BICD 100 Writing Assignment #1 PDF

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Professor Lisa McDonnell...

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Phoebe Zhang A13866116 B10 1. Author:

Place of work:

Christopher L. King

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106 Veterans Affairs Medical Center, Cleveland, OH 44106

John H. Adams

College of Public Health, University of South Florida, Tampa, FL 33612

Jia Xianli

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106

Brian T. Grimberg

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106

Amy M. McHenry

College of Public Health, University of South Florida, Tampa, FL 33612

Lior J. Greenberg

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106

Asim Siddiqui

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106

Rosalind E. Howes

Department of Zoology, University of Oxford, Oxford OX1 2JD, United Kingdom

Monica da Silva-Nunes

Departamento de Parasitologia, Instituto de Ciencias Biom>dicas, Universidade de S?o Paulo, 05508-900, S?o Paulo, Brazil

Marcelo U. Ferreira

Departamento de Parasitologia, Instituto de Ciencias Biom>dicas, Universidade de S?o Paulo, 05508-900, S?o Paulo, Brazil

Peter A. Zimmerman

Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106

2. 3. The primary author is typically a younger student or colleague who performed the research and contributed most to the published research. The last listed author is typically the senior, correspondent author who provided input and revisions and oversaw the project. 4. Three pieces of work are cited in this paragraph. 5. Citation #8 tells the reader that the information that P. vivax malaria can occur independently of the Duffy antigen came from source #8: M>nard D, et al. (2010) Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people. Proc Natl Acad Sci USA 107:5967–5971. 6. Word-for-word plagiarism is taking a series of specific words from a source without identifying the passage, citing the author, and providing the reference. Paraphrasing plagiarism is summarizing a source without citing the author and providing the reference. 7. Information is facts and statements, but ideas are derived methods, processes, theories, and conclusions. General common knowledge is information considered to be well-known in the public, and field-specific common knowledge is information considered to be well-known within a specific field. 8. Information that isn’t common knowledge, ideas, and exact words from a source stating common knowledge need a cited source in writing. Version A: Claim: There is a relationship between FY antigen genotype and malaria caused by P. vivax; individuals are most likely to be infected with P. vivax malaria if they have the FY*B allele, somewhat likely with the FY*A allele, and least likely with the FY*B ES allele. The European population is most susceptible to malaria caused by P. vivax. Evidence: Figure 1 shows P. vivax Duffy Binding II (PvDBPII) binding to red blood cells to be approximately 7.0 × 104 for individuals with two FY*B alleles, 6.0 × 104 for individuals with one FY*A and one FY*B allele, 4.0 × 104 for individuals with two FY*A alleles, 2.0 × 104 for individuals with one FY*A and one FY*BES allele, and nearly 0 for individuals with two FY*BES alleles. [1] Figure 4 shows the incidence of P. vivax malaria is approximately 0.45 for individuals with two FY*B alleles, 0.40 for individuals with one FY*B and one FY*BES allele, 0.30 for individuals with one FY*A and one FY*B allele, 0.25 for individuals with two FY*A alleles, and 0.03 for individuals with one FY*A and one FY*BES allele. The graph states that the data is statistically significant. [1] Figure 5 shows that areas of allelic homogeneity for FY*A include most of North and South America, Asia, and Australia. Additionally, the figure shows that areas of allelic homogeneity for FY*B include Europe and small parts in North and South America. Furthermore, the figure shows that areas of homogeneity for FY*BES include Africa and small parts in South America. The figure also shows that areas of heterogeneity for FY alleles include mostly Northern Africa and the Middle East. [1] Explanation: Given studies on non-human primates indicating that FY*B is the ancestral allele, we hypothesized that FY*A decreased the efficiency of PvDBPII binding, thereby reducing susceptibility to infection of P. vivax malaria. Cross sectional association studies performed in the Brazilian Amazon region suggested that individuals expressing the FY*B compared with FY*A antigen may be more susceptible to P. vivax infection. The FY*B allele is most commonly found in European popula-

tions. Therefore, individuals in Europe are most likely to be prone to infection of P. vivax malaria. What is wrong: The explanation includes a word-for-word copy of paragraph #4 but doesn’t cite the work or list the reference, which is dishonest because the source isn’t credited for the ideas taken. Version B: Claim: There is a relationship between FY antigen genotype and malaria caused by P. vivax; individuals are most likely to be infected with P. vivax malaria if they have the FY*B allele, somewhat likely with the FY*A allele, and least likely with the FY*B ES allele. The European population is most susceptible to malaria caused by P. vivax. Evidence: Figure 1 shows P. vivax Duffy Binding II (PvDBPII) binding to red blood cells to be approximately 7.0 × 104 for individuals with two FY*B alleles, 6.0 × 104 for individuals with one FY*A and one FY*B allele, 4.0 × 104 for individuals with two FY*A alleles, 2.0 × 104 for individuals with one FY*A and one FY*BES allele, and nearly 0 for individuals with two FY*BES alleles. [1] Figure 4 shows the incidence of P. vivax malaria is approximately 0.45 for individuals with two FY*B alleles, 0.40 for individuals with one FY*B and one FY*BES allele, 0.30 for individuals with one FY*A and one FY*B allele, 0.25 for individuals with two FY*A alleles, and 0.03 for individuals with one FY*A and one FY*BES allele. The graph states that the data is statistically significant. [1] Figure 5 shows that areas of allelic homogeneity for FY*A include most of North and South America, Asia, and Australia. Additionally, the figure shows that areas of allelic homogeneity for FY*B include Europe and small parts in North and South America. Furthermore, the figure shows that areas of homogeneity for FY*BES include Africa and small parts in South America. The figure also shows that areas of heterogeneity for FY alleles include mostly Northern Africa and the Middle East. [1] Explanation: It’s likely that FY*B increases PvDBPII binding, which increases the likelihood of being infected with P. vivax malaria. Individuals with the FY*B allele are likely more prone to Pv infection compared to individuals with the FY*A allele and/or FY*BES allele. The FY*B allele is most commonly found in European populations. Therefore, individuals in Europe are most likely to be prone to infection of P. vivax malaria. What is wrong: The explanation contains a rewording of paragraph #4 but doesn’t cite the work or list the reference, which is dishonest because the source isn’t credited for the ideas taken.

Version C: Claim: There is a relationship between FY antigen genotype and malaria caused by P. vivax; individuals are most likely to be infected with P. vivax malaria if they have the FY*B allele, somewhat likely with the FY*A allele, and least likely with the FY*B ES allele. The European population is most susceptible to malaria caused by P. vivax.

Evidence: Figure 1 shows P. vivax Duffy Binding II (PvDBPII) binding to red blood cells to be approximately 7.0 × 104 for individuals with two FY*B alleles, 6.0 × 104 for individuals with one FY*A and one FY*B allele, 4.0 × 104 for individuals with two FY*A alleles, 2.0 × 104 for individuals with one FY*A and one FY*BES allele, and nearly 0 for individuals with two FY*BES alleles. [1] Figure 4 shows the incidence of P. vivax malaria is approximately 0.45 for individuals with two FY*B alleles, 0.40 for individuals with one FY*B and one FY*BES allele, 0.30 for individuals with one FY*A and one FY*B allele, 0.25 for individuals with two FY*A alleles, and 0.03 for individuals with one FY*A and one FY*BES allele. The graph states that the data is statistically significant. [1] Figure 5 shows that areas of allelic homogeneity for FY*A include most of North and South America, Asia, and Australia. Additionally, the figure shows that areas of allelic homogeneity for FY*B include Europe and small parts in North and South America. Furthermore, the figure shows that areas of homogeneity for FY*BES include Africa and small parts in South America. The figure also shows that areas of heterogeneity for FY alleles include mostly Northern Africa and the Middle East. [1] Explanation: Since PvDBPII and red blood cell binding is greatest in individuals with two FY*B alleles and second greatest in those with one FY*B allele [1], the event of having malaria caused by Pv is likely to be increased the FY*B allele. The FY*A allele is associated with intermediate levels of binding compared to FY*B and FY*BES [1] so it’s likely the FY*A allele is more likely than FY*BES but less likely than FY*B to lead to Pv malaria infection. The incidence of P. vivax malaria is highest in individuals with two FY*B alleles, high in individuals with one FY*B allele, and low in individuals with no FY*B allele [1]. Therefore, the incidence of P. vivax malaria likely increases with the number of FY*B alleles present. The incidence of P. vivax malaria is greater with two FY*A alleles than one FY*A and one FY*BES allele [1] so the FY*A allele is more likely to cause susceptibility to P. vivax malaria infection than the FY*BES allele. However, the FY*B allele is more likely to lead to infection than the FY*A allele because the presence of one FY*B allele leads to higher incidence of malaria than the presence of one or even two FY*A alleles. Additionally, since having two FY*B alleles is most commonly found in European populations and having one FY*B allele is commonly found in Northern Africa, the Middle East, and parts of North and South America [1], individuals in these areas are most likely to be susceptible to infection of P. vivax malaria, with Europeans being the most prone. Reference: [1] King CL, Adams JH, Jia X, Grimberg BT, McHenry AM, Greenberg LJ, Siddiqui A, Howes RE, da Silva- Nunes M, Ferreira MU, Zimmerman PA. Fya/Fyb antigen polymorphism in human erythrocyte Duffy antigen affects susceptibility to Plasmodium vivax malaria. Proceedings of the National Academy of Sciences (2011) 108: 477-487....