Publications by authors named "Kelsey LeVault"

Erythema ab igne (EAI) is a typical example of an environmental-induced dermatosis secondary to overexposure of a particular part of the skin to heat. Once a familiar entity in the precentral heating era, it seems to be making a comeback with prolonged usage of electronic devices close to the body surface as well as usage of alternative methods of pain relief being sought by patients. We describe a case of a 39-year-old female who presented to our clinic with a mottled reticulate rash on her back after five years of using heating pads for her chronic backache.

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Perceptions of harms and social norms influence the use of conventional tobacco cigarettes, but little research is available about their combined relationship with e-cigarette and smokeless tobacco use. We conducted a cross-sectional survey of 309 individuals from central Illinois. We explored (1) demographic predictors of perceived harms and social norms related to e-cigarette and smokeless tobacco use, and (2) whether perceived harms, social norms, or both were important predictors of e-cigarette and smokeless tobacco use.

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Background: Electronic cigarettes (e-cigarettes) are often marketed as safe and effective aids for quitting cigarette smoking, but concerns remain that use of e-cigarettes might actually reduce the number of quit attempts. To address these issues, we characterized the utilization and demographic correlates of dual use of e-cigarettes and traditional cigarettes (referred to here as simply “cigarettes”) among smokers in a rural population of Illinois.

Methods: The majority of survey participants were recruited from the 2014 Illinois State Fair and from another event—the Springfield Mile (a motorcycle racing event)—in Springfield, Ill.

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It is unclear whether pre-symptomatic Alzheimer's disease (AD) causes circadian disruption or whether circadian disruption accelerates AD pathogenesis. In order to examine the sensitivity of learning and memory to circadian disruption, we altered normal lighting phases by an 8 h shortening of the dark period every 3 days (jet lag) in the APPSwDI NOS2-/- model of AD (AD-Tg) at a young age (4-5 months), when memory is not yet affected compared to non-transgenic (non-Tg) mice. Analysis of activity in 12-12 h lighting or constant darkness showed only minor differences between AD-Tg and non-Tg mice.

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Background: Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (GC) are the most reported diseases in the United States, and emergency departments (ED) serve a population presenting with increased infection risk. However, identifying patients for whom sexually transmitted infection (STI) screening is appropriate requires accurate sexual history reporting.

Study Objectives: To examine the consistency with which ED patients answer general and specific sexual activity questions, and how responses relate to perceived STI risk.

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Aging, a major risk factor in Alzheimer's disease (AD), is associated with an oxidative redox shift, decreased redox buffer protection, and increased free radical reactive oxygen species (ROS) generation, probably linked to mitochondrial dysfunction. While NADH is the ultimate electron donor for many redox reactions, including oxidative phosphorylation, glutathione (GSH) is the major ROS detoxifying redox buffer in the cell. Here, we explored the relative importance of NADH and GSH to neurodegeneration in aging and AD neurons from nontransgenic and 3xTg-AD mice by inhibiting their synthesis to determine whether NADH can compensate for the GSH loss to maintain redox balance.

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To determine whether glutathione (GSH) loss or increased reactive oxygen species (ROS) are more important to neuron loss, aging, and Alzheimer's disease (AD), we stressed or boosted GSH levels in neurons isolated from aging 3xTg-AD neurons compared with those from age-matched nontransgenic (non-Tg) neurons. Here, using titrating with buthionine sulfoximine, an inhibitor of γ-glutamyl cysteine synthetase (GCL), we observed that GSH depletion increased neuronal death of 3xTg-AD cultured neurons at increasing rates across the age span, whereas non-Tg neurons were resistant to GSH depletion until old age. Remarkably, the rate of neuron loss with ROS did not increase in old age and was the same for both genotypes, which indicates that cognitive deficits in the AD model were not caused by ROS.

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The brain depends on redox electrons from nicotinamide adenine dinucleotide (reduced form; NADH) to produce ATP and oxyradicals (reactive oxygen species [ROS]). Because ROS damage and mitochondrial dysregulation are prominent in aging and Alzheimer's disease (AD) and their relationship to the redox state is unclear, we wanted to know whether an oxidative redox shift precedes these markers and leads to macromolecular damage in a mouse model of AD. We used the 3xTg-AD mouse model, which displays cognitive deficits beginning at 4 months.

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