Publications by authors named "K A Crandall"

With climate and land use changes, tick-borne pathogens are expected to become more widely distributed in Canada. Pathogen spread and transmission in this region is modulated by changes in the abundance and distribution of tick and host populations. Here, we assessed the relationships between pathogens detected in and mammal hosts at sites of different levels of disease risk using data from summer field surveys in Ontario and Quebec, Canada.

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Freshwater ecosystems are highly biodiverse and important for livelihoods and economic development, but are under substantial stress. To date, comprehensive global assessments of extinction risk have not included any speciose groups primarily living in freshwaters. Consequently, data from predominantly terrestrial tetrapods are used to guide environmental policy and conservation prioritization, whereas recent proposals for target setting in freshwaters use abiotic factors.

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Background: Brown-Séquard syndrome (BSS) is a rare neurological condition characterized by injury to one-half of the spinal cord. In the context of trauma, BSS is typically seen with penetrating injuries. Here, the authors present the unique case of a patient presenting with BSS after blunt trauma.

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Background: Predicting phenotypes from genetic variation is foundational for fields as diverse as bioengineering and global change biology, highlighting the importance of efficient methods to predict gene functions. Linking genetic changes to phenotypic changes has been a goal of decades of experimental work, especially for some model gene families, including light-sensitive opsin proteins. Opsins can be expressed in vitro to measure light absorption parameters, including λmax-the wavelength of maximum absorbance-which strongly affects organismal phenotypes like color vision.

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Obesity and fatty liver diseases-metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH)-affect over one-third of the global population and are exacerbated in individuals with reduced functional aldehyde dehydrogenase 2 (ALDH2), observed in approximately 560 million people. Current treatment to prevent disease progression to cancer remains inadequate, requiring innovative approaches. We observe that Aldh2 and Aldh2Sptbn1 mice develop phenotypes of human metabolic syndrome (MetS) and MASH with accumulation of endogenous aldehydes such as 4-hydroxynonenal (4-HNE).

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