Fire service administration Essay Example | Topics and Well Written Essays - 500 words - 5

Fire service administration - Essay Example f fire extinguisher, burglar detection system in place and how the insured came to know about the fire, are essential for investigation (Redsicker & O’Connor, 2010). The fire fighters officially need no warrant to enter in a building for a specific time having reasons to be there to investigate the matter. If the above persons are in a state of doubt, they have every right to arrange administrative or criminal search warrant as the case may be for necessary searches by intimating to the office of Prosecutor. For more elaborate investigation, they seek permission of district attorney coupled with crime specialists and legal experts to face the questionnaire relating to affected scene (Davis, 1978). If search needed, it should be specific in respect of the ingredients that are location of the property to be searched and specific items that require searching. If there is no reason or evidence available, the investigator may have some probable cause (Davis, 1978). A Probable Cause Affidavit should contain many aspects such as when and where the incidence took place; relevant information should be in chronological order leading to the ending point of ample evidence for a particular location; if other investigator need to investigate the place of incidence, it requires the following conditionality and in order to ensure maximum effectiveness, it should be with the consensus of all the stakeholders; Investigators are duty bound to keep that cause of fire for examination later on; the mentioned laws allow sharing of information between the police and fire investigator besides the investigators of the insurance company (Davis, 1978). The key aim is to ensure flow of vital information between the law enforcers and the insurers. It provides opportunity to the insurer or other persons connected with fires that seem to be suspicious in its originality. It permits insurer to inform the state organs about fire and share the information that has developed during the course

Case study Economics Essay Example | Topics and Well Written Essays - 1000 words

Case study Economics - Essay Example The first term on the right hand side depicts the amount that is demanded if the product is freely available, i.e if p = 0, Qd = 100. Since, this term is oblivious to price movements, and it is the coefficient of the second term on the right hand side that actually determines the extent of influence price changes can exert on demanded quantities, the second term is relatively much more important from the aspect of decision making perspective of the suppliers in particularly deciding the price to charge. More than the direction of the relation (inverse in general), it is the exact nature of the relation reflected in the extent to which demand is influenced by price movements which is considered important in most cases and in our case specially as we are dealing with the issue of tax incidences. This extent of influence that price changes have on the quantity demanded, or in other words, the degree of responsiveness of quantity demanded to price changes is known as the price elasticity of demand. In more specific terms, the percentage change in quantity demanded due to a percentage change in price is known as the price elasticity of demand. There are two alternative ways in which we can calculate such percentage changes: Observe in this measure, the elasticity of demand is measured for a particular point only. For a different value of p in the function, we are measuring the elasticity for a different point on the demand curve1 and get different values of price elasticity. For this very reason this particular measure of price elasticity is known as ‘point price elasticity of demand’. The alternative that shows the way out of this difficulty is the ‘arc’ elasticity measure. It measures the elasticity over an arc of the demand curve using the midpoint of the arc as a reference. The p and Q values are essentially averages of their

Not So Sure It’s Ernest Essay Example for Free

Not So Sure It’s Ernest Essay In The Importance of Being Earnest (1985) by Oscar Wilde (1854 – 1900) and Sure Thing (1988) by David Ives (1950 ) we witness characters attempting to negotiate personal relationships under the heavy weight of contemporary perceptions. The Importance of Being Earnest takes place in Victorian England, roughly between 1850 and 1900, and Sure Thing is a contemporary play that debuted in 1988. In both plays we are forced over and over again to take an honest look at what is important in the lives of two people who hope to make a love connection. In the Oscar Wilde play in the end we discover that all was not, or rather that all was what it seemed, even if it was not really meant to be. In David Ives one act play we go through the rigors of what we all have come to believe is considered acceptable and end up being forced to look inside of ourselves as the play evolves. Both plays present a brilliant satire on pompousness and the expectations of society. Not So Sure It’s Ernest Although born and raised an entire century apart from one another, both Oscar Wilde and David Ives hit upon a similar note of social cynicism in their respective celebrated plays; The Importance of Being Earnest (1895), and Sure Thing (1988) Both deal with the heavy impact that social mores contemporary to their day seem to have upon the intimate union of man and woman. They both feature characters that seem to question the earnest nature of their own relationships. While Wilde’s London characters appear to be more deeply involved, and to have perhaps more at sake in their remotely settled Eighteenth Century Victorian lives, Ives on the other hand presents an almost transient view of contemporary Post Modern urban life in the mid 1980’s. Make no mistake about it, his is a view poised from the super-charged post-Future Shock-internet age. Yet, together they present a vision of society that is often rather similar in its critique. These are characters whose only options seem to be raw cynicism or stark narcissism, as if the weight of life leaves them with no other choice. Ultimately, both narratives involve a world where the characters try their best to reinterpret what is truly important in their own lives; in order to escape the neurosis that surrounds them. In each plot, comedy plays a fascinating role as if to help us adjust to the psychological dilemma that we witness unfolding before our eyes. As the characters on the stage embark upon a mission to reinvent themselves, triggered either by a startling revelation that all is not quite what it actually seems or simply by the ringing of a bell, we see that happiness is all about what you are willing to believe. These are plays about relationships, and the sometimes overwhelming influence that social and class perceptions have upon whether that ‘love connection’ actually happens or not. Both playwrights take direct satirical aim at male-female relationships and the often bogus nature of courtship and just what it may entail. It is as if love and marriage, or perhaps the respective contemporary mores governing love and marriage is viewed by both of these men with a fundamental contempt. The women appear for the most part strong and somewhat liberated. However, this is satire by the way, and the language involved helps to construct two moral universes with a vision of life that is actually deserving of mockery. In Sure Thing this is aided with the immediacy of a bell which interrupts and determines the success or failure of each exchange. For the cast of The Importance of Being Earnest, we are led to believe that there is actually much more at stake; simply because we are taken through a narrative that is about much more their lives. Wilde wrote during one of Great Britain’s celebrated golden ages. It was the Victorian Age, a time when England commanded the sea and had very few rivals in the world. It was a time of great economic consolidation for the UK, and a time of great expectation and upward mobility for a bourgeoning English middle class. The Germans were often considered crude, and the French were frequently called vulgar in their appetite for free expression. This was the dawn of the modern industrial age, and in Great Britain unlike the character in Wilde’s play, it was really deemed improper in polite company for a man to directly propose marriage to a young woman. Usually, her parents would be the first to know of a man’s intentions for their child, and for the young woman this was actually supposed to come as quite a surprise. Oscar Wilde was one to write narratives that poked fun at English culture and ran contrary to these notions of propriety. This is what much of his literature is all about. The short one-act play Sure Thing, takes place in a post-modern urban American setting. We are simply led into a coffee shop where a prototypical rendezvous takes place between a man and a woman. It is one generation after the sexual revolution, and the nature of boy meets girl is summed up for us in a series of one-liners or pick up lines from Bill to Betty. His success or failure is determined by a bell and also by his and our relative proximity to current perceptions of what is actually socially acceptable and perhaps politically correct. So it is that everything, from his knowledge of literature, to where he grew up, his grade point average, and where he went to school, all elicit relative scrutiny from the overly cynical bell ringer. This is done well within ear shod of an audience that is quickly fit to express its own cynicism as well. It is as if we become Betty’s parents as we look on, in the hopes that Bill will finally get it right and make a proper connection. In the end, Ives is cleverly allowing us to poke fun at ourselves.

Effect of Mutant EDA-A1 Gene on Huvecs

Effect of Mutant EDA-A1 Gene on Huvecs Effect of EDA-A1 gene mutant on proliferation and cell cycle distribution of cultured human umbilical vein endothelial cell Running title: The effect of mutant EDA-A1 gene on HUVECs. Ke Lei, MM; Lunchang Wang, MD; Bing Ma, MM; Ping Shi, MD; Longjiang Li, MD; Tuanjie Che, MD; Xiangyi He, MD Highlights: EDA-A1 gene mutant significantly decreased proliferation of human umbilical vein endothelial cells (HUVECs). HUVECs of mutant group were blocked at G0/G1 and S phase. HUVECs of wild group accumulated in S phase and decreased in G2/M phase. Abstract Background: To investigate the effect of ectodysplasin A gene (EDA-A1) on proliferation and cell cycle of human umbilical vein endothelial cells (HUVECs) and explore the possible mechanism underlying this process. Methods: Recombinant eukaryotic expression vectors pcDNA3.1(-)-EDA-A1-M/W (mutant, M; wild, W) containing the coding sequence of EDA-A1-M/W were transfected into HUVECs. EDA-A1-M/W genes were amplified by reverse transcription polymerase chain reaction (RT-PCR), and the proteins were detected by western blot. Then MTT assay for cell proliferation of HUVECs in each group was performed and cell cycle was detected using flow cytometry. Results: The EDA-A1 gene and protein were detected respectively by RT-PCR and western blot in HUVECs transfected with pcDNA3.1(-)-EDA-A1-M/W, but not in HUVECs transfected with empty plasmid pcDNA3.1(-) (control group) and cells without transfection. Compared with control group, EDA-A1 gene mutant significantly decreased proliferation of HUVECs and the inhibition rate was 45.70% (PEDA-A1 gene did not cause such growth inhibition (P>0.05). A significant increase of the G0/G1 and S fraction was seen in the HUVECs of mutant group, compared with wild group with an accumulation in S phase and a concomitant decrease in G2/M phase population (P Conclusion: Compared with the wide-type, the mutant EDA-A1 gene could inhibit the proliferation and cell cycle of the HUVEC. Key words: EDA-A1 gene; Mutant; Human umbilical vein endothelial cell; Cell cycle; Proliferation Introduction Hypohidrotic ectodermal dysplasia (HED), also called anhidrotic ectodermal dysplasia (AED) or Christ-Siemens-Touraine Syndrome, is a kind of X-linked recessive genetic disease (XLHED) (1). HED is a rare congenital genetic disorder with a birth incidence of 1/100,000-1/10,000 (2, 3). It is characterized by the diminution or absence of eccrine sweat glands, oligodontia and peg shaped teeth and sparse hair (1, 4). Previous study indicates that XLHED is caused by the ectodysplasin A gene (EDA-A1) mutant (5). EDA-A1, a major causative gene of HED, locates in Xq12-13.1 and encodes a novel tumor necrosis factor (TNF) ligand family protein ectodysplasin A (EDA-A1) and this protein is associated with the nuclear factor-ÃŽ ºB (NF-ÃŽ ºB) signaling mechanisms (5-9). Bayes M et al. (10) indicates that the full-length of EDA-A1 is 5296bp (http://www.ncbi.nlm.nih.gov/, AH007059, Gene ID 4007891), the open reading frame (ORF) of EDA-A1 is 1176bp, and it encoding the protein with 391 amino acids (EDA-A1, GeneID1896). Studies showed the combination of EDA-A1 and ectodysplasin receptor (EDAR) could promote programmed cell death and active the signaling of NF-ÃŽ ºB (8, 11). Recently, the related research on HED are mostly for mutation analysis of EDA-A1, and more than 100 mutations in the EDA gene have been reported to cause XLHED up to now (12, 13). However, there have few reports relating to the function of mutant EDA-A1, and the exact pathological mechanism of mutant EDA-A1 on HED is still unclear. In the present study, EDA-A1 mutant (pcDNA3.1 (-)-EDA-A1-M) and wild type (pcDNA3.1(-)-EDA-A1-W) eukaryotic expression vector that we used were constructed in our previous study (14). Then the function of transfected EDA-A1 and its mutant for cell proliferation and cell cycle of HUVECs were analyzed. The aim of this study was to investigate the effect of EDA-A1 on proliferation and cell cycle of HUVECs and explore the possible mechanism underlying this process. Material and Method Cell culture HUVECs were kindly provided by professor Wang chunming (Lanzhou University, China). HUVECs were cultured in RPMI-1640 (Huamei Company, Shanghai, China) Medium. The medium were consisted of 10% fetal bovine serum (FBS) (Evergreen Company, Hangzhou) and 100U/ml penicillin/streptomycin. All these cells were maintained in humidified incubator of 5% CO2 at 37à ¢Ã¢â‚¬Å¾Ã†â€™ (0.25% trypsin digestion overnight). Inverted microscope was used for the cell morphology investigation. All the experiments were performed at least in triplicate and repeated at least twice. Plasmid extraction EDA-A1 mutant (pcDNA3.1(-)-EDA-A1-M) and wild type (pcDNA3.1 (-)-EDA-A1-W) eukaryotic expression vector that we used were constructed in our previous study (14). Totally 3ÃŽ ¼l mutant (M) and Wild-type (W) plasmid DNA was extracted respectively from transfected HUVECs, followed by the sterile deionized water diluted to 1ml. The values of à ¢Ã¢â€š ¬Ã¢â‚¬ ¹Ãƒ ¢Ã¢â€š ¬Ã¢â‚¬ ¹A260nm and A280nm were measured by UV spectrophotometer. Plasmid DNA concentration (ÃŽ ¼g / ÃŽ ¼l) = A260 Ãâ€" dilution factor Ãâ€" 50/1000. The plasmid DNA (positive recombinants and empty control) was precipitated by ethanol. Then the DNA pellet was resuspended in sterile deionized water. Cell transfection Cell transfection was carried out according to the instructions of QIAGEN-Effectene Transfection Reagent Kit (QIAGEN). Transfection was carried out when the cell density was up to 70% after 24 hour-cell passaging. Cells were transferred into a complete medium (CM) 2 hours before transfection. Totally 2.5 µg mutant (M) and Wild-type (W) plasmid DNA was slowly added to the 2 M CaCl2 solution (stand for 10 minutes). DNA-CaCl2 solution was slowly added dropwise to the 2 Ãâ€" HeBS (stand for 30 minutes) until the precipitation of tiny particles. The precipitate was uniformly dropwise added to the culture flasks. After a 12 hours growth under standard conditions, cells were washed 2 times with HeBS, followed by the cultured in CM. HUVECs transfected with empty vector were used as the control group. Semi-quantitative real-time PCR To identify the expression levels of EDA-A1 in HUVECs, semi-quantitative real-time PCR (SqRT-PCR) analysis was performed. Total RNA was extracted from cultured cells in each group (cultured for 48 hours) by using reverse transcription (RT) kit (Fermentas Company), followed by the EDA-A1 primers designation (Primer Premier 5.0 software) and synthesis (Shanghai Biological Engineering Company ). The primers used were as follows, EDA-A1 (408bp): 5’- CGC AGG ATC CAT GGG CTA CCC GGA GGT -3’ (forward) and 5’- ATT AAG CTT GCC AAG CGG GCA CCA GGG AGA C -3’ (reverse), ÃŽ ²-actin (230bp): 5’- ACG CAT TTG GTC GTA TTG GG-3’ (forward) and 5’- TGA TTT TGG AGG GAT CTC GC-3’ (reverse). The 50ÃŽ ¼l PCR reaction system were: cDNA template (2ÃŽ ¼l), 10 Ãâ€" PCR Buffer (5ÃŽ ¼l), dNTP (1ÃŽ ¼l), primer (up and downstream, 1ÃŽ ¼l), Taq DNA polymerase (1ÃŽ ¼l), ddH2O (39ÃŽ ¼l). Products were subjected to electrophoresis (1.5% agarose gel, 120V, 90mA). Western blot analysis For Western blot analysis, proteins were extracted from HUVECs in each group. Proteins were collected after cell lysis. Protein concentration was determined using the Bradford dye-binding method (15). The proteins were separated by SDS-PAGE and transferred to the 0.45ÃŽ ¼m pore size nitrocellulose (NC) membrane (RPN303E, Amersham Company). NC membranes were blocked with TBS buffer (5% milk and 0.5%-Tween) for 1 hour (37 °C). Then, the membrane was incubated overnight at 4à ¢Ã¢â‚¬Å¾Ã†â€™ with the rabbit antibodies EDA-A1 and ÃŽ ²-actin (1:200 dilution with TBST solution), followed by incubation at room temperature for 1h with an anti-rabbit secondary antibody (Sigma). Finally, the expression levels of the target proteins were visualized withchromogenic substrate. MTT assay for cell proliferation detection To determine the proliferation of HUVECs in each group, the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay was performed. The 24 hours-transfected and untransfected cells were seeded into 96-well plate with inculation density of 5000 cells/well and incubated at 37à ¢Ã¢â‚¬Å¾Ã†â€™. After 12 hours, 100 ÃŽ ¼l serum-free DMEM was added in each well. After 72 hours, 20 ÃŽ ¼l MTT was added into each well to continue incubation at 37à ¢Ã¢â‚¬Å¾Ã†â€™(4 hours). Then, the medium was removed and the precipitation was dissolved in DMSO. The absorbance at 560 nm was measured by SpectraMax 190 microplate reader (Moteular Devices Company) for colorimetric analysis. Inhibition rate of cell growth was calculated (n=10) based on the experimentally measured absorbance value (OD value). Cell cycle analysis Flow cytometry was used to detect the cell cycle.After incubation for 48 h, the cells were collected and washed with cold PBS. The washed cells were fixed in 70% cold ethanol with incubation overnight at 4à ¢Ã¢â‚¬Å¾Ã†â€™. To stain the cells, prodium iodide (PI) solution was added. Flow cytometer (Coulter Epics XL, Beckman Coulter Company) was used to analyze the samples. Cell Quest software was used to analyze the cell percentage of G0 / G1 phase, S phase, and G2 / M phase. Statistical analysis All assays were performed in triplicate and datawere expressed as mean values  ±s.d. The SPSS 13.0 software employing ANOVA was used to analyze all data which expressed as mean ±SD. P values less than 0.05 was considered as significantly different. Results EDA-A1 expression pattern in HUVECs influenced by plasmid-mediated transfection To identify the expression level of ED1-A1 in HUVECs transfected with vector pcDNA3.1(-)-EDA-A1-M or pcDNA3.1(-)-EDA-A1-W, the RNA samples with an OD260/OD280 ration of 1.8-2.0 were chosen for RT-PCR. The HUVECs with pcDNA3.1(-)-EDA-A1-M or pcDNA3.1(-)-EDA-A1-W transfection showed a band nearly 400 bp compared with control using semi-quantitative PCR and primers specific to EDA-A1 (Figure 1). Additionally, ÃŽ ²-actin band between 200 bp and 300 bp have been seen in all the groups. Then, EDA-A1 protein expression in HUVECs were detected by western blot. Figure 1 shows that the EDA-A1 protein was expressed in the transfected cells with pcDNA3.1(-)-EDA-A1-M or pcDNA3.1(-)-EDA-A1-W vector, however, it could not be achieved in control group. In conclusion, the EDA-A1 was expressed in HUVECs after exogenous delivered of EDA-A1, but not in the un-treated control cells. Overexpression of EDA-A1 affects HUVECs proliferation To elucidate the effect of EDA-A1 on HUVECs proliferation, the MTT assays were performed. As shown in Figure 2, the HUVECs viability at 96 h transfection was decreased significantly in the mutant group by comparison with wild type and control. The proliferation of mutant group cells was suppressed by 45.7% compaired to control, while the wild type group was suppressed by 16.0% (Table 1, Figure 3). EDA-A1 overexpression regulates the cell cycle of HUVECs To determine the role of plasmid-mediated EDA-A1 transfection in cell cycle of HUVECs, the flow cytometry was used (Figure 4). We observed that 25.45  ± 1.89 % cells were arrested at G0/G1 phase of cell cycle in the mutant group compared with 20.37  ± 0.6% and 20.30  ± 0.68% cells in wild type and control groups, respectively (Table 2). During S phase, both mutant and wild type groups showed significantly higher cell percentages (14.80  ± 1.45% and 12.4 0  ± 1.75%) than that of control (8.55  ± 0.57%). However, both transfection groups had lower cell percentages than control in G2/M phase. The lowest cell percentage with 62.15  ± 1.94% was showed in the mutant group during S phase. We could conclude that the cell cycle distribution in G0/G1, S, and G2/M of HUVECs were regulated by EDA-A1 overexpression. Discussion HED characterized by impaired development of hair, eccrine sweat glands and teeth is caused by mutations in the EDA-A1 gene (3, 16). Recently, the related research on HED are focused on the mutation analysis of EDA-A1, however, the exact pathological mechanism of HED caused by mutant EDA-A1 is still unclear (17). In this study, we investigated the effect of HED related gene EDA-A1 on proliferation and cell cycle of HUVECs. The results showed that mutant EDA-A1 gene significantly decreased proliferation of HUVECs (P EDA-A1 protein, a type à ¢Ã¢â‚¬ ¦Ã‚ ¡ transmembrane protein, is one of the TNF ligand family members involved in ectodermal development (18). EDA-A1 contains a TNF-like domain (aa: 245–391), a collagen domain, and a furin protease recognition sequence (7, 8, 19-21). The TNF-like domain is necessary and sufficient for receptor molecule EDAR binding (22, 23). Furthermore, EDA-A1 has been shown to specifically bind to EDAR, which could promote programmed cell death and active the signaling of NF-ÃŽ ºB (8, 11). In our study, the reason why EDA-A1 mutant could inhibit the proliferation and block the cell cycle progression in G0/G1 phase and S phase of HUVECs might be the change of protein spatial configuration and biological activity that caused by the EDA-A1 gene mutation and the changed protein could not combined with EDAR and thus inhibit the signaling of NF-ÃŽ ºB. Maria et al. found that HED was related with the blocked signaling pathway of NF-ÃŽ ºB (9). Pascal et al. found th at point mutations in the TNF-like domain of EDA-A1 strongly decreased EDAR binding to EDA-A1 by altering the folding of EDA (21). Moreover, the substitution of Gln306 with Pro in our study was found to be located in the TNF-like domain of EDA-A1 and may influence the epithelial signaling pathway required for the normal ectodermal development through altering the topology of EDA, which is consistent with previous study. HUVECs are cells derived from the endothelium of veins from the umbilical cord, and they are often used as a laboratory model system for the study of the function and pathology of endothelial cells (24). Some studies showed that during vascular development and pathological angiogenesis, the maintenance of blood vessel homeostasis and its functional execution depend on the integrity of vascular endothelium, which is affected by proliferation, migration and apoptosis of endothelial cells (25, 26). Furthermore, Jie et al. showed that recovery of injured endothelial cells through regulated endothelial cell proliferation plays significant roles in thrombosis disease (27). In our study, mutant EDA-A1 decreased the proliferation of HUVECs, therefore, we suspected that pathological mechanism underlying HED caused by EDA-A1 may be the growth inhibit of endothelial cells which could lead to the defection of eccrine sweat glandsis. Despite of all results mentioned above, there were still some l imitations in the present study, whether the EDA-A1 mutant blocked the combination of EDA-A1 with EDAR required further experiment. In conclusion, our study revealed EDA-A1 gene mutant could inhibit the proliferation and cell cycle of HUVECs. We explored the mechanism of HED caused by mutant EDA-A1. The substitution of Gln306 with Pro may influence the epithelial signaling pathway required for the normal ectodermal development through altering the topology of EDA, which could impair the binding of EDA-A1 to EDAR and further inhibit the signaling of NF-ÃŽ ºB. Our finding broadens the spectrum of EDA-A1 mutations and may help to understand the molecular basis of XLHED and aid genetic counseling. Acknowledgements We wish to express our warm thanks to Fenghe(Shanghai) Information Technology Co., Ltd. Their ideas and help gave a valuable added dimension to our research. Conflict of interest The authors have declared that no competing interests exist. Authors’ contributions KL and LW participated in the design of this study, and they both performed the statistical analysis. BM and TC carried out the study, together with PS, collected important background information, and drafted the manuscript. LL and XH conceived of this study, and participated in the design and helped to draft the manuscript. All authors read and approved the final manuscript. Figure legends: Figure 1 Detection of mRNA expression of EDA-A1gene in ECV304 cells by RT-PCR: M: mutant group; W: wild group; C: control group. Figure 2 Expression of ECV304 cells transfected with EDA-A1 gene and mutant: M: mutant group; W: wild group; C: control group. Figure 3 OD560 value of ECV304 cells transfected with EDA-A1 gene after cultured for 96h: M: mutant group; W: wild group; C: control group; a: compared with the control group, P Figure 4 The effect of EDA-A1 gene mutant on cell cycle in ECV304 cells. Table 1 OD560 value of ECV cells transfected with EDA-A1 gene after cultured for 96h Note: a: compared with control group, P Table 2 Effect of EDA-A1 gene mutant on cell cycle in ECV304 cells Note: a: compared with control group, P

The Old Man And The Sea Compared To Shipwrecked Sailor :: essays research papers

The Old Man and the Sea compared to â€Å"Shipwrecked Sailor† In the stories, The Old Man and the Sea by Ernest Hemmingway and â€Å"Shipwrecked Sailor† by Gabriel Garcia Marques, there are so many similarities, like their losses and their love for the creatures of the sea, that it its eerie. Although, there are many similarities, there are also some differences, such as the main characters’ love for the creatures of the sea. There are more similarities in these stories than differences, in my opinion.   Ã‚  Ã‚  Ã‚  Ã‚  A difference between Santiago in The Old Man and the Sea and the sailor in â€Å"Shipwrecked Sailor† is their knowledge of the sea. Santiago is expressed well as a fecund and resourceful old fisherman of the sea. This is prodigiously expressed when Santiago, †Hooked a patch of yellow Gulf weed with the gaff as they passed and shook it so that the small shrimps that were in it fell onto the planking of the skiff† (Hemmingway p.98). This is the act of a very intellectual and experienced fisherman. Unlike Santiago, the sailor in â€Å"Shipwrecked Sailor† is rather ignorant. Although, this is excused because the man hadn’t the experience at sea that Santiago had. His imbecility is shown when he, â€Å"Lay down at the side of the raft and took a few swallows of seawater† (Marques p.45). This was a rather fatuous action, because the salt dries the body and retains water. That action proves that he is not sea-worthy. So, Santiago i s the more experienced seaman of the two.   Ã‚  Ã‚  Ã‚  Ã‚  A similarity between The Old Man and the Sea and â€Å"Shipwrecked Sailor† was their losses. In the â€Å"Shipwrecked Sailor†, â€Å"The sharks had made off with my prey† (Marques p.44). This event marked the loss of the man’s food supply. It wasn’t a very crucial part of the story, because the man had earlier devoured some raw meat, which had satiated him. In The Old Man and the Sea, â€Å"He did not want to look at the fish. He knew half of him had been destroyed† (Hemmingway p.144). This was a very similar method of loss, which the shipwrecked sailor had faced. This was a tragic loss and abasement to both Santiago and his pride. He was tenacious and worked so hard to obtain the fish, only to have it taken away by sharks. The old man lost the fish, even though he fought valiantly to fend off the attacking sharks.

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Napoleon Bonaparte was a bewildering man of many achievements. He attended military school at the age of nine, and joined the French military when he was sixteen. His mother was named Letizia, and his father was named Carlos. He had seven siblings, named Joseph, Lucien, Elise, Louis, Pauline, Caroline, and Jerome. He also supported the revolution, which led to him attending several places during the initial part of the revolutionary wars. He became renowned after shielding the Nation Convention in 1795. One of his more significant feats was that he led effective campaigns against Austria, Sardinia, and Italy. As soon as other people became aware of his accomplishments, he very quickly became known as â€Å"the General.† His earlier military occupation included the Italian Campaigns: from 1796-1797, he dominated most of northern Italy for France, and had established a liking for leading. Another triumph from his early military career was the Egyptian Campaign. In 1798, he was defeated by a British navy, which was under the command of Admiral Horatio Nelson, who devastated the French fleet at the Battle of the Nile. Discarding his troops in Egypt, Napoleon returned to France and received a champion’s welcome. In 1796, Napoleon got married to Josephine. But by 1799, the dishonesty of the Directory along with the dwindling war effort against the Second Coalition left the government open for assaults. Napoleon was put in control of the military on November 9, 1799. The next day, he and his military took control by overtaking the government, which then decided to end the Directory. The Directory was swapped with three consuls, and Napoleon was elected First Consul. With the government in disorder, Napoleon launched a successful coup d’ et... ... European leaders at the Congress of Vienna tried to reestablish order and reestablish peace. The champions (mainly the alliance of Russia, Austria, Prussia, and Great Britain) restored the French boundaries of 1792 and the Bourbon dynasty. They made other modifications in the boundaries of Europe, founding Prussia as a "sentinel" against France, and produced a new kingdom out of Belgium and Holland. It was understood that the notion of the stability of power would preserve peace in Europe. But the demands of the conquerors, especially the Prussians and the Russians, for reimbursement threatened the balance. The Russian demands for Poland and the Prussian wish for Saxony led to conflict among the powers. Castlereagh, Metternich, and Talleyrand forced Russia and Prussia into a compromise whereby Russia got part of Poland and Prussia received two-fifths of Saxony.

Dostoevsky: Psychiatric Genius?

The book Crime and Punishment and its author, Fyodor Dostoevsky, both came many years before their time. In the book, Dostoevsky clearly describes the medical disorders we now know today as schizophrenia, bipolar disorder, and dissociative identity disorder which is also known as multiple personality disorder. The book was first published in 1866, however, schizophrenia was first described officially in 1887 by Dr.Emile Kraepelin and not given the name â€Å"schizophrenia† until Eugene Bleuler coined the term in 1911 (The History of Schizophrenia). And it was not until the late 19th and early 20th century that Pierre Janet coined the term dissociative identity (Pendergrast). Bipolar Disorder was also a relatively new disorder being that it was officially described in 1854 (â€Å"A Brief History of Bipolar Disorder†).The character of Raskolnikov is a good example of these three disorders because of the way he acts towards others or towards himself and then suddenly has a change of feelings or mindset. Schizophrenia is defined as a common type of psychosis, characterized by abnormalities in perception, content of thought, and thought processes (hallucinations and delusions) and by extensive withdrawal of interest from other people and the outside world, with excessive focusing on one's own mental life (WebMD LLC).In the beginning of the book, the narrator talks about how Raskolnikov has â€Å"become so completely absorbed in himself, and isolated from his fellows that he dreaded meeting, not only his landlady, but anyone at all† (Dostoevsky 1). This is the first sign of schizophrenia that Dostoevsky shows in Raskolnikov, it is obvious that Raskolnikov has become isolated and does not want to be around any other people. Next, Raskolnikov’s illness is almost completely caused by his hallucinations, delusions, and dreams.This is seen in part two, chapter one after Raskolnikov has committed the murders â€Å"He sat down on the sofa in exh austion and was at once shaken by another unbearable fit of shivering†¦he covered himself up with his winter coat and once more sank into drowsiness and delirium. † (92). This is also seen in chapter three after he returns to his room and has a dream about his landlady being beaten, â€Å"He was not completely unconscious, however, all the time he was ill; he was in a feverish state, sometimes delirious, sometimes half conscious. † (120).Raskolnikov continues to focus on his own mental state throughout the novel and he does not truly become well until the end of the story when he confesses, suffers, and becomes educated. Raskolnikov also has many symptoms of dissociative identity disorder, which is defined as a severe form of dissociation, a mental process, which produces a lack of connection in a person's thoughts, memories, feelings, actions, or sense of identity. Dissociative identity disorder is thought to stem from trauma experienced by the person with the dis order (WebMD LLC).Raskolnikov’s condition has obviously stemmed from the trauma Raskolnikov experienced after having committed the murders which is a major sign of dissociative identity disorder, and there are instances where Raskolnikov will do something and immediately completely regret his decision such as when he gives money to Marmeladov and then wants to go up to the room to take his money back â€Å"Raskolnikov had time to put his hand into his pocket, to snatch up the coppers he had received in exchange for his rouble in the tavern and to lay them unnoticed on the window.Afterwards, on the stairs he changed his mind and would have gone back† (Dostoevsky 26-27). Rakolnikov also has a form of dissociation because he gets into moods when he is thinking about certain things but disregarding other important details such as closing the door at the pawnbroker’s, locking his own door the night of the murder, and checking his clothes for blood. A third disorder t hat Dostoevsky describes through the character of Raskolnikov is bipolar disorder.Bipolar disorder is a major affective disorder, or mood disorder, characterized by dramatic mood swings. Bipolar disorder is a serious condition, when mania causes sleeplessness, sometimes for days, along with hallucinations, psychosis, grandiose delusions, and/or paranoid rage (WebMD LLC). Raskolnikov has many mood swings throughout the story. One of the first examples is when he is debating whether he should go talk to his friend Razumikhin, he changes his mind several times and then decides not to see him.Raskolnikov also switches moods about his â€Å"act† that he is planning to commit which we come to know is the murder of Alonya Ivanova. He switches his decision several times and finally commits to killing her when he finds out that she will be alone at seven o’ clock, â€Å"he felt suddenly in his whole being that he had no more freedom of thought, no will, and that everything was suddenly and irrevocable decided† (Dostoevsky 65). We also know that Raskolnikov suffered from hallucinations, delusions, and paranoid rage that he used to kill Alonya.These hallucinations included the dream of the horse getting beaten, the dream that his landlady was being beaten, and the nightmare when Raskolnikov is trying to kill the pawnbroker but she does not die, she only laughs. Dostoevsky helped to pave the way for other doctors and scientists to discover all of the symptoms of these mental illnesses we now know as schizophrenia, dissociative identity disorder, and bipolar disorder. This shows how much Dostoevsky knew about human nature. He was able to pick out tendencies that many mentally ill people have.Not only did he describe these three, he also described alcoholism very accurately by using the character Marmeladov to show that alcoholism only leads to suffering and the more one continues to drink, the more suffering they endure, â€Å"â€Å"the more I drink, the more I feel it. That’s why I drink too. I try to find sympathy and feeling in drink†¦. I drink so that I may suffer twice as much! † And as though in despair he laid his head down on the table† (14). Dostoevsky was a very extraordinary man and he gave mankind many contributions.Psychology was an important part of Crime and Punishment, but it is also clear that Dostoevsky is a very intelligent writer and incorporates many different themes into his works. ? Works Cited â€Å"A Brief History of Bipolar Disorder. † Today’s Caregiver. 2009. http://www. caregiver. com/channels/bipolar/articles/brief_history. htm. Dostoevsky, Fyodor. Crime and Punishment. Ed. Bantam Classic Reissue. New York: Bantam Dell, 2003. â€Å"The History of Schizophrenia. † Schizophrenia. com. 2004. http://www. schizophrenia. com/history. htm .Pendergrast, Mark. Victims of Memory. Upper Access Books, 1996. â€Å"Schizophrenia. † Dictionary. com. 2009. http:// dictionary. reference. com/browse/schizophrenia. WebMD LLC. â€Å"Bipolar Disorder. † WebMD. 2009. http://www. webmd. com/depression/guide/bipolar-disorder-manic-depression. WebMD LLC. â€Å"Dissociative Identity Disorder. † WebMD. 2009. http://www. webmd. com/mental-health/dissociative-identity-disorder-multiple-personality-disorder. WebMD LLC. â€Å"Medical Dictionary: Schizophrenia. † WebMD. 2009. http://dictionary. webmd. com/terms/schizophrenia.