Violence In Entertainment Essays - Dispute Resolution, Criminology

Violence In Entertainment Violence In Entertainment And Its Effect On Society Does entertainment influence society's attitude towards violent behavior? In order to fully answer this question we must first understand what violence is. Violence is the use of one's powers to inflict mental or physical injury upon another, examples of this would be rape or murder. Violence in entertainment reaches the public by way of television, movies, plays, and novels. Through the course of this essay it will be proven that violence in entertainment is a major factor in the escalation of violence in society, once this is proven we will take all of the evidence that has been shown throughout this paper and come to a conclusion as to whether or not violence in entertainment is justified and whether or not it should be censored. Television with its far reaching influence spreads across the globe. Its most important role is that of reporting the news and maintaining communication between people around the world. Television's most influential, yet most serious aspect is its shows for entertainment. Violent children's shows like Mighty Morphin Power Rangers and adult shows like NYPD Blue and Homicide almost always fail to show human beings being able to resolve their differences in a non-violent manner, instead they show a reckless attitude that promotes violent action first with reflection on the consequences later. In one episode of NYPD Blue three people were murdered in the span of an hour. Contemporary television creates a seemingly insatiable appetite for amusement of all kinds without regard for social or moral benefits (Schultze 41). Findings over the past twenty years by three Surgeon Generals, the Attorney General's Task Force on Family Violence, the American Medical Association, the National Institut e of Mental Health, the American Psychiatric Association, the American Psychological Association, the American Academy of Pediatrics, and other medical authorities indicate that televised violence is harmful to all of us, but particularly to the mental health of children (Medved 70-71). In 1989 the results of a five year study by the American Psychological Association indicated that the average child has witnessed 8,000 murders and 100,000 other acts of violence on television by the time he or she has completed sixth grade. In further studies it was determined that by the time that same child graduates from high school he or she will have spent 22,000 hours watching television, twice as many hours as he or she has spent in school (Bruno 124). In a study by the Centers for Disease Control, published by the JAMA (Journal of the American Medical Association), it was shown that homicide rates had doubled between the introduction of television in the 1950's and the end of the study in 1994. In that same study other possible causes for the vast increases in violence were studied, the 'baby boom' effect, trends in urbanization, economic trends, trends in alcohol abuse, the role of capital punishment, civil unrest, the availability of guns, and exposure to television(Lamson 32). Each of these purported causes was tested in a variety of ways to see whether it could be eliminated as a credible contributor to doubling the crime rate in the United States, and one by each of them was invalidated, except for television. Children average four hours of television per day, and in the inner city that increases to as much as eleven hours a day, with an average of eight to twelve violent incidents per hour. It is also interesting to note tha t violence occurs some fifty-five times more often on television than it does in the real world (Medved 156). FBI and census data show the homicide arrest rate for seventeen-year-olds more than doubled between 1985 and 1991, and the rates for fifteen-and sixteen-year-olds increased even faster. Movies also add their fair share to the problem of violence in society. Researchers have established that copycat events are not an anomaly. Statistically-speaking, they are rare, but predictable, occurences. Television shows, novels, but especially movies-all can trigger copycat violence (Medved 72). As recently as November of 1995, New York City officials believed that the burning of a toll-booth clerk was a result of copycat violence, resulting from a similar scene in the movie Money Train. In 1994,

T. Roosevelt, a legacy essays

T. Roosevelt, a legacy essays The Presidency of Theodore Roosevelt The turn of the century has always been a big deal for modern civilizations. One hundred years of life is quite large compared with the average 70 or so given to most. Because of that, people tend to look in trends of decades, rather than centuries or millennia. When it does come time for a new century, when that second digit rotates, as it does so seldom, people tend to look for change. Events tend to fall before or after the century, not on top of it, and United States history, particularly, has had a tendency for sudden change at the century marks. Columbus' accidental discovery of the West Indies in 1492 brought on the exploration age in the 1500s. Jamestown colony, founded in 1607, was England's first foothold on the New World. A massive population surge, brought on in part by the import of fricans, marks entry into the 18th century. Thomas Jefferson's presidency, beginning in 1800, changed the face of American politics. 1900 was a ripe year for change, but needed someone to help the change arrives. That someone was Theodore Roosevelt. Roosevelt's political presence altered the course of the United States, transforming it into a superpower fully ready to handle the challenges of any opposition, and changed the role of the president and executive branch of US government, making it a force with As the first president with progressive views, Roosevelt enacted the first regulatory laws and prosecuted big businesses who had been violating them and others for years. Roosevelt also initiated the United States' active interests in other countries, and began to spread the benefits of democracy throughout the world. Before Roosevelt, the United States was an inward-looking country, largely xenophobic to the calls of the rest of the world, and chiefly concerned with bettering itself. As one critic put it, "Roosevelt was the first mode...

Virtual Workshops Essay Example | Topics and Well Written Essays - 1750 words

Virtual Workshops - Essay Example My formal categories were designed to show frequency in the video that highlighted rage and hostility and frequency of video which illustrated sympathy or disturbed reactions to the verdict. The content analysis format allowed me to establish the precise number of times that the news organization opted to illustrate any of these factors. One of my categories dealt with the social status of the trial participants (career, relationship to Saddam, etc.), which achieved no results in trying to determine whether people varying social status held differing opinions about the death sentence. Other than Saddam and the presiding judge, I could make no determination about social status as the media opted not to offer background information regarding the other trial participants. This failure could be remedied in further analyses by formulating categories for research that can be more readily displayed in the chosen data used for observation. In terms of future research, I might suggest that us ing the category of "intensity" might offer further data regarding whether the instances of emphasizing a media agenda are witnessed in terms of how media interactions take place. For instance, facial grimaces or smiles (in this case applying to the Saddam verdict) and their frequency within a form of media might suggest the emphasis being placed on fulfilling a biased media agenda. Virtual Workshop 3: Observation This is a content analysis report based on the observation carried out on people using a public transport.

Public speaking Essay Example | Topics and Well Written Essays - 1000 words

Public speaking - Essay Example The two goals contradicted each other, as Vietnams had threatened to attack US if their troops were not to be withdrawn from South Vietnams. For that reason, Nixon addressed the issue with a two sided mind. Paradoxically, Nixon imparts a withdrawal mode to his audience, a strategy that makes them feel like he cares so much for the Americans, and especially the American men in Vietnam. He acknowledges that American troops stand a higher risk in the attacked zones but concludes the sentence by mentioning that withdrawing implies a greater risk to the natives of the attached zones. Nixon considers it wise to analyse the situation in two ways to make the audience understand that withdrawal, as the solution suggested earlier, is a controversial action that worsens the situation. As matter of fact, the Nixon understands that his audience are Americans, who would want their men protected but keeps in mind that the outside world is also watching his action. Therefore, the speech is planned n ot only to please the immediate audience but ensure that the problem is effectively addressed. Nixon confidently convinces the audience that his speech is well advised, by mentioning that the decision being presented wasn’t his own opinion but an informed discussion with national Security Council, other crucial personnel as well as the president’s advisers. To ensure this confidence, the speech creates some sense of inductive reasoning, by first defining the problem, analysing the available solutions and drawing a generalised conclusion later on. Nixon explains the problem by describing the actions and motives of the enemy. According to Nixon, America has no enmity whatsoever with North Vietnam, in the past there had been no troops moving to attack Vietnam, neither had the south Vietnams attacked their opponents before . He at the same time mentions the existence of alliance with South Vietnams. These create some sense of reasoning to the audience that

Malcolm Gladwell's David and Goliath presentation Assignment

Malcolm Gladwell's David and Goliath presentation - Assignment Example David’s brand is an underdog in this presentation that serves to show the upper hand he had against Goliath. Contextually, Gladwell argues that nimble, newcomers with new answers to old challenges frequently beat giant risks or barriers. David’s strong suit originated from his ability to break the presumptions of conventional battle strategies that size means power.2 Here, Gladwell says that being the underdog creates a situation that shows why there is always more than meets the eye. Using context to express an analysis of the account of David and Goliath makes Gladwell’s work convincing.3 The presentation is essentially about spiritual weapons as well as how affective and imaginative desires are as equally important as financial or material desires. In the absence of physical advantages, one has ideas, imagination, perseverance, devotion, and excitement to keep going. A critical look at the story of David and Goliath underscores this near rationale as I was convinced to appreciate my ideal and imaginative gifts as they are, as should any other historian or even

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

Consider the theme of loneliness in Of Mice and Men. How does it Essa

Consider the theme of loneliness in 'Of Mice and Men'. How does it affect the friendships and relationships in the novel? This novel that was written by John Steinbeck which was set in the 1930s in Salinas Soledad which is in California. The novel consists of many historical factors which have affected the characters in this novel and one of them includes "the great depression" Which leads the novels inspiration for the famous writer John Steinbeck which he mainly based on his own experience. In those days people travelled a lot differently to how we travel now. In those days migrant workers travelled extravagant distances looking for a job. There are many different themes in which are based throughout the whole book, such as loneliness, happiness, nature, dreams and reality: - Which even lead to catastrophe. Many of the people in this novel have very lonely lives mainly because they are migrant workers and as we know they don't have time to make any friends or have any time to spend with their families. There are many characters that are lonely due to age, sex, and race. Two good examples would be Candy because of his age and Crooks because of his race. This novel consists of two main characters George and Lennie, who are an anomalous pair of migrant workers that look after each other. They are completely the reverse of each other. George is the one who has the communicative face and thinks of all of their problems and ideas and tells the other one what to do. Being like this all of the time, in what ever the story it is, always pictures that you would be the small quick one with sharp features. Lennie is the guy that is tall and always does what he is told and has an ill-defined, solid, a... ... gets treated like a little girl. Curley's wife often dreams about herself becoming an actress. At the end of the novel, her loneliness causes Lennie's death. Before Lennie's death, Curley's wife and Lennie were talking in the barn whilst everyone else was playing games. They began talking to each other about each others dreams. They both talked about each others dreams and what they wanted to do in their life. Lennie has a fascination of stroking things. He was stroking Curley's wife's hair, he began to stroke her hair so hard, that he lost control and broke her neck. This has a big impact on George, Lennie and Candy's relationship, as Curley wants to kill Lennie. As a result to this, George has to kill Lennie before he gets killed by Curly. Loneliness will always end in tragedy and dreams will rarely become reality. Friendship never ends.