Publications by authors named "Kelsey Taylor"

We report the application of a Pictet-Spengler reaction to the synthesis of covalent organic frameworks (COFs) using functionalized terephthalaldehydes. The COFs produced show an increased propensity to generate screw dislocations and produce multilayered flakes when compared with other 2D-COFs. Using HRTEM, definitive evidence for screw dislocations was obtained and is presented.

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Human Lyme disease-primarily caused by the bacterium Borrelia burgdorferi sensu stricto (s.s.) in North America-is the most common vector-borne disease in the United States.

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Prior studies have established that broader incorporation of active surveillance, guided by additional prognostic tools, may mitigate the growing economic burden of localized prostate cancer in the USA. This study sought to further explore the potential of a particular gene expression-based prognostic tool to address this unmet need. A deterministic, decision-analytic model was developed to estimate the economic impact of the Prolaris test on a US commercial health plan.

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One of the most popular policy mechanisms for greenhouse gas emissions regulation is cap-and-trade which is a market-based approach that has come to dominate partially because of its flexibility. With flexibility, however, comes the potential for the clustering of greenhouse gas emissions. To understand whether emissions trading leads to localized clustering of emissions changes, we perform a systematic, spatio-economic assessment of the European Union Emissions Trading Scheme (EU ETS).

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Polychlorinated biphenyls (PCBs) are persistent organic pollutants known to cause adverse health effects and linked to neurological deficits in both human and animal studies. Children born to exposed mothers are at highest risk of learning and memory and motor deficits. We developed a mouse model that mimics human variation in the aryl hydrocarbon receptor and cytochrome P450 1A2 (CYP1A2) to determine if genetic variation increases susceptibility to developmental PCB exposure.

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Insomnia, or inadequate or poor sleep leading to significant distress or impairment in functioning, is a prevalent disorder treated by primary care providers (PCPs). With millions of people across the United States suffering from insomnia, PCPs must understand the disorder's pathophysiology, perpetuating factors, and treatment, as well as its effect on patient health and the economy. Although PCPs traditionally treat insomnia with pharmaceuticals, behavioral measures are effective and should be used whenever possible.

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During larval molts, Caenorhabditis elegans exhibits a sleep-like state (termed lethargus) that is characterized by the absence of feeding and profound locomotion quiescence. The rhythmic pattern of locomotion quiescence and arousal linked to the molting cycle is mediated by reciprocal changes in sensory responsiveness, whereby arousal is associated with increased responsiveness. Sensory neurons arouse locomotion via release of a neuropeptide (PDF-1) and glutamate.

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C. elegans undergoes periods of behavioral quiescence during larval molts (termed lethargus) and as adults. Little is known about the circuit mechanisms that establish these quiescent states.

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Animals undergo periods of behavioral quiescence and arousal in response to environmental, circadian, or developmental cues. During larval molts, C. elegans undergoes a period of profound behavioral quiescence termed lethargus.

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Deficiency in human mitochondrial Complex-1 has been linked to a wide variety of neurological disorders. Homozygous deletion of the Complex-1 associated protein, Ndufaf2, leads to a severe juvenile onset encephalopathy involving degeneration of the substantia nigra and other sub-cortical regions resulting in adolescent lethality. To understand the precise role of Ndufaf2 in Complex-1 function and its links to neurologic disease, we studied the effects on Complex-1 assembly and function, as well as pathological consequences at the cellular level, in multiple in vitro models of Ndufaf2 deficiency.

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We report here the preparation of ratiometric luminescent probes that contain two well-separated emission peaks produced by a sequential bioluminescence resonance energy transfer (BRET)-fluorescence resonance energy transfer (FRET) process. The probes are single soluble fusion proteins consisting of a thermostable firefly luciferase variant that catalyze yellow-green (560nm maximum) bioluminescence and a red fluorescent protein covalently labeled with a near-infrared fluorescent dye. The two proteins are connected by a decapeptide containing a protease recognition site specific for factor Xa, thrombin, or caspase 3.

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