The Great Gatsby - Male And Female Interactions Essays -

The Great Gatsby - Male and Female Interactions Through the interactions between male and female characters, Fitzgerald depicts a variety of social expectations regarding "typical" male behavior in the 1920's. In the novel The Great Gatsby, characters such as Tom Buchanan, Jay Gatsby, George Wilson and Nick Carraway demonstrate behavior that acts to maintain and live up to expectations inherent in society. Through their controlling ways, these characters strive to define the "typical" man in the 1920's. The notion that a man's success can be measured by his possessions becomes evident through the actions of Tom, Gatsby and Wilson. These characters strive to obtain more than just material possessions. For example, Tom seems to view the women in his life as mere possessions, a sign of his success and wealth. His attitude and interactions with Daisy, his wife, and Myrtle, his mistress, demonstrate this. Through out the story, Tom does not show respect or genuine caring for either woman. Rather, he commits open adultery with Myrtle. Tom makes this affair public because it is just another way of showing-off, another of his possessions and thus boosting his ego. Tom does this without regard for the shame his affairs may bring onto his wife. Daisy comes to represent a treasured and sought possession for both Tom and Gatsby. Although on the surface it appears that Gatsby has an ever-lasting love for Daisy, I feel that his longing for Daisy stems from his need to recapture a possession which he lost during his youth. Nick comments "He talked a lot about the past and I gathered that he wanted to recover something, some idea of himself perhaps, that had gone into loving Daisy" (117). Furthermore by possessing Daisy's love, Gatsby can reject defeat and feel successful as a man. In the novel, Gatsby goes as far as to view the green light as a symbolic way of holding onto his possession and keeping Daisy in some way close to him. After obtaining his dream of being reunited with Daisy, the green light begins to lose its symbolic strength. "Now it was again a green light on a dock. His count of enchanted objects had diminished by one" (98). Now that the realization of his dream has begun, Gatsby needs to feel a greater sense of possession or control over Daisy. He may feel the need to obtain another enchanted object to replace the loss of the symbolic meaning of the light. Now the only enchanted object which he is left to obtain is Daisy's complete and everlasting. Likewise, Tom refuses to forfeit Daisy to another man or even believe that she could love another. Tom states "But all the rest is a God damnened lie. Daisy loved me when she married me and she loves me now." (138). If Tom were to give up Daisy to another man, this would surely be a sign of defeat and failure like losing a football or polo trophy. Instead of admitting defeat, Tom rationalizes Daisy's behavior by demeaning her will. For example, he states "The trouble is that sometimes she gets foolish ideas in her head and doesn't know what she's doing" (138). Another social expectation of "typical" male behavior in the 1920's depicted in The Great Gatsby is the notion that a "real" man should be in control of the woman in his life at all times. This notion is exemplified through the struggling relationship between George and Myrtle Wilson. Although Fitzgerald describes George as "one of these worn-out men...He was his wife's man and not his own." (144), a need for control takes over George when he discovers his wife had "some sort of life apart from him in another world." (131) with perhaps another man. To gain control over this situation and thus live up to the social expectation, George takes drastic measures. He states "I've got my wife locked up in there. She's going to stay up there till the day after tomorrow and then we 're going to move away." (143). Through his actions, George forces his will on his wife and strives to maintain control over his possession, his wife. In addition, Tom demonstrates control over Myrtle when the issue of whether she has the right to

The aim of this research is, eventually, to Essays

The aim of this research is, eventually, to Essays The aim of this research is, eventually, to Essay The aim of this research is, eventually, to Essay Context of the intended research CRIT is a receptor that was foremost encountered on the surface of aSchistosomaspecies ; in theSchistosoma,it acts as a decoy C2-binding receptor in order to protect this parasite from complement onslaught by viing with C4 for the binding of C2 ( Inal and Schifferli, 2002 ) . Complement is, basically, an enzyme system that is triggered upon immune system onslaught: most of the enzymes in this system are identified through standardised labeling: they are labelled C followed by a figure and so a codification based on the cleavage merchandises when proteolysed, for illustration, C5b-9. Complement onslaught ( Carroll, 1998 ) plays a major function in supporting hosts from immune onslaught, in footings of extinguishing foreign encroachers, and involves a complex tract of interactions, in order that the procedure does non take to self devastation: so, unregulated complement action can take to autoimmune diseases ( Ohet al. ,2003 ) , and other conditions/diseases such as bosom onslaught ( K ilgoreet al. ,1994 ) , Alzheimer’s disease ( Bradtet al. ,1998 ) . CRIT ( or Sh-TOR as it was antecedently known ) was found inSchistosoma,as a complement C2 protein, that could barricade complement activation, therefore bring oning bilharzia in worlds ; it was hypothesized that the CRIT blocked complement activation through its C2 binding site ; CRIT look in the parasite therefore acts as a steerer C2 binding receptor, protecting the parasite against complement onslaught by viing with C4 for the binding of C2, at the ed1 sphere ( Hui, 2005 ) . CRIT has later been found that other animate beings, that are suited as theoretical account systems for analyzing CRIT action besides express CRIT, for illustration, the rat andTrypanosoma.Recent work has besides shown that worlds have a CRIT factor, labeled ( Hu ) -CRIT which is expressed in a broad scope of human cells, particularly in hematopoietic cells ( Inalet al. ,2005 ) . Further elaborate surveies of CRIT have shown that it is a transmembrane receptor with two extracellular and two in intracellular spheres with an active 11 amino-acid peptide subdivision ( called CRIT-H17 ) which is hypothesized to be involved in the complement suppression activity of CRIT ( Hui, 2005 ) . Much work has been undertaken on clarifying the mechanism of action of CRIT, in footings of it being a potentially utile molecule in handling immunological diseases and other diseases, such as malignant neoplastic disease. For illustration, Inalet Al.( 2005 ) have shown that CRIT barricading can take to deprotection in CRIT-expressing human myeloid cell lines and in monocytes, ensuing in a greater susceptibleness to complement-mediated lysisin vitro. Other research, such as that by Mollet Al.( 2006 ) has shown that CRIT look is different in patients with kidney upsets, through assorted alterations in up- or down-regulation of CRIT look, taking to the suggestion that the upregulation of CRIT in activated podocytes might stand for a self-defense mechanism, stand foring a ‘last line’ of defense mechanism in membranous kidney disease of the kidney. Other surveies have looked at the existent mechanism of operation of the CRIT tract, for illustration Huiet Al.( 2005 ) looked at the look of a functional recombinant von Willebrand factor-A sphere from human complement C2, in footings of this being a possible binding site for C4 and CRIT. As we have seen, CRIT competes with C4b for the binding of C2, with the major adhering site on C2 being located on a short peptide sequence that was antecedently of unknown beginning ; Huiet al. ,( 2005 ) , nevertheless, looked at a part on C2 that was known to hold binding capacity, the von Willebrand Factor-A, and found that, so, this peptide sequence inhibits complement activity ; utilizing a cloned von Willebrand Factor-A sequence, Huiet Al.( 2005 ) were able to look in item at the interactions between C2 and CRIT and C4b. This pilot survey that is intended to be undertaken as portion of this reappraisal of CRIT is intended to take this work of Huiet Al.( 2005 ) farther. As will be seen, on adh ering the serum complement protein, C2, the CRIT peptide, H17 can cut down complement-mediated redness in vivo [ 7 ] and it is intended that CRIT-ed1 and H17 will be tested as possible distinction therapeutics peculiarly aiming monocytic leukemia. To better the efficaciousness of these peptides, structural information on the manner they interact with C2, such that this can be ‘tweaked’ to increase efficiency of binding. The CRIT-H17 peptide will be synthesized full length as an 11-mer, but besides as a 10-mer, 9-mer and 8-mer. We will besides mutate to alanine the amino acids believed to interact with the vWFA sphere of C2. CRIT-H17 will farther be synthesized as a head-to-toe cyclised version of H17 ( to mime the native CRIT molecule ) . Prior to the structural surveies, nevertheless, these peptides will be tested for their efficaciousness at cut downing complement activationin vitro. In add-on, interactions of these peptides with C2 vWFA sphere will be monitored for by a novel technique utilizing electrospray ionization mass spectroscopy ( developed within the Institute for Health Research A ; Policy at LMU by Dr. A. Bligh ) [ 8 ] . This technique can besides observe the presence of two adhering sites and if there are two ligands whether they bind competitively and with what affinity. To supervise conformational alterations on interaction, in add-on to working out dynamicss of interaction, we will utilize Double Polarisation Interferometry ( AnaLight Quantum ) through coaction with Dr. R.B. Sim ( MRC Immunochemistry Unit, Univ. of Oxford ) . Prof. Peter Gros ( Centre for Biomolecular Research, Utrecht ) has approached the applier for CRIT peptides for co-crystallisation with an available C2a ( von Willebrand Factor A [ vWFA ] and serine peptidase ) concept and we expect this coaction to continue and to finally demo the points of contact between CRIT-ed1 and C2 ( via the vWFA sphere ) . It is hoped that this methodological analysis will let a deeper apprehension of how CRIT binds with other molecules in the complement tract, and how this tract is regulated in footings of supplying a intervention option for some of the diseases/conditions that are known to develop following perturbation, or irregular operation of, this complement tract. Introduction The purpose of this research is, finally, to transport out a pilot survey to back up preliminary grounds that the complement receptor CRIT ( Complement C2 Receptor Inhibitor Trispanning ) plays a function in monocyte/macrophage terminal distinction. We aim to demo that by triping distinction through CRIT, it is possible to suppress the proliferation of myeloid leukemia cells. This could hold of import deductions for an alternate intervention agenda for monocytic leukemia. By the terminal of this survey we expect to demo the undermentioned: I ) that monocytes which can adhere C2 through CRIT maintain monocytic phenotypein vitroorin vivo ;II ) that monocytes can be induced to terminally distinguish by barricading the interaction of CRIT with its blood relation ligand, complement C2 or as monocytes move into an extravascular environment devoid of C2 ; that a knockdown of CRIT look in monocyte carcinoma cell lines or physical blocking of CRIT-C2 interaction induces them to terminally dis tinguish, and that, likewise, a blocking of CRIT-C2 interaction on leukaemic monocytes will halt proliferation and bring on distinction ; and, in conclusion, that, conversely, monocytes that are C2-/- , can non be induced to terminally distinguish by barricading the interaction of CRIT with its ligand, C2, nevertheless on traveling into an extravascular environment, other excess mechanisms, such as interaction of monocyte integrins with VCAM molecules on endothelial cells, may still bring on distinction. In consequence, basically, either barricading ligand interaction with CRIT or cut downing CRIT look should excite cell rhythm apprehension ( irreversible block at G1 ) and terminal distinction into cells with a macrophage phenotype. These conditions represent a fresh tract for monocyte/macrophage terminal distinction, based on the theoretical account proposed, and affecting the complement receptor, CRIT. In footings of monocyte leukemia, besides advancing cell rhythm apprehension, barricading CRIT with anti-CRIT-ed1 has the added benefit of rendering the cell more susceptible to complement-mediated cytolysis, as described antecedently for monocyte carcinoma cell lines ( U937 and THP-1 ) and primary monocytes showing CRIT [ 1 ] . It is intended that this research will lend to a deeper apprehension of how the complement tract works in worlds, in peculiar with respect to how abnormalities in the operation of the complement tract can do disease, and how CRIT look modulates the operation of the complement tract in human systems. The informations obtained from this pilot survey will be used to look into five chief issues: I ) The function of CRIT in myeloid distinction The function of CRIT in myeloid distinction has been studied with an antagonist CRIT-based peptide termed H17 ( NH2-HEVKIKHFSPY-CO2H ) consisting the 11aa C-terminus of CRIT-ed1. Preliminary work suggests that in adhering to C2 and therefore barricading the interaction of C2 with CRIT [ 1 ] , H17 may bring on the distinction of monocytes/promonocytic cell lines along the tract of macrophage distinction, and significantly, inhibit cell proliferation. The different curative attacks that are presently used in handling acute leukemia include cytotoxicity, programmed cell death and distinction. Differentiation therapy was developed over a decennary ago and Acts of the Apostless by bring oning cell rhythm apprehension and hence distinction in leukaemic monocytes [ 2 ] , therefore elegantly avoiding cytotoxicity effects. Retinoids, such as all-trans-retinoic acid ( ATRA ) are used to handle promyelocytic leukemia by specifically aiming neoplastic cells whilst non impacting normal mature ce lls. Many successes in the intervention of monocytic leukaemias have been reported since [ 3-5 ] . We suggest that a CRIT-based peptide ( H17 or an H17 derived function ) could finally offer an of import alternate intervention for monocytic leukemia by bring oning distinction of monocytic cells. The peptide will be tested entirely and in combination with ATRA in a mouse theoretical account of acute promyelocytic leukemia [ 6 ] . two ) The construction of CRIT peptides ( ed1 and H17 ) and of CRIT peptides interacting with the von Willebrand Factor A ( vWFA ) sphere of complement C2 On adhering the serum complement protein, C2, the CRIT peptide, H17 can cut down complement-mediated redness in vivo [ 7 ] and we will prove CRIT-ed1 and H17 as possible distinction therapeutics peculiarly aiming monocytic leukemia. To better the efficaciousness of these peptides, we aim to utilize structural information on the manner they interact with C2. The CRIT-H17 peptide will be synthesized full length as an 11-mer, but besides as a 10-mer, 9-mer and 8-mer. We will besides mutate to alanine the amino acids believed to interact with the vWFA sphere of C2. CRIT-H17 will farther be synthesized as a head-to-toe cyclised version of H17 ( to mime the native CRIT molecule ) . Prior to structural surveies, these peptides will be tested for their efficaciousness at cut downing complement activation in vitro. Interactions of these peptides with C2 vWFA sphere will be monitored for by a novel technique utilizing electrospray ionization mass spectroscopy ( developed within the Institute for Health Research A ; Policy at LMU by Dr. A. Bligh ) [ 8 ] . This technique can besides observe the presence of two adhering sites and if there are two ligands whether they bind competitively and with what affinity. To supervise conformational alterations on interaction, in add-on to working out dynamicss of interaction, we will utilize Double Polarisation Interferometry ( AnaLight Quantum ) through coaction with Dr. R.B. Sim ( MRC Immunochemistry Unit, Univ. of Oxford ) . Prof. Peter Gros ( Centre for Biomolecular Research, Utrecht ) has approached the applier for CRIT peptides for co-crystallisation with an available C2a ( von Willebrand Factor A [ vWFA ] and serine peptidase ) concept and we expect this coaction to continue and to finally demo the points of contact between CRIT-ed1 and C2 ( via the vWFA sphere ) . three ) Expression profile of CRIT in autoimmune disease and malignant neoplastic disease With a position to understanding the function of CRIT in autoimmune disease and malignant neoplastic disease, the applier is join forcesing on a Swiss National Foundation funded undertaking with Prof. J. Schifferli ( Univ. Hospital Basel ) to do a CRIT smasher mouse. To happen an association between CRIT look degrees and the disease procedure, a comparing of CRIT look ( messenger RNA and protein ) in normal tissue with that in autoimmune disease and malignant neoplastic disease will be made. In situ hybridization surveies every bit good as immunohistochemistry, utilizing dual staining and/or staining of consecutive subdivisions with anti-CRIT and cell specific markers, will be conducted to corroborate look in sertoli cells, podocyte cells, keratinocytes, encephalon [ 1 ] . The distribution of CRIT in normal and morbid tissue will be studied, peculiarly tissues injured by inflammatory or necrotic procedures: joints-synovium in arthritis, myocardial infarction etc. Previously, we carri ed out a survey along these lines, which looked at CRIT look in assorted kidney diseases [ 9 ] . This survey revealed CRIT upregulation in membranous kidney diseases on glomerular podocyte cells. Unlike CR1, hitherto the lone other complement regulator described on podocytes, and which is non upregulated in membranous nephropathy, we believe that CRIT on podocytes represents a last line of defense mechanism against onslaught by complement. Functional information back uping this was later obtained ( manuscript in Complement regulators are frequently upregulated in malignant neoplastic disease [ 10 ] and so expression degrees of CRIT in assorted human malignances will be assessed excessively. Critically, CRIT is upregulated in liver malignant neoplastic disease ( Fig. 4 ) and thyroid malignant neoplastic disease ( non shown ) . As obstruction of CRIT with antibody sensitises cells to complement lysis [ 1 ] , such findings may hold applications in malignant neoplastic disease. Already schemes to barricade complement regulators with specific antibodies have been used successfully with a position to developing fresh malignant neoplastic disease immunotherapies [ 11,12 ] . In a recent development, membrane-bound complement regulative proteins ( mCRP ) have been downregulated by siRNA to render tumour cells sensitive to complement [ 13 ] . Therefore we will bring forth vector-based shRNAs ( utilizing psiRNA vector [ In vivo Gen ] ) to stably strike hard down CRIT look and see the consequence on tumor cells. four ) CRIT extracellular peptide ( H17 ) and its usage in modulating complement-mediated redness in in vivo theoretical accounts of autoimmune disease With a position to therapeutically suppress redness due to classical tract activation in theoretical accounts of complement-mediated autoimmune disease, CRIT has been targeted to suppress the Reversed Passive Arthus Reaction in mice [ 7 ] . By disposal of an counter peptide, H17, which binds complement C2 and prevents its activation it was possible to significantly cut down complement-mediated redness. To prove this peptide as a curative against autoimmune diseases in which the classical tract is peculiarly of import we are join forcesing with labs that have the appropriate animate being theoretical accounts. Experimental autoimmune myasthenia gravis ( EAMG ) is an antibody-mediated autoimmune disease impacting the neuromuscular junction. The disease, which is besides T cell-dependent, is an accurate theoretical account in footings of its pathology and clinical result of human myasthenia gravis ( MG ) . We have been approached by Prof. P. Christadoss and Dr. E. Tuzun of the Universit y of Texas, Galveston to prove H17 in their mouse theoretical account of MG [ 14,15 ] and will continue with this coaction. 1.2.5 Does CRIT adhere other serum proteins through its extracellular spheres? In a collaborative survey with Prof. Marina Botto ( Imperial College ) we will look into whether CRIT is a receptor for any other proteins beside complement C2 and FB, with which it binds with high and low affinity, severally. To prove whether the extracellular spheres of CRIT have other adhering spouses, receptor affinity chromatography [ 16 ] will be used to see whether ed1 binds other proteins from the serum of a C2 deficient ( C2D ) patient or of a combined C2/FB smasher mouse [ 17,18 ] . As the function of the 2nd extracellular sphere, ed2 has non been established, normal serum will be used ab initio to place ed2-binding proteins adhering to ed2 affinity columns by standard mass-spec designation protocols. Further experiments will be conducted to see if CRIT binds integrins. The principle for this is that CRIT-ed1 binds the vWFA1 sphere of complement C2 [ 19 ] and vWFA spheres are typically found in integrins, such as Very Late Antigen 4 ( VLA-4 ) on monocytes. The interaction w ith vascular cell adhesion molecule-1 ( VCAM-1 ) molecules on the endothelium is believed to non merely intercede attachment [ 20 ] and transendothelial migration [ 21 ] but besides to excite distinction [ 22 ] . Methodology to be utilized in the survey of the purposes of the undertaking: I ) The function of CRIT in myeloid distinction As we have seen, the function of CRIT in myeloid distinction has been studied with an antagonist CRIT-based peptide termed H17 ( NH2-HEVKIKHFSPY-CO2H ) consisting the 11aa C-terminus of CRIT-ed1. Preliminary work suggests that in adhering to C2 and therefore barricading the interaction of C2 with CRIT [ 1 ] , H17 may bring on the distinction of monocytes/promonocytic cell lines along the tract of macrophage distinction, and significantly, inhibit cell proliferation. It is intended that this pilot survey will go on the work that has been started in this respect, and will lend original research findings to the intervention of diseases that are caused by failures in the proper operation of the complement tract in worlds. The different curative attacks that are presently used in handling acute leukemia include cytotoxicity, programmed cell death and distinction. Differentiation therapy was developed over a decennary ago and Acts of the Apostless by bring oning cell rhythm apprehension and hence distinction in leukaemic monocytes [ 2 ] , therefore elegantly avoiding cytotoxicity effects. Retinoids, such as all-trans-retinoic acid ( ATRA ) are used to handle promyelocytic leukemia by specifically aiming neoplastic cells whilst non impacting normal mature cells. Many successes in the intervention of monocytic leukaemias have been reported since [ 3-5 ] . We suggest that a CRIT-based peptide ( H17 or an H17 derived function ) could finally offer an of import alternate intervention for monocytic leukemia by bring oning distinction of monocytic cells. The peptide will be tested entirely and in combination with ATRA in a mouse theoretical account of acute promyelocytic leukemia [ 6 ] . This will take to cons equences which could be of great usage in developing alternate therapies for handling conditions that arise as a consequence of failure of the right operation of the complement tract in worlds. two ) The construction of CRIT peptides ( ed1 and H17 ) and of CRIT peptides interacting with the von Willebrand Factor A ( vWFA ) sphere of complement C2 As has been seen, Huiet Al.( 2005 ) looked at the look of a functional recombinant von Willebrand factor-A sphere from human complement C2, in footings of this being a possible binding site for C4 and CRIT. As we have seen, CRIT competes with C4b for the binding of C2, with the major adhering site on C2 being located on a short peptide sequence that was antecedently of unknown beginning ; Huiet al. ,( 2005 ) , nevertheless, looked at a part on C2 that was known to hold binding capacity, the von Willebrand Factor-A, and found that, so, this peptide sequence inhibits complement activity ; utilizing a cloned von Willebrand Factor-A sequence, Huiet Al.( 2005 ) were able to look in item at the interactions between C2 and CRIT and C4b. The current survey will take the work of Huiet Al.( 2005 ) further, by looking in item at the CRIT tract, in footings of adhering the serum complement protein, C2, the CRIT peptide, H17 can cut down complement-mediated rednessin vivo[ 7 ] and we will prove CRIT-ed1 and H17 as possible distinction therapeutics peculiarly aiming monocytic leukemia. To better the efficaciousness of these peptides, we aim to utilize structural information on the manner they interact with C2. The CRIT-H17 peptide will be synthesized full length as an 11-mer, but besides as a 10-mer, 9-mer and 8-mer. We will besides mutate to alanine the amino acids believed to interact with the vWFA sphere of C2. CRIT-H17 will farther be synthesized as a head-to-toe cyclised version of H17 ( to mime the native CRIT molecule ) . Prior to structural surveies, these peptides will be tested for their efficaciousness at cut downing complement activation in vitro. Interactions of these peptides with C2 vWFA sphere will be moni tored for by a novel technique utilizing electrospray ionization mass spectroscopy ( developed within the Institute for Health Research A ; Policy at LMU by Dr. A. Bligh ) [ 8 ] . This technique can besides observe the presence of two adhering sites and if there are two ligands whether they bind competitively and with what affinity. To supervise conformational alterations on interaction, in add-on to working out dynamicss of interaction, we will utilize Double Polarisation Interferometry ( AnaLight Quantum ) through coaction with Dr. R.B. Sim ( MRC Immunochemistry Unit, Univ. of Oxford ) . Prof. Peter Gros ( Centre for Biomolecular Research, Utrecht ) has approached the applier for CRIT peptides for co-crystallisation with an available C2a ( von Willebrand Factor A [ vWFA ] and serine peptidase ) concept and we expect this coaction to continue and to finally demo the points of contact between CRIT-ed1 and C2 ( via the vWFA sphere ) . three ) Expression profile of CRIT in autoimmune disease and malignant neoplastic disease With a position to understanding the function of CRIT in autoimmune disease and malignant neoplastic disease, the applier is join forcesing on a Swiss National Foundation funded undertaking with Prof. J. Schifferli ( Univ. Hospital Basel ) to do a CRIT smasher mouse. To happen an association between CRIT look degrees and the disease procedure, a comparing of CRIT look ( messenger RNA and protein ) in normal tissue with that in autoimmune disease and malignant neoplastic disease will be made. In situ hybridization surveies every bit good as immunohistochemistry, utilizing dual staining and/or staining of consecutive subdivisions with anti-CRIT and cell specific markers, will be conducted to corroborate look in sertoli cells, podocyte cells, keratinocytes, encephalon [ 1 ] . The distribution of CRIT in normal and morbid tissue will be studied, peculiarly tissues injured by inflammatory or necrotic procedures: joints-synovium in arthritis, myocardial infarction etc. Previously, we carri ed out a survey along these lines, which looked at CRIT look in assorted kidney diseases [ 9 ] . This survey revealed CRIT upregulation in membranous kidney diseases on glomerular podocyte cells. Unlike CR1, hitherto the lone other complement regulator described on podocytes, and which is non upregulated in membranous nephropathy, we believe that CRIT on podocytes represents a last line of defense mechanism against onslaught by complement. Functional information back uping this was later obtained ( manuscript in Complement regulators are frequently upregulated in malignant neoplastic disease [ 10 ] and so expression degrees of CRIT in assorted human malignances will be assessed excessively. Critically, CRIT is upregulated in liver malignant neoplastic disease ( Fig. 4 ) and thyroid malignant neoplastic disease ( non shown ) . As obstruction of CRIT with antibody sensitises cells to complement lysis [ 1 ] , such findings may hold applications in malignant neoplastic disease. Already schemes to barricade complement regulators with specific antibodies have been used successfully with a position to developing fresh malignant neoplastic disease immunotherapies [ 11,12 ] . In a recent development, membrane-bound complement regulative proteins ( mCRP ) have been downregulated by siRNA to render tumour cells sensitive to complement [ 13 ] . Therefore we will bring forth vector-based shRNAs ( utilizing psiRNA vector [ In vivo Gen ] ) to stably strike hard down CRIT look and see the consequence on tumor cells. four ) CRIT extracellular peptide ( H17 ) and its usage in modulating complement-mediated redness in in vivo theoretical accounts of autoimmune disease With a position to therapeutically suppress redness due to classical tract activation in theoretical accounts of complement-mediated autoimmune disease, CRIT has been targeted to suppress the Reversed Passive Arthus Reaction in mice [ 7 ] . By disposal of an counter peptide, H17, which binds complement C2 and prevents its activation it was possible to significantly cut down complement-mediated redness. To prove this peptide as a curative against autoimmune diseases in which the classical tract is peculiarly of import we are join forcesing with labs that have the appropriate animate being theoretical accounts. Experimental autoimmune myasthenia gravis ( EAMG ) is an antibody-mediated autoimmune disease impacting the neuromuscular junction. The disease, which is besides T cell-dependent, is an accurate theoretical account in footings of its pathology and clinical result of human myasthenia gravis ( MG ) . We have been approached by Prof. P. Christadoss and Dr. E. Tuzun of the Universit y of Texas, Galveston to prove H17 in their mouse theoretical account of MG [ 14,15 ] and will continue with this coaction. 1.2.5 Does CRIT adhere other serum proteins through its extracellular spheres? In a collaborative survey with Prof. Marina Botto ( Imperial College ) we will look into whether CRIT is a receptor for any other proteins beside complement C2 and FB, with which it binds with high and low affinity, severally. To prove whether the extracellular spheres of CRIT have other adhering spouses, receptor affinity chromatography [ 16 ] will be used to see whether ed1 binds other proteins from the serum of a C2 deficient ( C2D ) patient or of a combined C2/FB smasher mouse [ 17,18 ] . As the function of the 2nd extracellular sphere, ed2 has non been established, normal serum will be used ab initio to place ed2-binding proteins adhering to ed2 affinity columns by standard mass-spec designation protocols. Further experiments will be conducted to see if CRIT binds integrins. The principle for this is that CRIT-ed1 binds the vWFA1 sphere of complement C2 [ 19 ] and vWFA spheres are typically found in integrins, such as Very Late Antigen 4 ( VLA-4 ) on monocytes. The interaction w ith vascular cell adhesion molecule-1 ( VCAM-1 ) molecules on the endothelium is believed to non merely intercede attachment [ 20 ] and transendothelial migration [ 21 ] but besides to excite distinction [ 22 ] . CRIT is a receptor that was foremost encountered on the surface of aSchistosomaspecies ; in theSchistosoma,it acts as a decoy C2-binding receptor in order to protect this parasite from complement onslaught by viing with C4 for the binding of C2 ( Inal and Schifferli, 2002 ) . Complement is, basically, an enzyme system that is triggered upon immune system onslaught: most of the enzymes in this system are identified through standardised labeling: they are labelled C followed by a figure and so a codification based on the cleavage merchandises when proteolysed, for illustration, C5b-9. Complement onslaught ( Carroll, 1998 ) plays a major function in supporting hosts from immune onslaught, in footings of extinguishing foreign encroachers, and involves a complex tract of interactions, in order that the procedure does non take to self devastation: so, unregulated complement action can take to autoimmune diseases ( Ohet al. ,2003 ) , and other conditions/diseases such as bosom onslaught ( K ilgoreet al. ,1994 ) , Alzheimer’s disease ( Bradtet al. ,1998 ) . CRIT ( or Sh-TOR as it was antecedently known ) was found inSchistosoma,as a complement C2 protein, that could barricade complement activation, therefore bring oning bilharzia in worlds ; it was hypothesized that the CRIT blocked complement activation through its C2 binding site ; CRIT look in the parasite therefore acts as a steerer C2 binding receptor, protecting the parasite against complement onslaught by viing with C4 for the binding of C2, at the ed1 sphere ( Hui, 2005 ) . CRIT has later been found that other animate beings, that are suited as theoretical account systems for analyzing CRIT action besides express CRIT, for illustration, the rat andTrypanosoma.Recent work has besides shown that worlds have a CRIT factor, labeled ( Hu ) -CRIT which is expressed in a broad scope of human cells, particularly in hematopoietic cells ( Inalet al. ,2005 ) . Further elaborate surveies of CRIT have shown that it is a transmembrane receptor with two extracellular and two in intracellular spheres with an active 11 amino-acid peptide subdivision ( called CRIT-H17 ) which is hypothesized to be involved in the complement suppression activity of CRIT ( Hui, 2005 ) . Much work has been undertaken on clarifying the mechanism of action of CRIT, in footings of it being a potentially utile molecule in handling immunological diseases and other diseases, such as malignant neoplastic disease. For illustration, Inalet Al.( 2005 ) have shown that CRIT barricading can take to deprotection in CRIT-expressing human myeloid cell lines and in monocytes, ensuing in a greater susceptibleness to complement-mediated lysisin vitro. Other research, such as that by Mollet Al.( 2006 ) has shown that CRIT look is different in patients with kidney upsets, through assorted alterations in up- or down-regulation of CRIT look, taking to the suggestion that the upregulation of CRIT in activated podocytes might stand for a self-defense mechanism, stand foring a ‘last line’ of defense mechanism in membranous kidney disease of the kidney. Introduction The purpose of this research is, finally, to transport out a pilot survey to back up preliminary grounds that the complement receptor CRIT ( Complement C2 Receptor Inhibitor Trispanning ) plays a function in monocyte/macrophage terminal distinction. We aim to demo that by triping distinction through CRIT, it is possible to suppress the proliferation of myeloid leukemia cells. This could hold of import deductions for an alternate intervention agenda for monocytic leukemia. By the terminal of this survey we expect to demo the undermentioned: I ) that monocytes which can adhere C2 through CRIT maintain monocytic phenotypein vitroorin vivo ;II ) that monocytes can be induced to terminally distinguish by barricading the interaction of CRIT with its blood relation ligand, complement C2 or as monocytes move into an extravascular environment devoid of C2 ; that a knockdown of CRIT look in monocyte carcinoma cell lines or physical blocking of CRIT-C2 interaction induces them to terminally dis tinguish, and that, likewise, a blocking of CRIT-C2 interaction on leukaemic monocytes will halt proliferation and bring on distinction ; and, in conclusion, that, conversely, monocytes that are C2-/- , can non be induced to terminally distinguish by barricading the interaction of CRIT with its ligand, C2, nevertheless on traveling into an extravascular environment, other excess mechanisms, such as interaction of monocyte integrins with VCAM molecules on endothelial cells, may still bring on distinction. In consequence, basically, either barricading ligand interaction with CRIT or cut downing CRIT look should excite cell rhythm apprehension ( irreversible block at G1 ) and terminal distinction into cells with a macrophage phenotype. These conditions represent a fresh tract for monocyte/macrophage terminal distinction, based on the theoretical account proposed, and affecting the complement receptor, CRIT. In footings of monocyte leukemia, besides advancing cell rhythm apprehension, barricading CRIT with anti-CRIT-ed1 has the added benefit of rendering the cell more susceptible to complement-mediated cytolysis, as described antecedently for monocyte carcinoma cell lines ( U937 and THP-1 ) and primary monocytes showing CRIT [ 1 ] . Bradt, B.M.et al. ,1998. Complement-dependent proinflammatory belongingss of the Alzheimer’s disease B-peptide.J. Exp. Med.188, pp.431. Carroll, M.C. , 1998. The function of complement and complement receptors in initiation and ordinance of unsusceptibility.Ann Rev Immun16,pp.545-568. Hui, K-M. , 2005. Biochemical and functional surveies of a fresh complement inhibitor, CRIT, with its interaction spouses. Dissertation submitted to the University of Basel, 2005. Hui, K-M.et al. ,2005. Expression of functional recombinant von Willebrand factor-A sphere from human complement C2: a possible binding site for C4 and CRIT.Biochem J.389, pp.863-868. Inal, J.M. , 2005. Complement C2 receptor inhibitor trispanning: from adult male to schistosome.Springer Seminars in Immunology27 ( 3 ), pp.320-331. Inal, J.M.et al. ,2005. Complement C2 receptor inhibitor trispanning: a fresh human complement inhibitory receptor.Journal of Immunology74, pp.356-366. Inal, J.M. and Schifferli, J.A. , 2002. Complement C2 receptor inhibitor trispanning and the B-chain of C4 portion a binding site for complement C2.Journal of Immunology168, pp.5213-5221. Kilgore, K.S.et al. ,1994. The complement system in myocardial ischaemia/reperfusion hurt.Cardiovasc Research28, pp.437. Makrides, S.C.et al. ,1992. Cell surface look of the C3b/C4b receptor ( CR1 ) protects the hamster ovary cells from lysis by human complement.J.Biol.Chem.34, pp.24754-24761. Moll, S.et al. ,2006. CRIT is expressed on podocytes in normal human kidney and upregulated in membranous kidney disease.Kidney International69,pp.1961-1968. Oh, K-S.et al. ,2003. Inhibition of complement activation by recombinant Sh-CRIT-ed1 parallels.Immunology110, pp.73-79.

Political climate of Venezuela Essay Example | Topics and Well Written Essays - 250 words

Political climate of Venezuela - Essay Example Various articulations in regards to democracy have been under the limelight, keeping in mind that political unrest violence is the main issue that brings about further curtailment of democracy in this nation. Venezuela is among the countries that take into account the virtue of multiparty and hence leading to the imposition of martial law as well as curtailing democratic rights in Venezuela. The United States of America that is the superpower has been against those people in support of President Chavez, who has been at large providing leadership full of poor governance. Elections held in the year 2012 was full of conspicuous results in that the Venezuela government have been forced out to permit the essence of the audit which is known to have been articulated fraudulent activities hence this could in turn help in revising the outcome of the elections (Valente, 23-29). Political unrest has been the subject as far as the political climate of Venezuela is of concern. Chavez on the other hand in his regime has worked diligently to make sure that his supporters believe that what he has achieved in his political system was not through deception and collusion with independent media. Some of the crucial negative insist that Venezuela political system has deployed includes the termination of popular Chavista social programs well known as Misiones Bolivarianas should the opposition takes into account the victory on the prevailing elections. I concur with L Philharmonic under heavy criticism over political climate of Venezuela.

Jaguar Land Rover Management Essay Example | Topics and Well Written Essays - 4000 words

Jaguar Land Rover Management - Essay Example Supply chain is defined as the a system involving the use of information, activities, people, organization and resources that work to ensure that products or services is moved from the supplier to the consumer. They are the link between the supplier and the consumer by ensuring that the supplier gets the goods to the target market and that the consumer can easily access the goods and services they need with ease. With this in mind, supply chain management would therefore refer to all attempts by the management and planning department of an organization to procure, coordinate, and convert and all other management activities that will ensure the success of the supply. It fosters coordination of activities with and across the various sectors of production, transportation, storage and distribution of goods and services. Channel partners may include intermediaries, suppliers, service provider and consumers which form a chain-like link through which the producer and the consumer are connec ted.Supply chain management has continued to be the most convenient way through which organizations can be able to gain knowledge they need in decision making (Wu & Blackhurst, 2009). The decision making process includes all activities which help us make informed choices that will lead to the overall success of the organization. In the automotive sector, there has been consumer demand for better quality product which meets the client needs of security, comfort, class, and has reduced negative effects on the environment

Basically Good, Bad, or Both Essay Example | Topics and Well Written Essays - 750 words

Basically Good, Bad, or Both - Essay Example Human beings are a combination of both, good and evil because they are neutral and they have the free will and determination to adopt any. In order to be civilized humans have set boundaries and rules that determine good and evil. Aristotle argued that since man is a social animal and setting boundaries for good and evil is but natural because they are essential for humans remain civilized. Humans are neutral because they are equally capable and free to make a rational choice between good and evil. It is the society, upbringing and biological factors that affect a human's ability to think and decide. So it's these factors that are to be accredited blamed or for good or evil, respectively. It has been proved that the human mind is not a blank slate by Steven Pinker in his book "The Blank Slate" and the other factors like the surroundings, sociological and biological factors affect the mind's ability to think. Humans are not born good or born evil because they are capable of both as th ey grow up into adults. Education and guidance have an effect on the mind's capability to decide and choose between good and evil. ... Whereas, the developed world is a different scenario and people are usually educated and well- brought up even well-fed and well-provided with all the needs and wants and it's a fact that these people are sensitive and have made rational decisions to do good and avoid evil. Both the qualities of good and evil are present within us and we must make a choice. There are outside influences that affect the nature of the choice. The most controversial example is George W. Bush who is civilized and a good man in the eyes of many and especially his relatives but he is responsible for waging wars for oil and millions have been killed in his quest. He is a combination of good and evil. Bush is a good person to some people and maybe he himself believes that he is working in the best interests of his people and his country. But the fact remains that his actions were evil and millions of innocent lives have been lost. There is a reason for human nature to take this form and there are several theo ries to explain it. The philosophical naturalism believes that humans are superior beings and they are the result of evolution. Humanist philosophers argue that good and evil are simply labels and made up boundaries in order to civilize this world. It is the brain and the society at work that bring out this distinction. These influences affect our decisions to be good or to be evil. Man was born free and free will according to Thomism by Aquinas explains that a free will is the only essential proof of the existence of a soul. Aristotle supported this theory as well since according to his concept of hylomorphism the soul is significant and also universal and the soul makes every human being different. Therefore, when every one of us is different, every one of us has a

Country Comparison of Economic Development Data

Country Comparison of Economic Development Data QUESTIONS: You are required to collect comprehensive economic development data for year 2012 2013 of Malaysia and two countries of your choice and discuss which country is better in terms of†¦Ã¢â‚¬ ¦(based on economic performance da ta collected) and discuss possible ways to improve your country’s economic development and standard of living. Malaysia Malaysia have 4 types of GDP which is purchasing power parity, official exchange rate, real growth rate and per capita PPP. For purchasing power parity in 2012 estimation is $501.5 billion and in 2013 estimation is $525 billion. In 2012 and 2013 estimation for the official exchange rate is $312.4 billion. For the real growth rate in 2012 estimation is 5.6% and in 2013 estimation is 4.7%. For the per capita PPP in 2012 is $17,000 and 2013 estimation is $17,500. Besides that, Malaysia have many different economy categories such as unemployment rate, population below poverty line. For the unemployment rate in 2012 estimation is 3% and in 2013 estimation is 3.1%. For the population below poverty line in 2012 and 2013 estimation is at 4.0% . Furthermore, for the budget consists of 2 categories which are revenues and expenditures. For the revenues in 2012 and 2013 estimation is $ 65.72 billion. For the expenditures in 2012 and 2013 estimation is $ 79.4 billion. In conjunction with the budget expenditures there is taxes which applies on the expenditures as well. For the taxes and other revenues is 21% GDP and for the budget deficit is -4.4% of GDP. For the consumer prices will have inflation rate as well. In 2012 estimation is 1.7% and in 2013 estimation is 2.2%. Lastly is the exports and imports for the country in Malaysia. For the exports in 2012 estimation is $227.7 billion and in 2013 estimation is $230.7 billion. For the imports in 2012 estimation is $186.9 billion and in 2013 estimation is $192.9 billion. The next category is people and society. There is 5 categories which is population, human development index, human poverty index, poverty rates and population growth rates. For the population in Malaysia for 2012 and 2013 estimation is 30,073,353 people. For the human development index in 2012 and 2013 estimation is 0.769. For the poverty rates in 2012 and 2013 estimation is 1.7%. Finally, for the population growth rates in 2012 and 2013 estimation 1.7%. Finally, for the population growth rates in 2012 and 2013 estimation is 1.47%. Japan Japan have 4 types of GDP which is purchasing power parity, official exchange rate, real growth rate and per capita PPP. For purchasing power parity in 2012 estimation is $4.638 trillion and in 2013 estimation is $4.729 trillion. In 2012 and 2013 estimation for the official exchange rate is $5.007 trillion. For the real growth rate in 2012 and 2013 estimation is 2% For the per capita PPP in 2012 is $36,300 and 2013 estimation is $37,100. Besides that, Malaysia have many different economy categories such as unemployment rate, population below poverty line. For the unemployment rate in 2012 estimation is 4.4% and in 2013 estimation is 4.1%. For the population below poverty line in 2012 and 2013 estimation is at 16%. Furthermore, for the budget consists of 2 categories which are revenues and expenditures. For the revenues in 2012 and 2013 estimation is $1.739 trillion. For the expenditures in 2012 and 2013 estimation is $2.149 trillion. In conjunction with the budget expenditures there is taxes which applies on the expenditures as well. For the taxes and other revenues is 34.7% GDP and for the budget deficit is -8.2% of GDP. For the consumer prices will have inflation rate as well. In 2012 estimation is 0% and in 2013 estimation is 0.2%. Lastly is the exports and imports for the country in Malaysia. For the exports in 2012 estimation is $776.6 billion and in 2013 estimation is $697.0 billion. For the imports in 2012 estimation is $830.1 billion and in 2013 estimation is $766.6 billion. The next category is people and society. There is 5 categories which is population, human development index, human poverty index, poverty rates and population growth rates. For the population in Malaysia for 2012 and 2013 estimation is 127,103,388 people. For the human development index in 2012 and 2013 estimation is 0.912. For the poverty rates in 2012 and 2013 estimation is 11.1%. Finally, for the population growth rates in 2012 and 2013 estimation 15.7%. Finally, for the population growth rates in 2012 and 2013 estimation is 0.13%. United States United States have 4 types of GDP which is purchasing power parity, official exchange rate, real growth rate and per capita PPP. For purchasing power parity in 2012 estimation is $16.47 trillion and in 2013 estimation is $16.72 trillion. In 2012 and 2013 estimation for the official exchange rate is $16.72 trillion. For the real growth rate in 2012 is 2.8% and 2013 estimation is 1.6%. For the per capita PPP in 2012 is $52,400 and 2013 estimation is $52,800. Besides that, Malaysia have many different economy categories such as unemployment rate, population below poverty line. For the unemployment rate in 2012 estimation is 8.1% and in 2013 estimation is 7.3%. For the population below poverty line in 2012 and 2013 estimation is at 15.1%. Furthermore, for the budget consists of 2 categories which are revenues and expenditures. For the revenues in 2012 and 2013 estimation is $2.849 trillion. For the expenditures in 2012 and 2013 estimation is $3.517 trillion. In conjunction with the budget expenditures there is taxes which applies on the expenditures as well. For the taxes and other revenues is 17% GDP and for the budget deficit is -4% of GDP. For the consumer prices will have inflation rate as well. In 2012 estimation is 2.1% and in 2013 estimation is 1.5%. Lastly is the exports and imports for the country in Malaysia. For the exports in 2012 estimation is $1.561 trillion and in 2013 estimation is $1.575 trillion. For the imports in 2012 estimation is $2.303 trillion and in 2013 estimation is $2.273 trillion. The next category is people and society. There is 5 categories which is population, human development index, human poverty index, poverty rates and population growth rates. For the population in Malaysia for 2012 and 2013 estimation is 127,103,388 people. For the human development index in 2012 and 2013 estimation is 0.912. For the poverty rates in 2012 and 2013 estimation is 11.1%. Finally, for the population growth rates in 2012 and 2013 estimation 15.7%. Finally, for the population growth rates in 2012 and 2013 estimation is 0.13%. 5 Ways To Improve Your Country’s Economic Development And Standard Of Living 1. Wage your levies: An efficient tax collection and management system is important for a country’s economy growth. Besides exports, the majority of revenue is from taxation, without taxation, the government cannot invest in infrastructure, social programs or compensate government officials. Sales taxes, income taxes, payroll taxes and wealth taxes are made by taxpayer into the economy to improve the collective standard of living. This includes the benefit from getting better roads, schools, hospitals and a welfare system. 2. Animate within your means: By saving money and keeping your debt lower than your disposable income, you will be less vulnerable recession. For example, if your credit cards, mortgage loans, the outstanding balance of auto loans and student loans is more than your savings, investments and property combined, then the problem will come to you. It means you may have a dissatisfied conditions, as like a sudden drop in unexpectedly financial obligations. 3. Acquire valuable teaching: The education level is highly associated to the economic growth. In other words, the more skilled of the population is (composed for example of engineers, physicists, agricultural biologists, construction workers, etc), the more productive, competitive and autonomous that a country can be. For example, with the right expertise, food security can be guaranteed by increasing agricultural production; a plenty of goods can be manufactured and exported; and natural resources can safely use and local change. So by getting a professional education that is in demand, you will help your country to get productivity and a strategic advantage. 4. Devour properties and facilities created locally: By selecting to buy a five-dollar t-shirt made in your country instead of the exact same t-shirt selling for one dollar but made abroad, you just made a major positive impact: the money stayed in the local economy, domestic jobs were compensated and small businesses remain open. 5. Chosen administration bureaucrats in errand of financial development: All of the advice above cannot be effective without leaders who fight for corruption, foster a fair trade and business agreements, promote financial transparency, support for protectionist labor laws, avoid excessive public and consumer debt, engage in a prudent monetary and fiscal policy development, boost job creation, ease access to important sectors of education and healthcare, subsidize vital industries and help small businesses. 2. What is ‘Dumping’ and why do countries implement ‘Anti-dumping’ legislation? Do you think such legislations are required in today’s free trade world market? Discuss with supporting data and relevant duties What is dumping? Dumping happens when the export price of the goods in Malaysia is lower than the usual price of the similar or alike artefact in the inland market in the nation of export or basis. In other words, dumping is an global value discernment which the corporation custodies more in its inland marketplace than in the export marketplace. What is export price? Export price is actually the value that salaried or owed for the topic merchandise (supposedly vended at dumping values in Malaysia for overseas products) . In cases the export price may be built on the topic merchandise are first resold to an self-governing purchaser on basis of price. What is subject merchandise ? Subject merchandise means the lesson or kind of merchandise imported or vended imported into Malaysia that is the topic of any countervailing or anti-dumping responsibility act under Act 504. What is like product? Like product means a product which is alike or like in all compliments to the topic merchandise, and comprise other artefact which comprise bodily, technical or biochemical physiognomies, applications or uses that nearly alike to those the topic merchandise. What is normal value? Normal value is the value salaried in the normal course of interchange in the inland marketplace of the nation of export. Auctions used to verify the usual price which must be lucrative and unaffected by any association between the purchaser and vender. Nations comply ‘anti-dumping’ lawmaking because to authorizing the Examining Specialist to take corrective events against unfair interchange by overseas builders/exporters and to deliver a outline for examining accusations of damage caused by dumped or funded imports. I think such legislations are required in today’s free trade world market due to: Anti-dumping actions (Legal issues) If a corporation exports a artefact at a worth that is fewer than the worth it usually custodies in its own home-based marketplace, or vended properties at a worth which does not encounter its filled cost of manufacture, it is called as dumping the artefact. It is a sub-section of numerous forms of worth discernment and is registered as third gradation worth discernment. Many administrations take act against dumping to defend inland business and the WTO contract concentration is on how administrations can or cannot respond to dumping. It disciplines anti-dumping contract. The administration must compute the boundary of dumping (how much lower of the export worth compared to the exporter’s home-based marketplace worth), and show that the injured of dumping. References: Fatima, R. (2014). MITI. Retrieved 12 May 2014, from http://www.miti.gov.my/cms/content.jsp?id=com.tms.cms.section.Section_e2f9c09d-c0a8156f-282d282d-9947bc72 Adkins, T., Alvin, M. (2009). Dumping Definition | Investopedia. Retrieved 12 May 2014, from http://www.investopedia.com/terms/d/dumping.asp Azhar, A., Reserve, T. (2014). Govt imposes anti-dumping duty on FCB from Thailand. Free Malaysia Today. Retrieved 12 May 2014, from http://www.freemalaysiatoday.com/category/business/2013/11/29/govt-imposes-anti-dumping-duty-on-fcb-from-thailand/ Gwet, M., Gwet, M. (2013). 5 things you can do to help your country’s economy BobbyFinance. BobbyFinance. Retrieved 13 May 2014, from http://bobbyfinance.com/2013/05/24/5-things-you-can-do-to-help-your-countrys-economy/# Britt S.L. (2014). The World Factbook. Retrieved 2 June 2014, from https://www.cia.gov/library/publications/the-world-factbook/geos/my.html

Free Essays - Individual vs. Society in Catcher in the Rye :: Catcher Rye Essays

Individual vs. Society in Catcher in the Rye In the novel Catcher in the Rye, many differences exist within the plot and between the characters. This makes the book so interesting. But what interest me, is that the main character, Holden, is the most distinctive example of a difference. Usually, societies approve of a level of uniqueness. But when individuality turns into clear differences of attitude and opinion, conflict starts to arise. Because Holden's morals and beliefs are those different from the society in which he lives in, he can't function in that particular society. Throughout the book, certain values of Holden start to show through. He speaks a lot about how he dislikes "phonies" and tries to separate himself from them. Every time Holden tries to run away from these "phonies," it starts to give you an idea about how he values honesty and his reaction towards people who don't have this particular value. In chapter seventeen, Holden tries to rationalize himself being kicked out of school by saying he wants to accomplish something different and not just be a phony. "It's full of phonies, and all you do is study so that you can learn enough to be smart enough to be able to buy a goddam Cadillac some day, and you have to keep making believe you give a damn if the football team loses, and all you do is talk about girls and liquor and sex all day, and everybody sticks together in these dirty little goddam cliques (Salinger 131)." In life, and as his days go by, he will realize that many people in society and people who run it, are indeed n ot genuine. The reality angers Holden and he fantasizes about running away, escaping from society, and living in a cabin away from everybody. This is a far-fetched idea that is hardly even an option for him. He decides that if he can't fit in a society where he isn't wanted, then he won't be a part of it. This thought would have never come across Holden's mind if he was like everybody else, but he isn't. Holden obviously can't deal with the environment around him and one day may lash out to the elements of life that aren't in agreement with him. Free Essays - Individual vs. Society in Catcher in the Rye :: Catcher Rye Essays Individual vs. Society in Catcher in the Rye In the novel Catcher in the Rye, many differences exist within the plot and between the characters. This makes the book so interesting. But what interest me, is that the main character, Holden, is the most distinctive example of a difference. Usually, societies approve of a level of uniqueness. But when individuality turns into clear differences of attitude and opinion, conflict starts to arise. Because Holden's morals and beliefs are those different from the society in which he lives in, he can't function in that particular society. Throughout the book, certain values of Holden start to show through. He speaks a lot about how he dislikes "phonies" and tries to separate himself from them. Every time Holden tries to run away from these "phonies," it starts to give you an idea about how he values honesty and his reaction towards people who don't have this particular value. In chapter seventeen, Holden tries to rationalize himself being kicked out of school by saying he wants to accomplish something different and not just be a phony. "It's full of phonies, and all you do is study so that you can learn enough to be smart enough to be able to buy a goddam Cadillac some day, and you have to keep making believe you give a damn if the football team loses, and all you do is talk about girls and liquor and sex all day, and everybody sticks together in these dirty little goddam cliques (Salinger 131)." In life, and as his days go by, he will realize that many people in society and people who run it, are indeed n ot genuine. The reality angers Holden and he fantasizes about running away, escaping from society, and living in a cabin away from everybody. This is a far-fetched idea that is hardly even an option for him. He decides that if he can't fit in a society where he isn't wanted, then he won't be a part of it. This thought would have never come across Holden's mind if he was like everybody else, but he isn't. Holden obviously can't deal with the environment around him and one day may lash out to the elements of life that aren't in agreement with him.