black Jamaican rights and freedom. Through her works, Edna was able to show the world that Black Jamaicans were capable and ready to make a contribution to the Jamaican society and the world as a whole. These works represented the quest for a new order in the Jamaican society. Two of such