Putting it Graphically: Fidelity in Graphic Novel Adaptations of Classic German Literature

The rise of the graphic novel as a new genre of the arts has prompted many questions surrounding it – about its nature, relationship to other genres, effect on audiences, etc. In our research, we specifically examined graphic novel adaptations of classic German works that are part of the “canon” of German literature. We first read the original work and then the graphic novel adaptation. Our aim was to determine how faithful the adaptation was to the original using four criteria: style (character perspective/representation), use of original text, plot additions or subtractions, and use of color. in each of the four works, we analyzed these criteria as they appeared (or did not appear) in the graphic novel and then discussed how they served (or did not serve) to portray the original novel faithfully. From our analysis, we concluded that graphic novel adaptations of classic “canon” works of German literature are largely faithful to the original works, and that they use style, original text, plot, and color to achieve this faithful portrayal

Lymphoma and the Kidney: A Kidney Biopsy Teaching Case

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Observing the Reionization Epoch Through 21 Centimeter Radiation

We study the observability of the reionization epoch through the 21 cm hyperfine transition of neutral hydrogen. We use a high-resolution cosmological simulation (including hydrodynamics) together with a fast radiative transfer algorithm to compute the evolution of 21 cm emission from the intergalactic medium (IGM) in several different models of reionization. We show that the mean brightness temperature of the IGM drops from dT_b~25 mK to dT_b~0.01 mK during overlap (over a frequency interval of ~25 MHz), while the root mean square brightness temperature fluctuations on small scales drop abruptly from ~10 mK before overlap to ~0.1 mK at the end of overlap. We show that 21 cm observations can efficiently discriminate models with a single early reionization epoch from models with two distinct reionization episodes.Comment: 10 pages, 7 figures, submitted to MNRA

Fitness Cost of Resistance to Bt Cotton Linked with Increased Gossypol Content in Pink Bollworm Larvae

Fitness costs of resistance to Bacillus thuringiensis (Bt) crops occur in the absence of Bt toxins, when individuals with resistance alleles are less fit than individuals without resistance alleles. As costs of Bt resistance are common, refuges of non-Bt host plants can delay resistance not only by providing susceptible individuals to mate with resistant individuals, but also by selecting against resistance. Because costs typically vary across host plants, refuges with host plants that magnify costs or make them less recessive could enhance resistance management. Limited understanding of the physiological mechanisms causing fitness costs, however, hampers attempts to increase costs. In several major cotton pests including pink bollworm (Pectinophora gossypiella), resistance to Cry1Ac cotton is associated with mutations altering cadherin proteins that bind this toxin in susceptible larvae. Here we report that the concentration of gossypol, a cotton defensive chemical, was higher in pink bollworm larvae with cadherin resistance alleles than in larvae lacking such alleles. Adding gossypol to the larval diet decreased larval weight and survival, and increased the fitness cost affecting larval growth, but not survival. Across cadherin genotypes, the cost affecting larval growth increased as the gossypol concentration of larvae increased. These results suggest that increased accumulation of plant defensive chemicals may contribute to fitness costs associated with resistance to Bt toxins

Evolution of increased mutation rates in asexual populations: Causes and consequences

The rate at which mutations arise is under the control of complex biological systems, and is thus subject to adjustment by natural selection. The effects of beneficial and deleterious mutations counter exert opposing forces on the direction of such selection; understanding the balance of these forces is key to understanding the evolution of mutation rates. This work concentrates on understanding the processes that result in the evolution of high mutation rates in asexual populations. An in-depth study is made of the population dynamics surrounding the fixation of three different alleles conferring high mutation rates in experimental bacterial populations. The results of this study are consistent with the hypothesis that high mutation rates evolved, not because of any inherent fitness advantage to the phenotype, but because of fortuitous association with other mutations of beneficial effect. Two of the three alleles studied were found to have arisen independently in a small repeat region within the same DNA repair gene; while the coincidence is striking, analysis of the repeat region as well as the nature of selective dynamics in asexual populations make it extremely unlikely that the DNA repeat has been maintained by selection to provide a region of hypervariability. Other work described here includes an experimental analysis of the dynamics of adaptation in populations of high versus low mutation supply rates; a theoretical treatment of the effect of environment-specific changes in mutation rate on the accumulation of deleterious load during times of physiological stress; and a simulation-based analysis of the estimation of mutation rates from experimental data when the data are subjected to realistic levels of noise and distortion

Evolution of increased mutation rates in asexual populations: Causes and consequences

The rate at which mutations arise is under the control of complex biological systems, and is thus subject to adjustment by natural selection. The effects of beneficial and deleterious mutations counter exert opposing forces on the direction of such selection; understanding the balance of these forces is key to understanding the evolution of mutation rates. This work concentrates on understanding the processes that result in the evolution of high mutation rates in asexual populations. An in-depth study is made of the population dynamics surrounding the fixation of three different alleles conferring high mutation rates in experimental bacterial populations. The results of this study are consistent with the hypothesis that high mutation rates evolved, not because of any inherent fitness advantage to the phenotype, but because of fortuitous association with other mutations of beneficial effect. Two of the three alleles studied were found to have arisen independently in a small repeat region within the same DNA repair gene; while the coincidence is striking, analysis of the repeat region as well as the nature of selective dynamics in asexual populations make it extremely unlikely that the DNA repeat has been maintained by selection to provide a region of hypervariability. Other work described here includes an experimental analysis of the dynamics of adaptation in populations of high versus low mutation supply rates; a theoretical treatment of the effect of environment-specific changes in mutation rate on the accumulation of deleterious load during times of physiological stress; and a simulation-based analysis of the estimation of mutation rates from experimental data when the data are subjected to realistic levels of noise and distortion

Spontaneously Arising mutL Mutators in Evolving Escherichia coli Populations Are the Result of Changes in Repeat Length

Over the course of thousands of generations of growth in a glucose-limited environment, 3 of 12 experimental populations of Escherichia coli spontaneously and independently evolved greatly increased mutation rates. In two of the populations, the mutations responsible for this increased mutation rate lie in the same region of the mismatch repair gene mutL. In this region, a 6-bp repeat is present in three copies in the gene of the wild-type ancestor of the experimental populations but is present in four copies in one of the experimental populations and two copies in the other. These in-frame mutations either add or delete the amino acid sequence LA in the MutL protein. We determined that the replacement of the wild-type sequence with either of these mutations was sufficient to increase the mutation rate of the wild-type strain to a level comparable to that of the mutator strains. Complementation of strains bearing the mutator mutations with wild-type copies of either mutL or the mismatch repair gene uvrD rescued the wild-type mutation rate. The position of the mutator mutations—in the region of MutL known as the ATP lid—suggests a possible deficiency in MutL's ATPase activity as the cause of the mutator phenotype. The similarity of the two mutator mutations (despite the independent evolutionary histories of the populations that gave rise to them) leads to a discussion of the potential adaptive role of DNA repeats