Causes and Effects of Water Pollution in Lake Huron Essay

Causes and Effects of Water Pollution in Lake Huron - Essay Example Its drainage region is large in comparison to other Great Lakes since it covers parts of Ontario and Michigan lakes. Its waters are useful to several people who bound it especially the farmers. However, the Lake has been facing some water pollution challenges that make its waters disastrous. The ultimate aim of this context is to examine the sources that lead to pollution of Lake Huron and the Great lakes. It then looks at the effects of this pollution and winds up by providing recommendations on what can be done to save Lake Huron (Buchsbaum, 2009). Causes of Water Pollution on Lake Huron Several pollutants caused by human activities around the region have affected Lake Huron. Some of the most common pollutants are as mentioned below. Chemical Contamination Lake Huron is fed by contaminants, which initiate from several sources among them being spills, municipal discharges, industrial discharges, landfills, agricultural runoff and storm sewers (Krantz & Kifferstein, 2010). These cont aminants get into Lake Huron through several trails including atmospheric deposition, direct liberation and river discharge. In comparison to Lakes Ontario, Michigan and Erie, pollutant concentrations are comparatively low in Lake Huron. However, public health consultative exists concerning utilization of trout and all Areas of Concern (AOCs). Atmospheric Deposition Besides, its massive surface area, like the other Great Lakes, has made it susceptible to atmospheric deposition of pollutants. It has a large surface area and comparatively few regional pollutant point sources (Mahler, Metre & Callender, 2006). Loading to Lake Huron from water basis are stumpy of all the Great Lakes, but air basis are highest. Bio-accumulative Substances From the late 1970s to around 1990s, the concentrations of bio-accumulative matters like DDT, PCBs, dioxins, dieldrin, and furans turned down considerably in Lake Huron lake trout. Nevertheless, whereas the concentrations of DDT have persistently deteri orated, PCB concentrations have not fallen off considerably since the mid-1980s. DDE inclinations in Lake Huron herring gull eggs display a marked reduction in concentration since 1970s. According to other inclinations, concentrations decreased considerably in the late 1970s but continued to be comparatively stable (Mahler, Metre & Callender, 2006). Continuing basis of pollutants is mainly from sediments polluted by historic liberation, airborne deposition industrial and municipal librations and land runoff. Initially, there were six main Great Lakes regions of considerable environmental pollution or Areas of Concern (AOCs) on Lake Huron. The St. Mary River is named as an Area of Concern since it contains pollutants from municipal discharges and non point source contamination sources (Buchsbaum, 2009). Management of industrial point sources is developing, and pollution consignments are being minimized. The St. Clair River is named as an AOC because of the contamination difficulties on the eastern side of the river. Severn Sound and Spanish are the two other Canadian Areas of Concern that are reacting positively to the remedial activities and displaying recovery (Mahler, Metre & Callender, 2006). The only Area of Concern exclusively in Michigan, Saginaw Bay or river, is modeled as an AOC mainly because of polluted deposits and non point contamination sou

Molecular Mechanisms of Sepsis

Molecular Mechanisms of Sepsis Title: Protein-protein interaction network and functional module analysis to reveal the mechanism of sepsis in polytrauma patients Highlights: We explored the molecular basis of sepsis induced by polytrauma using PPI network. A total of 342 DEGs including 110 up- and 232 down-regulated genes were obtained. TRAF3 was related with the innate immune responses in sepsis. ITGB3 was the key gene involved in coagulation dysregulation in sepsis. CASP6 and RASA1 played key roles in the cell apoptosis mechanism of sepsis. Abstract Objective Sepsis represents the systemic inflammatory response to microbial infection. The pathogenesis of sepsis remains unclear. In this study, we aimed to explore the molecular mechanism of sepsis inpolytrauma patients. Methods The differentially expressed genes (DEGs) between the polytrauma patients with and without sepsis were identified by analyzing the GSE12624 microarray data using the limma package of R. The protein-protein interaction (PPI) network was extracted from the human PPI datasets by using MATLAB. The functional modules in the PPI network were identified by the MCODE network clustering algorithm. The KEGG pathway analysis was performed in each module. The phylogenetic tree was constructed using phylogeny inference package (PHYLIP). Result Total of 342 DEGs including 110 up- and 232 down-regulated genes were obtained. The PPI network identified several hub genes which had more interactions with others, such as TRAF3, ITGB3, CASP6 and RASA1. Further phylogenetic analysis indicated the high conservation of these hub genes. In the module analysis, four significant modules were identified. All the genes (COL1A2, FN1, ITGA2B, ITGB3 and CD36) in module 2 were enriched in extracellular matrix (ECM)-receptor interaction pathway. In module 4, CASP6 and CASP3 were enriched in apoptosis pathway. Conclusion We predicted genes such as TRAF3, ITGB3, CASP6 and RASA1 which were closely associated with sepsis induced by polytrauma. Among them, ITGB3 may play key role in the coagulation dysregulation of polytrauma patients with sepsis, and CASP6 and RASA1 may be the key genes in the cell apoptosis mechanism of sepsis. Keywords Sepsis, DEGs, GO, PPI network, phylogenetic tree Introduction Polytrauma is a syndrome of multiple injuries exceeding a defined severity with sequential systemic reactions that can lead to dysfunction or failure of remote organs and vital systems, which have not themselves been directly injured [1]. Sepsis, as one of the complications of polytrauma [2], is the systemic inflammatory response to microbial infection that often leads to increasing susceptibility to secondary infections, multiorgan failure, and death [3]. A sixteen years clinical study indicated that 10.2% of polytrauma patients infected sepsis during their hospital course [4]. Polytrauma is a major cause of morbidity and mortality in global and sepsis (3.1-17%) is one of the predominant causes of late death in polytrauma patients [5]. The disease severity is increasing according to the order of sepsis, severe sepsis and septic shock in the systemic inflammatory response syndrome (SIRS) [6]. Mortality has been reported to be as high as 45.6% for patients with severe sepsis or septic shock [7]. Based on the pathogenesis of sepsis, many therapies have been applied in the clinical practice such as antimicrobial therapy [8, 9] and hemodynamic support and adjunctive therapy [10, 11]. Currently, the Surviving Sepsis Campaign (SSC) has attempted to increase the awareness and establish the practice guidelines to improve the recognition and treatment for the patients with sepsis [12, 13]. At present, there are four approved mechanisms in the pathogenesis of sepsis [14]. The first one is dysregulated coagulation. Sepsis patients frequently manifest disseminated intravascular coagulation (DIC) with consumption of platelets and prolongation of clotting times [15]. The second one is inflammatory response. The inflammatory response is an important and central component of sepsis because the elements of response drive the physiological alterations that manifest as the SIRS [16]. Third, many cellular aspects become dysfunctional in sepsis which behave either excessive activation or depressed function [17]. The last one is metabolic alterations. It was reported that endogenous glucose production was markedly increased in the patients [18]. However, the specific molecular mechanisms of them remain entirely unclear. In this study, the differentially expressed genes (DEGs) between the polytrauma patients with sepsis and without sepsis were identified. Gene ontology (GO) analysis , protein-protein interaction (PPI) network and phylogenetic tree construction were performed to explore the molecular basis of sepsis induced by polytrauma. Materials and methods Microarray data The gene expression profile of GSE12624 based on the CodeLink UniSet Human I Bioarray platform (GE Healthcare/Amersham Biosciences) was downloaded from National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database (http://www.ncbi.nlm.nih.gov/geo/). The dataset available in this analysis contained 70 samples including 34 polytrauma patients with sepsis and 36 polytrauma patients without sepsis. Data preprocessing and DEGs screening For the microarray data, Robust Multichip Average (RMA) in the Affy package of R was used to compute normalized expression measures from the raw expression values. Probe annotation was obtained by using the Bioconductor package. The limma package was used to identify the DEGs with p-value 1 [19]. GO enrichment analysis of DEGs GO analysis was performed using the DAVID online tool (http://david.abcc.ncifcrf.gov/) [20]. For GO enrichment of DEGs, we selected GOTERM_BP_FAT, GOTERM_CC_FAT and GOTERM_MF_FAT as the gene set categories. A p-value of less than 0.05 was set as the cut-off criterion. PPI network construction The human PPI datasets with 108477 interacting protein pairs were downloaded from PINA2 (http://cbg.garvan.unsw.edu.au/pina/interactome.stat.do) at December 26, 2013. The PPI networks of the DEGs in sepsis were extracted from the human PPI datasets by usingMATLAB [21]. The proteins in the network served as nodes and the degree of a node corresponded to the number of interactions with other proteins [22]. The protein with high degree was considered as the hub node. Identification of functional modules in PPI network PPI network visualization and network parameters evaluation were performed by using Cytoscape software. The modules were identified by the MCODE (a cytoscape plug-in) network clustering algorithm with the default parameters [23]. The module with score larger than 2 was considered as significant. KEGG pathway analysis of each module was performed by applying the DAVID annotation tool. Phylogenetic tree construction In this study, we constructed the phylogenetic tree based on the nucleotide sequences to investigate the sequence conservation of the DEGs whosedegree were large than 30. The BLAST program is used to search for homologous sequences of these DEGs. The DNA sequence of these DEGs and their homologous genes in FASTA format were obtained from the nucleic acid database in NCBI (http://www.ncbi.nlm.nih.gov/nuccore). The phylogenetic tree was constructed by using phylogeny inference package (PHYLIP) with the default parameters [24]. The gene conservation was estimated by the distance from gene to the phylogenetic tree root. Result DEGs between the patients with and without sepsis After statistical analysis of the microarray data, a total of 342 DEGs were screened out. Among them, 110 were down-regulated and 232 were up-regulated in sepsis. The top 20 significantly up- and down-regulated DEGs are shown in Table 1. GO enrichment analysis The 342 DEGs were significantly enriched into 95GOterms including 81 biological processes terms, 10 cellular component terms and 4 molecular function terms. The top 10 GO biological processes termswere mainly related to the purine base (purine base biosynthetic process, purine base metabolic process, purine nucleoside monophosphate biosynthetic process and purine ribonucleoside monophosphate biosynthetic process), nucleobase (nucleobase metabolic process and nucleobase biosynthetic process) and regulation of protein modification (regulation of protein modification process and positive regulation of protein modification process). The 10 significantly enriched GO terms of cellular component included four lumen related terms (organelle lumen, membrane-enclosed lumen, intracellular organelle lumen and nuclear lumen), two membrane related terms (extrinsic to membrane and plasma membrane part) and four other cellular component terms (peroxisome, microbody, nuclear body and Golgi apparatus) . For molecular function, four significant GO terms were enriched finally. They were acyl-CoA binding, sons of mothers against decapentaplegic homologue (SMAD) binding, aryl hydrocarbon receptor binding and potassium channel inhibitor activity (Table 2). PPI network of DEGs A PPI network consisting of 225 DEGs and 1048 non-DEGs is shown in Fig. 1. This network included 1145 gene nodes and 1273 interactions. The connectivity degree of each node in this PPI network was calculated and the results of top 20 nodes are listed in Table 3. Among them, the genes CRK (encoding CDC2 related protein kina), RASA1 (encoding RAS p21 protein activator 1), TRAF3 (encoding tumour-necrosis-factor receptor associated factor 3), ZHX1 (encode zinc-fingers and homeoboxes), ITGB3 (encoding integrin ÃŽ ²3), RPA1 (encoding replication protein A1), JAK3 (encoding Janus kinases 3), and CASP6 (encoding caspase-6) with the degree over 30 were selected as the hub genes. Module analysis of PPI network A total of 7 modules were constructed by using MCODE plug-in. After excluding the modules with the score less than 2, 4 significant modules were considered as functional ones associated with sepsis (Table 4). According to the Fig. 2, the numbers of nodes and edges were similar in each model. The detailed results of KEGG pathway analysis for each module are provided in Table 5. For module 1, no pathway was enriched in the KEGG pathway analysis. For module 2, a total of 14 significant enriched pathways were identified. Among them, all the genes in this module were enriched in the pathway of extracellular matrix (ECM)-receptor interaction. In addition, except CD36 (encoding glycoprotein IV), the other four genes (ITGB3 and ITGA2B encoding integrin ÃŽ ±IIbÃŽ ²3, COL1A2 encoding the ÃŽ ± 2 chain of type 1 collagen and FN1 encoding fibrinogen 1) were enriched in the focal adhesion and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. There were three significant enriched pathways in module 3. HIF1A (encoding hypoxia inducible factor-1), ARNT (encoding arylhydrocarbon receptor nuclear translocator) and ARNT2 (encoding arylhydrocarbon receptor nuclear translocator 2) were enriched in the pathway of renal cell carcinoma and pathways in cancer. HIF1A and ARNT were enriched in the pathway of Hypoxia-inducible factor 1 (HIF-1) signaling. For the module 4, five significant pathways were found. Among them, CASP3 (encoding caspase 3) and BIRC5 (encoding baculoviral IAP repeat–containing 5 and also called survivin) were enriched in the pathway of colorectal cancer, hepatitis B and pathways in cancer. CASP6 and CASP3 were enriched in apoptosis pathway. CASP3 and RASA1 were enriched in the mitogen-activated protein kinase (MAPK) signaling pathway (Table 5). Phylogenetic tree analysis Based on the result of PPI network analysis, the selected hub genes were chosen to construct the phylogenetic tree. The phylogenetic tree of ZHX1 was unable to be constructed, as only three homologous sequences were searched out. The phylogenetic trees of the other seven hub genes were constructed by the DEGs and their top nine significant homologous genes. The results showed that CRK, RASA1, TRAF3, ITGB3, RPA1 and CASP6 were the genes that were closer to tree roots indicating that the conservation of these genes was high during evolution. However, the conservation of JAK3 was low because of appearing in the late period of evolution (Fig. 3). Discussion Currently, sepsis remains a serious clinical problem. The four approved mechanisms of sepsis were dysregulated coagulation, inflammatory response, and cellular dysfunctional and metabolic alterations. However, the specific molecular mechanisms are still incompletely understood. For better understanding the pathogenesis, we identified and analyzed the DEGs between the patients with and without sepsis. As a result, a total of 342 DEGs including 110 up-regulated genes and 232 down-regulated genes were found. These genes were significantly enriched in GO terms including purine base biosynthetic process, regulation of protein modification process and peroxisome. Among them, the process of purine base biosynthesis is the most significantly enriched process. It was reported that de novo purine biosynthesis was essential for infectivity, growth and virulence of many bacteria in mammals [25]. The pathogenesis of sepsis was related with the bacterial infection [26]. Therefore, the purine base biosynthesis process may associate with sepsis based on the tissue response to bacterial infection. For the regulation of protein modification, Wu et al. reported that the alterations in the phosphorylation of myofibrillar proteins and the Ca2+ sensitivity of myofibrillar ATPase might contribute to alter cardiac function during the progression of sepsis [27]. The cardiac dysfunction was the clinical characteristic in severe sepsis and septic shock [28]. Thus, the phosphorylation of myofibrillar proteins may be related with the sepsis-induced cardiac dysfunction. Furthermore, we mapped the DEGs to the PPI network and identified high conserved hub genes. Among them, the high conservation of CRK, RASA1, TRAF3, ITGB3, RPA1 and CASP6 were proved by the phylogenetic tree analysis. They may be the crucial genes in the pathogenesis of sepsis. For TRAF3, it is a member of the TNF receptor (TNFR) associated factor (TRAF) protein family [29]. This protein participates in the activation of the innate immune response [30]. In the PPI network, TBK1 (encoding TANK-binding kinase 1) was a non-DEG interacted with TRAF3. It was reported that TIR domain-containing adaptor-inducing IFN-ÃŽ ² (TRIF) could interact with noncanonical IKKs (IKKà Ã‚ µ and TBK-1) and IKKÃŽ ¹ (also called IKKà Ã‚ µ) through TRAF3 in the Toll-like receptors (TLR) signaling pathway [31]. The innate immune system constitutes the first line of defense by rapidly detecting invading pathogens through the TLR [32] and is a danger signal in systemic inflammatory response syndrome and sepsi s [33]. Thus, TRAF3 may be the mediator of innate immune responses in sepsis induced by polytrauma. We also performed the modular analysis of the PPI network and four functional modules were identified. Based on the result of the KEGG pathway analysis of each module, we found that the pathways in module 2 and 4 were more related with sepsis. The ECM-receptor interaction pathway was the most significant pathway in module 2 and all the genes of this module were enriched in this pathway. Fibronectin and collagen are the components of ECM [34]. Integrin family are the receptors transducing signals from the ECM [35]. Among them, integrin ÃŽ ±IIbÃŽ ²3 is the platelet integrin promoting theaggregation of platelets [36-38]. Moreover, it was reported that collagen type I could induce the aggregation of platelet [39]. Integrin ÃŽ ±IIbÃŽ ²3 is one of the platelet collagen receptors in platelets [40]. It was reported that platelet-specific elements initiated at the cytoplasmic domains of integrin ÃŽ ±IIbÃŽ ²3, which was a signal that leaded to conformational changes within the extracellular do mains of integrin and expression of the fibrinogen receptor, then the simultaneous occupancy on adjacent platelets of receptors with dimeric fibrinogen molecules leaded to platelet aggregation [41]. In addition, CD36 is spatially associated with the ÃŽ ±IIbÃŽ ²3 integrin on the surface of platelets [42]. Thus, we speculated that the binding of collagen type I and ÃŽ ±IIbÃŽ ²3 might need the participation of CD36, and then conformational changes within the extracellular domains of integrin and the binding between fibrinogen and fibrinogen receptor could lead to platelet aggregation. Disseminated platelet aggregation is one of the characteristics of the DIC in sepsis [43, 44]. The up-regulated expression of ITGB3 in sepsis may lead to the disseminated platelet aggregation. Hence, we concluded that the coagulation dysregulation in the polytrauma patients with sepsis may be associated with the increase of disseminated platelet aggregation caused by the up-regulated expression of ITGB3. Thus, ITGB3 may play key roles in the coagulation dysregulation of the polytrauma patients with sepsis. Hub nodes CASP6 and RASA1 were predicted to be closely interacted with each other in module 4. Besides, CASP3, TOP1, BIRC5 and AURKB (Aurora B kinase) were also included in module 4. Among them, CASP6 and CASP3 were enriched in apoptosis pathway. It was reported that CASP6 may be associated with the cell apoptosis in sepsis [45] and blocking caspases might have some beneficial effects in decreasing cell apoptosis in sepsis [46]. Thus, we further confirmed that the up-regulated expression of CASP6 may promote cell apoptosis in sepsis. Besides, TOP1 is cleaved late during cell apoptosis by CASP6 and CASP3 [47]. The TOP1 cleavage complexes contribute to cell apoptosis [48]. Therefore, the increase of these complexes induced by the up-regulated CASP6 can promote the cell apoptosis in sepsis. Moreover, full-length TOP1 could induce DNA cleavage by single-strand breaks which is the signal of cell apoptosis [49, 50]. Therefore, the exaggerated gene expression of TOP1 in our study might cont ribute to cell apoptosis in sepsis. In addition, it was reported that CASP3 could modulate a given set of proteins to generate, depending on the intensity of the input signals, opposite outcomes (survival vs death) through differential processing of RASA1 [51]. Some articles reported that low CASP3 activity leaded to the cleavage of the RASA1 protein into an amino-terminal fragment [52, 53]. RASA1 bound BIRC5 is a bifunctional protein complex that can suppress cell apoptosis and regulated cell division, so as to generate anti-apoptotic signals [54]. AURKB exists in a complex with BIRC5 [55]. Considering the up-regulated expression of RASA1 and AURKB, we speculated that there may be a switch mechanism of CASP3-RASA1 in cell apoptosis and BIRC5 and AURKB might play roles in the anti-apoptosis mechanism of RASA1. In summary, CASP6 and RASA1 are the key genes in the pathogenesis of sepsis induced by polytrauma. Conclusion In this study, we obtained four key genes related with pathogenesis of sepsisinduced by polytrauma. Among them, TRAF3 was related with the innate immune responses in sepsis,ITGB3 may play key role in the coagulation dysregulation of the polytrauma patients with sepsis and CASP6 and RASA1 were associated with the mechanism of cell apoptosisin sepsis. For further investigating the association of these hub nodes with sepsis and verifying the role of the interactions among the genes in the pathogenesis of sepsis, more studies are required in the future.

Great Britain Essay examples -- History, British Empire

Ever since its creation in 1707, the United Kingdom of Great Britain has been a powerful union of many different nations and identities, including the English, Scots, Welsh and later Irish. From the Middle Ages until the Second World War this union had not only fortified its domestic political power but also expanded its reign across the entire world, resulting in the world’s largest and mightiest empire, the British Empire. This great achievement of the union was mainly due to the remarkable sense of unity of its people who considered themselves primarily as British and secondly as Scots, Welsh or Irish. By the end of the Second World War, however, the domestic governance stability also threatened to collapse as many foreign colonies of the Empire seized independence. The Scots, Welsh and the Northern Irish started demanding more and more political independence from Westminster and by the end of the 20th century they were finally granted own national parliaments. After this p rocess of devolution, the English people started questioning their own identity and what distinguished them from the Scots, Welsh and the Northern Irish. But is there a national identity in England and if yes can this national identity be politically mobilized in the near future? When investigating English national identity and its possible future political mobilization it is crucial to analyze its meaning and history in the first part. Bechhofer and McCrone (2009) explain national identity as a political, sociological, cultural and psychological construct which is highly influence by the media, political changes within a state and its institutions. National identity, therefore, stays in a very close connection to notions such as nation, nationhood and nati... ...necessary in the eyes of the English voters that mainly vote in regard of other more important issues and debates. Partly contradicting Copus, Kumar (2001) explains that a future English nationalism is does not have to be excluded and very possible, but no one can now say how this is reflected in the future. To put it in a nutshell, in my opinion a political mobilization of the English identity in the near future is rather not probable since the English people are clearly not in the need of it an English parliament. Not only due to the multicultural aspect of its society today but also due to its imperialistic past, the English identity has become multifaceted and interpreted in many ways which makes it much harder for the English nationalism to evolve compared to Scotland, Wales and Ireland. Therefore, a unified mobilization is in the near future not thinkable.

Analysis of Willie Stark’s Life as a Politician Essay

Can it be right to do wrong? Can we have a square circle? Can we move backwards and forwards at the same time? During Plato’s time (c. 429-347 B.C.) a long discussion had begun and carried throughout the Middle Ages that affirmed that the ruler ought to embody noble ideals and values. This tradition focuses on the virtues of justice and mercy as essential for good government. However, during the Renaissance period the author Niccolo Machiavelli turned away from these traditions and considers in The Prince what is necessary to be successful in a corrupt world. Machiavelli proclaims in his book The Prince, â€Å"A man who wishes to make a profession in everything must necessarily come to grief among so many who are not good. Therefore, it is necessary†¦to learn how not to be good, and to use this knowledge and not use it, according to the necessity of the case†. Essentially, it is the situation at the moment that determines which actions are necessary. For Machiavelli, the goal is success, not the virtue or vice of the act. He does not advocate that the successful prince should always violate the rights of others but, rather, calculate what course of action will enhance the strength and vitality of the state. In the book All the King’s Men by Robert Penn Warren, the character Willie Stark is similar to the prince; he exemplifies and exercises Machiavelli’s ideals. In All the King’s Men by Robert Penn Warren, Machiavelli’s ideals are dealt with through the political career of Willie Stark, a man that was transformed from an idealist to an opportunist because of power, a man who ultimately was assassinated, but not before he could achieve the goodness he sought to make possible. Willie Stark, the son of a farmer, began his political career when becoming the County Treasurer of Mason City. As the Treasurer of Mason City, he was an idealist, guided more by ideals than practical considerations. Willie Stark remained an idealist up until he discovered the truth about politics. He than started to believe that goodness derives from evil because there is nothing else from which to make it. This idea comes from the mature, disillusioned Willie, who had become a tough-minded politician after losing his first political job and after discovering he was manipulated by the bosses who wanted to split rural votes. After he learned about the scheme and analyzing the situation, Willie Stark realized what Machiavelli’s theory proclaimed, â€Å"A man who wishes to make a profession in everything must necessarily come to grief among so many who are not good†. Willie encountered and experienced the â€Å"grief among so many who are not good,† he encountered Harrison and his men and their political methods to try and win an election which was all made possible by corrupt men, bad men. This was a turning point in Willie’s career and life since he how believed, â€Å"Man is conceived in sin and born in corruption and he passeth from the stink of the didie to the stench of the shroud.† As he sees it, goodness is not an inherent human characteristic. People, basically, are prone to corruption and evil. Goodness has to be made. Because of the scheme Willie’s blindfold he had as an idealist was gone and he now knew that politics were not at all what he though it to be and that he had to change the way he was conducting his political campaign if he was to get anything done around here. Although Willie withdrew his name from the ballot for the Governor race, he still came out of that ordeal as a winner. Stark exposed the dirty tricks of Harrison and his men and in the process gained support from the public, therefore leading to his ultimate election for Governor the second time he ran for the position. By this time Willie, â€Å"learn how not to be good, and to use this knowledge and not use it†¦Ã¢â‚¬  He exposed to the public the corrupt men of Harrison who coerced him to run for Governor only to be â€Å"used and abused in the process;† by blowing the whistle Willie became a bad man who turned against the people who helped him come into the political spot light. Instead of being seen with bad eyes, the public sympathized with him. With all the sympathy he gained Willie managed to win the race for Governor. Once Willie became Governor he became an opportunist because of the lack of support he received and because his power was growing. Willie essentially started off as a man who rose to power by offering to save the people from their distress, during his struggles, he became corrupted by power. Willie became corrupted because he realized that in order for him to help out the people he wanted to help out the most, he had to play a â€Å"little dirty†. He was forced to bribe the state legislators in order to get his bills passed; he even went as far as blackmailing some in order to achieve his goals. Willie Stark exemplifies Machiavelli’s discourse, â€Å"to learn †¦ not to be good †¦and not use it, according to the necessity of the case†. He was vicious and ruthless at times to his enemies and then he befriended those who opposed him within the state legislator. He learned when it was appropriate to be good to people and when it was necessary to be bad to people according to each situation because he could not afford to unbalance one with the other since both were essential for being a great governor. Willie Stark was an opportunist because of power. As Machiavelli’s theory stated one must use the knowledge of when to be good and when to be bad, â€Å"according to the necessity of the case,† and when the situation presented itself, Willie was ready to follow accordingly. When the plan to build a hospital presented itself, Willie wanted to keep the hospital clean, he did not want politics involved with the hospital especially , corrupt contractors. That is why Willie did not want to give Gummy Larson, a corrupt contactor to build his hospital. In this case Willie became a bad man who turned on a man that was much like him. Both had been involved in dirty politics, but now Willie chose to be a bad man in order to keep his hospital free from corruption and politics. While dealing with this situation, Willie also chose to be a good man by trying to persuade Adam Stanton, a romantic and idealist to be the Director of his hospital, but when Adam refused the offer, Willie indirectly used incriminating information about his father, a former governor who was involved in a bribe and cover up, in order to convince him to accept the position. Ironically, Adam Stanton, the man Willie wanted to Direct his hospital ended up assassinating him. In return Willie’s men ended up killing Adam. Both were destined to kill each other since they were complete opposites, one was a man of ideas and the other was a man of fact. In the end, by the author of All the King’s Men adhering Willie’s life to Machiavelli theory of how a ruler should govern and obey by; Willie life was destined to become righteous and end up dying because of it. Willie wanted to help out the poor by building a school house, a hospital for the poor, and reworking the state’s tax structure in favor of the poor. But by the means he achieved these goals were wrong and bad which ultimately lead to his death. Even a man who wants to do good things, but uses bad methods ends up paying a harsh price for being bad while trying to do some good. In conclusion, Willie Stark was a character of good intentions who becomes tainted by the system. He was a human being who had dreams, a family he loved, and passions he yields to, among them a desire for power. The author, Warren shows Willie as a man torn between his visions of an ideal society and stark reality- what it takes in the real world to fulfill one’s dreams. Willie sacrifices his ideals for action. He is a man of stark fact, and he wants results. In the end, Willie reevaluates his life’s goals. But it is too late for change. Willie is not given a second chance. For Willie’s political activity is much like Machiavelli political activity which is like a game of chess with its rules, its proven gambits, and its successful strategies. The master player knows how to exploit the weaknesses and blunders of his opponents to maximum advantage. The goal is finding the best move, the move that wins. The qualities needed to win may be judged as vices by others, but, as Machiavelli puts it in The Prince, they are â€Å"the vices by which you are able to rule.† The crimes committed in order to preserve one’s country are â€Å"glorious crimes.† Willie essential would have believed, â€Å"a multitude is more easily governed by humanity and gentleness than by haughtiness and cruelty,† the point is that a wise ruler does whatever is necessary.

Codification Master Glossary Essay

Question 1 Is the Enterprise a VIE as defined in the Codification Master Glossary? If so, what criteria cause it to be deemed a VIE? Assume that (1) the Enterprise does not qualify for any scope exceptions and (2) the equity investment by the Nominee Shareholders in the Enterprise represents equity investment at risk. The enterprise is a VIE as defined in the codification of the master glossary. From the narrative, nominee equity holders do not absorb the losses of the enterprise and do not benefit from the residual gain the residual gain rather goes to the WFOE. The nominee equity holders though they own 100% of the share cannot run the activities of the enterprise; the activities are run by the WFOE as they provide the intellectual property, employees, resources and other services to run the schools. The nominee shareholders equally pledge their equity rights to the WFOE and cannot transfer, sell or give their equity for encumbrance. This descriptions in the narrative are in line with the def inition of a VIE as per ASC 810-10. Question 2 If the Enterprise is deemed to be a VIE, would the WFOE (excluding any related party or de facto agency relationships) consolidate the Enterprise? The WFOE would consolidate the enterprise following ASC 810-10-25-38 because it says a reporting entity shall consolidate a VIE if the reporting entity has a variable interest that absorb a majority of the VIE’s expected losses, receives a majority of the VIE’s expected residual income or both. The WFOE receives a majority of the enterprise residual income and so should consolidate the enterprise. Question 3 What impact, if any, does the POA agreement have on the conclusion reached in Question 2? The POA does not change the conclusion reached in question 2 because the nominee shareholders still act on behalf of the WFOE and the provisions that made the enterprise a VIE does not change with the POA 4. Does the accounting analysis or conclusion change for each of the questions above when analyzed in accordance with IFRS? IFRS does not have VIEs they  have special purpose entities which are similar to VIEs. According to IAS 27 SPEs should be consolidated where substance of the relationship indicates that the SPE is controlled by the reporting entity. This may arise even where the activities of the SPE are predetermined or where the majority of the voting or equity are not held by the reporting entity.