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Liberty, MO, United States

William Jewell College is a private, four-year liberal arts college of 1,100 undergraduate students located in Liberty, Missouri, U.S. It was founded in 1849 by members of the Missouri Baptist Convention and other civic leaders, including Robert S. James, a Baptist minister and father of the infamous Frank and Jesse James. It was associated with the Missouri Baptist Convention for over 150 years until its separation in 2003 and is now an independent institution. Wikipedia.


Braitman K.A.,William Jewell College | Chaudhary N.K.,Preusser Research Group Inc. | McCartt A.T.,Insurance Institute for Highway Safety
Traffic Injury Prevention | Year: 2014

Objective: To determine the association between passenger presence and risk of fatal crash involvement in relation to driver and passenger age and gender, focusing especially on drivers ages 65 and older. Methods: Data on US fatal crashes were obtained for 2002-2009. Using the quasi-induced exposure methodology, logistic regression analysis was used to predict the odds of fatal crash involvement as a function of driver age and gender as well as passenger age and gender. Results: Overall, risk of fatal crash involvement with passengers was 43 percent lower for drivers ages 65-74 and 38 percent lower for drivers 75 and older. Older drivers' risk of fatal crash involvement was lower with almost all combinations of passenger age and gender; there was no reduction in risk with passengers ages 75 and older. Effects were stronger at nonintersection locations than at intersection locations. Conclusion: Older drivers' crash risk is lower with almost every combination of passenger age group and gender. It is unclear whether the presence of passengers lowers older driver crash risk or whether safer drivers tend to ride with passengers. © 2014 Copyright Taylor & Francis Group, LLC. Source


Reynolds R.M.,University of Oregon | Reynolds R.M.,William Jewell College | Phillips P.C.,University of Oregon
PLoS ONE | Year: 2013

Genetic approaches (e.g. mutation, RNA interference) in model organisms, particularly the nematode Caenorhabditis elegans, have yielded a wealth of information on cellular processes that can influence lifespan. Although longevity mutants discovered in the lab are instructive of cellular physiology, lab studies might miss important genes that influence health and longevity in the wild. C. elegans has relatively low natural genetic variation and high levels of linkage disequilibrium, and thus is not optimal for studying natural variation in longevity. In contrast, its close relative C. remanei possesses very high levels of molecular genetic variation and low levels of linkage disequilibrium. To determine whether C. remanei may be a good model system for the study of natural genetic variation in aging, we evaluated levels of quantitative genetic variation for longevity and resistance to oxidative, heat and UV stress. Heritability (and the coefficient of additive genetic variation) was high for oxidative and heat stress resistance, low (but significant) for longevity, and essentially zero for UV stress response. Our results suggest that C. remanei may be a powerful system for studying natural genetic variation for longevity and oxidative and heat stress response, as well as an informative model for the study of functional relationships between longevity and stress response. © 2013 Reynolds, Phillips. Source


Price E.S.,University of Kansas | Price E.S.,William Jewell College | Aleksiejew M.,University of Kansas | Johnson C.K.,University of Kansas
Journal of Physical Chemistry B | Year: 2011

Fluorescence correlation spectroscopy (FCS) can be coupled with Förster resonance energy transfer (FRET) to detect intramolecular dynamics of proteins on the microsecond time scale. Here we describe application of FRET-FCS to detect fluctuations within the N-terminal and C-terminal domains of the Ca2+-signaling protein calmodulin. Intramolecular fluctuations were resolved by global fitting of the two fluorescence autocorrelation functions (green-green and red-red) together with the two cross-correlation functions (green-red and red-green). To match the Förster radius for FRET to the dimensions of the N-terminal and C-terminal domains, a near-infrared acceptor fluorophore (Atto 740) was coupled with a green-emitting donor (Alexa Fluor 488). Fluctuations were detected in both domains on the time scale of 30 to 40 μs. In the N-terminal domain, the amplitude of the fluctuations was dependent on occupancy of Ca2+ binding sites. A high amplitude of dynamics in apo-calmodulin (in the absence of Ca2+) was nearly abolished at a high Ca2+ concentration. For the C-terminal domain, the dynamic amplitude changed little with Ca2+ concentration. The Ca2+ dependence of dynamics for the N-terminal domain suggests that the fluctuations detected by FCS in the N-terminal domain are coupled to the opening and closing of the EF-hand Ca2+-binding loops. © 2011 American Chemical Society. Source


Sikkink K.L.,University of Oregon | Reynolds R.M.,University of Oregon | Reynolds R.M.,William Jewell College | Ituarte C.M.,University of Oregon | And 2 more authors.
G3: Genes, Genomes, Genetics | Year: 2014

Many organisms can acclimate to new environments through phenotypic plasticity, a complex trait that can be heritable, subject to selection, and evolve. However, the rate and genetic basis of plasticity evolution remain largely unknown. We experimentally evolved outbred populations of the nematode Caenorhabditis remanei under an acute heat shock during early larval development. When raised in a nonstressful environment, ancestral populations were highly sensitive to a 36.8° heat shock and exhibited high mortality. However, initial exposure to a nonlethal high temperature environment resulted in significantly reduced mortality during heat shock (hormesis). Lines selected for heat shock resistance rapidly evolved the capacity to withstand heat shock in the native environment without any initial exposure to high temperatures, and early exposure to high temperatures did not lead to further increases in heat resistance. This loss of plasticity would appear to have resulted from the genetic assimilation of the heat induction response in the noninducing environment. However, analyses of transcriptional variation via RNA-sequencing from the selected populations revealed no global changes in gene regulation correlated with the observed changes in heat stress resistance. Instead, assays of the phenotypic response across a broader range of temperatures revealed that the induced plasticity was not fixed across environments, but rather the threshold for the response was shifted to higher temperatures over evolutionary time. These results demonstrate that apparent genetic assimilation can result from shifting thresholds of induction across environments and that analysis of the broader environmental context is critically important for understanding the evolution of phenotypic plasticity. © 2014 Sikkink et al. Source


Many organisms can acclimate to new environments through phenotypic plasticity, a complex trait that can be heritable, subject to selection, and evolve. However, the rate and genetic basis of plasticity evolution remain largely unknown. We experimentally evolved outbred populations of the nematode Caenorhabditis remanei under an acute heat shock during early larval development. When raised in a nonstressful environment, ancestral populations were highly sensitive to a 36.8° heat shock and exhibited high mortality. However, initial exposure to a nonlethal high temperature environment resulted in significantly reduced mortality during heat shock (hormesis). Lines selected for heat shock resistance rapidly evolved the capacity to withstand heat shock in the native environment without any initial exposure to high temperatures, and early exposure to high temperatures did not lead to further increases in heat resistance. This loss of plasticity would appear to have resulted from the genetic assimilation of the heat induction response in the noninducing environment. However, analyses of transcriptional variation via RNA-sequencing from the selected populations revealed no global changes in gene regulation correlated with the observed changes in heat stress resistance. Instead, assays of the phenotypic response across a broader range of temperatures revealed that the induced plasticity was not fixed across environments, but rather the threshold for the response was shifted to higher temperatures over evolutionary time. These results demonstrate that apparent genetic assimilation can result from shifting thresholds of induction across environments and that analysis of the broader environmental context is critically important for understanding the evolution of phenotypic plasticity. Copyright © 2014 Sikkink et al. Source

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