The Technological Advances Of The Great Gatsby - 3475 Words

1. Introduction Ever since the fall we have not been unable to physically restore our glorious Eden experience, nor could we fix the mistake that Adam started with either good living or hard work. No council could be gathered; no theologian could negotiate his or her way out of our deserving judgment. We were indebted with sin, unable to choose right from wrong. God’s creation was just running around since birth with no clue as to who are or what was if any power was in us. We are like blind sheep aimlessly moving about with no direction, guidance or supervision. But is that the case? Are we helplessly wrapped in flesh and â€Å"totally depraved† as normal human beings? Depraved seems like such a solemn condition for such a sophisticated race of people who have achieved so many great things. Consider the technological advances we have accomplished, such as moving from horse driven wagons to electric powered cars or only communicating via close proximity to communicating via cell phones and email. There was a time when all people lived in tents or makeshift homes, however, now were capable of erecting buildings hundreds of stories in the air. Was God, not apart of this? Did He not use these people? Was He not aware of our abilities before we were conceived? The depraved state of humans would suggest we are in some parts incapable of good. How could one be total depraved, without hope, and still able to do all these things? Nevertheless, some would think that depravity means weShow MoreRelatedThe Great Gatsby By F. Scott Fitzgerald1271 Words   |  6 PagesAmerican Dream Essay By: Mary C. Watts In his novel,The Great Gatsby, F. Scott Fitzgerald attempted to explore the American Dream during a corrupt period of the 20’s. 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As a result, the American Dream slowly becomes less accessible to the lowerRead Moreâ€Å"the Great Gatsby Is a Story of Infatuation and Disenchantment†. How Far and in What Ways Do You Agree with This View of the Great Gatsby and One Other Novel You Have Read.2179 Words   |  9 Pagesâ€Å"The Great Gatsby is a story of infatuation and disen chantment†. How far and in what ways do you agree with this view of The Great Gatsby and one other novel you have read. The Great Gatsby is a novel that, superficially, seems like the tragic story of infatuation and misunderstanding. However, set in 1920s America, it can be read in a number of different ways. This post-war period was a time of economic boom and rapid change in technological advances led to fashionable, more affluent and carefreeRead MoreWomens Rights In The 1920s Essay1018 Words   |  5 PagesThe 1920s brought many positive changes that are important to Canadian history. 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Cyber Insurance Case Study - 1428 Words

Introduction: Data is the new gold and insuring data is the new billion-dollar line of business. Data protection methods aren’t unbreakable; they merely act as a deterrent for hackers. For disruptive cyber attacks, businesses need cyber insurance to help indemnify the loss of business, reputation, and to provide services to those breached. Cyber insurance offers the potential for extremely large losses that admitted carriers tend to avoid. Surplus lines companies are more willing to write reasonably high loss limits on these policies. Ironically, the issue with cyber liability coverage to date is a lack of data. Pricing this risk is incredibly difficult due to small sample sizes, reporting bias, lack of insurance specific data, and no†¦show more content†¦Rebuilding consumer trust after a cyber breach is crucial, which is why many companies offer free credit monitoring and identity theft monitoring. 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Pseudomonas Aeruginosa and Nosocomial Infections Free Essays

Bielecki et al. Research Paper Pseudomonas aeruginosa is a Gram-negative bacteria, particularly known for causing nosocomial infections (1). As a pathogen, it effectively causes disease by acquiring resistance to antibiotics that would otherwise inhibit growth (2). We will write a custom essay sample on Pseudomonas Aeruginosa and Nosocomial Infections or any similar topic only for you Order Now Reported rates of infection range from 0. 6 to 32% across various clinical environments because Pseudomonas aeruginosa has gained multi-drug resistance (2). Certain strains of Pseudomonas aeruginosa treated with gamma rays can break down the hydrocarbons in crude oil and are thus useful in cleaning up oil spills (3). The genome of Pseudomonas aeruginosa is 6. 3 million base pairs long, which is the largest bacterial genome to be sequenced (4). It contains about 5,570 open reading frames (4). Argyrin is a naturally synthesized antibiotic peptide extracted from myxobacteria (1). It has cytotoxic properties, suppresses the immune system, and is a highly active antibiotic used against Pseudomonas strains (1). Figure 1. Argyrin A structure. Bielecki et al chose to isolate these resistant clones in order to observe the mechanisms by which the P. eruoginosa acquires resistance to Argyrin A within the fusA1 gene (1). They isolated these clones by growing Pseudomonas aeruginosa strains on agar that contained Argyrin A (1). After incubation, the colonies that formed were able to grow in the presence of argyrin; these colonies were then streaked onto plates with Argyrin A again to ensure accuracy of obtaining resistant strains (1). A point mutation is an alteration of one base pair within a DNA sequence (5) . The point mutations, which caused changes in the amino acid sequence within the fusA1 gene, were different among the six isolates (1). They might have conferred resistance because the mutations caused the same impact on the resulting protein (1). The gene was identified by sequencing the whole genome of Pseudomonas aeruginosa strains with the bacterial target of Argyrin A, which showed mutations within fusA1 that encode for the elongation factor EF-G in resistant strains of Pseudomonas aeruginosa (1). The diagram below illustrates the process of elongation during the translational phase in EF-G along with EF-Tu (12). Figure 2. Elongation during ribosome-catalyzed translation (12). Bielecki et al confirmed the identity of the gene by using genetic maps. This required sequencing the resistant strain a second time to make a reference strain to compare the genes at a specific loci (1). Adding a mutation into the sensitive Pseudomonas aeruginosa strain demonstrated a resistance phenotype (1). Surface plasmon resonance is a lab technique that involves aiming a beam of light at a thin metal sheet, which catalyzes a reactio n by causing movement in the molecules behind the metal sheet (6). SPR was useful in this experiment because it confirmed that fusA1 is the target gene for Argyrin A, rather than fusidic acid, the antibiotic previously recognized (1). A heterologous protein, or a heterologue, is a protein that differs in structure and function relative to a given protein; not all proteins with different amino acid sequence necessarily differ in function (7). N-terminal His6-tags were fused to the fusA1 genes before undergoing the SPR experiments, causing the production of heterologous proteins in relation to the original fusA1 (1). According to Bielecki et al, the SPR procedures supported that Argyrin A binds to fusA1 by the resulting KD value (1). This shows that Argyrin A has a target on the heterologous protein (1). It is important to compare the variations made in the mutations because the other bacteria may have a different sequence that can still achieve resistance (1). It cannot be assumed that all bacterial strains will be identically resistant or sensitive because they all contain differences in their genomes (1). By mapping the mutated genes, the authors found the locations of the mutations in different domains (1). They deduced that the mutations exhibiting resistance to Argyrin A in Pseudomonas aeruginosa are found on opposite sides of the domain, despite the fact that most mutations involving fusidic acid and Argyrin A are located on the same side of the domain (1). This shows that the binding sites for fusidic acid and Argyrin A must be independent of each other (1). Both fusA1 and the second gene, fusA2, encode for the elongation factor EF-G (1). The fusA2 gene was expressed 30 times less in the strains of Pseudomonas aeruginosa than in the fusA1 gene, as shown by RNA sequencing (1). Homology modeling uses the model of a target protein to produce an estimated structure of a homologous template protein (8). After creating a homology model of Argyrin A’s protein structure, Bielecki et al concluded that it â€Å"most likely binds to a site distinct from that of fusidic acid, indicating a new mode of protein biosynthesis inhibition by Argyrin A† (11). Multi-drug resistant pathogens pose a very big risk on the world because they can easily mutate their genomes to adopt resistance to a given antibiotic and persist in causing harmful diseases (1). The authors used MDR clinic isolates in order to observe the mechanisms by which these pathogens mutate to build resistance to Argyrin. The fact that eleven of the twelve isolates showed sensitivity to Argyrin suggests that Argyrin is a useful antibiotic in preventing infections by Pseudomonas aeruginosa (1). There are other factors besides the uptake and export of Argyrin that affect Pseudomonas aeruginosa’s sensitivity to Argyrin, such as efflux pumps (1); however, the uptake and export of Argyrin in other bacteria does play a role in its sensitivity (9). A proteasome is a hollow protein complex with active sites that break down proteins by proteolysis (10). The degraded peptides that are produced can be used for other functions in the cell (10). Argyrin A is a factor used to inhibit proteasome function, yet there is no distinct evidence that Argyrin A binds to the site on the proteasome (1). This paper is important because it analyzes the resistance and sensitivity to Argyrin A in various strains of Pseudomonas aeruginosa. This bacteria has been a leading cause in nosocomial infections, so it is important to determine which antibiotics best work to stop the spread of disease (1). About ten percent of patients in hospitals across the United States obtain a significant nosocomial infection (13). Although there are effective methods to prevent the spread of pathogens in clinical environments (13), it is important to study how bacteria acquire resistance, so that scientists can develop ways to inhibit the spread of nosocomial infections by multi-drug resistant pathogens. Bibliography Bielecki, P. , Lukat, P. , Husecken, K. , Dotsch, A. , Steinmetz, H. , Hartmann, R. W. , Muller, R. , and Houssler, S. (2012) Mutation in elongation factor G confers resistance to the antibiotic Argyrin in the opportunistic pathogen Pseudomonas aeruginosa. Chembiochem. 13, 2339-2345. Obritsch, M. D. , Fish, D. N. , MacLaren, R. , and Jung, R. (2005) Nosocomial infections due to multidrug-resistant Pseudomonas aeruginosa: epidemiology and treatment options. Pharmacotherapy. 25, 1353-1364. Iqbal, S. , Khalid, Z. M. and Malik, K. A. (1995) Enhanced biodegradation and emulsification of crude oil and hyperproduction of biosurfactants by a gamma ray-induced mutant of Pseudomonas aeruginosa. Lett. Appl. Microbiol. 21,  176–179. C. K. Stover, X. Q. Pham, A. L. Erwin, S. D. Mizoguchi, P. Warrener, M. J. Hickey, F. S. L. Brinkman, W. O. Hufnagle, D. J. Kowalik, et al. (2000) Complete genome sequence of Pseudomonas aeruginosa PAO1, and opportunistic pathogen. Nature. 406, 959-964. Encyclopedia Britannica Online. Point mutation. Accessed 17 Oct. 2012 http://www. britannica. om/EBchecked/topic/54744/point-mutation Manfield, I. (2009) Biacore surface plasmon resonance. Univ. of Leeds, Astbury Centre for Structural Molecular Biology. Accessed 18 Oct. 2012 http://www. astbury. leeds. ac. uk/facil/SPR/spr_intro2004. htm Jackson, J. H. (1999) Terminologies for gene and protein similarity. Michigan State Univ. , Dept. of Microbiology. Accessed 19 Oct. 2012 https://www. msu. edu/~jhjacksn/Reports/similarity. htm Beva n, D. R. (2003) Homology modeling. Virginia Tech, Dept. of Biochemistry. Accessed on 19 Oct. 012 http://www. biochem. vt. edu/modeling/homology. html Sasse, F. , Steinmetz, H. , Schupp, T. , Petersen, F. , Memmert, K. , Hofmann, H. , Heusser, C. , Brinkmann, V. , von Matt, P. , Hofle, G. , and Reichenbach, H. (2002) Argyrins, immunosuppressive cyclic peptides from myxobacteria. I. Production, isolation, physico-chemical and biological properties. J. Antiobiot. 55, 543-551. Rape, M. , and Jentsch, S. (2002) Taking a bite: proteasomal protein processing. Nat. Cell Biol. 4, 113-116. Bielecki, P. , Lukat, P. , Husecken, K. , Dotsch, A. Steinmetz, H. , Hartmann, R. W. , Muller, R. , and Houssler, S. (2012) Mutation in elongation factor G confers resistance to the antibiotic Argyrin in the opportunistic pathogen Pseudomonas aeruginosa. Chembiochem. 13, 2340. Simonovic, M. and Steitz, T. A. (2009) A structural view on the mechanism of the ribosome-catalyzed peptide bond formation. BBA Gene Reg. Mech. 1789, 612-623. Abedon, S. T. (2009) Nosocomial infections. Ohio State University. Accessed on 27 Oct. 2012 http://www. mansfield. ohio-state. edu/~sabedon/biol2053. htm How to cite Pseudomonas Aeruginosa and Nosocomial Infections, Essay examples