Publications by authors named "Amanda Burns"

E-cigarette aerosol is a complex mixture of gases and particles with a composition that is dependent on the e-liquid formulation, puffing regimen, and device operational parameters. This work investigated mainstream aerosols from a third generation device, as a function of coil temperature (315-510 °F, or 157-266 °C), puff duration (2-4 s), and the ratio of propylene glycol (PG) to vegetable glycerin (VG) in e-liquid (100:0-0:100). Targeted and untargeted analyses using liquid chromatography high-resolution mass spectrometry, gas chromatography, in situ chemical ionization mass spectrometry, and gravimetry were used for chemical characterizations.

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Electronic (e-) cigarette aerosol (particle and gas) is a complex mixture of chemicals, of which the profile is highly dependent on device operating parameters and e-liquid flavor formulation. The thermal degradation of the e-liquid solvents propylene glycol and glycerol often generates multifunctional carbonyls that are challenging to quantify because of unavailability of standards. We developed a theoretical method to calculate the relative electrospray ionization sensitivities of hydrazones of organic acids and carbonyls with 2,4-dinitrophenylhydrazine based on their gas-phase basicities (Δ).

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The objective is to present historical asbestos airborne concentrations associated with activities involving presumably asbestos-containing materials in steel mills. A total of 138 historical industrial hygiene air samples collected in three US steel mills from 1972 to 1982 were analyzed. The majority of samples were collected during relining of open hearth furnaces, stoves, and blast furnaces by steel mill bricklayers and bricklayer helpers.

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Background: The rate of potential adverse drug events is reported to be 3 times higher among pediatric inpatients than among their adult counterparts. Various methods have been suggested to reduce medication errors in pediatric patients. One of the most influential of these strategies is inclusion of a clinical pharmacist on the multidisciplinary care team.

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Over time, concerns have been raised regarding the potential for human exposure and risk from asbestos in cosmetic-talc-containing consumer products. In 1985, the U.S.

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Premise Of The Study: California experienced severe drought between 2012 and 2016. During this period, we compared seasonal changes in tissue-water relations among eight fern species in the Santa Monica Mountains of southern California to elucidate differential mechanisms of drought survival and physiological performance during extreme water deficits.

Methods: We monitored seasonal changes in water potential (Ψmd) and dark-adapted chlorophyll fluorescence (Fv/Fm), assessed tissue-water relations including osmotic potential at saturation and the turgor loss point (Ψπ, sat and Ψπ, tlp), and measured, for two evergreen species, xylem-specific and leaf-specific hydraulic conductivity (Ks and Kl) and vulnerability of stem xylem to water stress-induced embolism (water potential at 50% loss hydraulic conductivity, Ψ50).

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Workplace air samples analyzed for benzene at four US refineries from 1976 to 2007 were pooled into a single dataset to characterize similarities and differences between job titles, tasks and refineries, and to provide a robust dataset for exposure reconstruction. Approximately 12,000 non-task (>180 min) personal samples associated with 50 job titles and 4000 task (<180 min) samples characterizing 24 tasks were evaluated. Personal air sample data from four individual refineries were pooled based on a number of factors including (1) the consistent sampling approach used by refinery industrial hygienists over time, (2) the use of similar exposure controls, (3) the comparability of benzene content of process streams and end products, (4) the ability to assign uniform job titles and task codes across all four refineries, and (5) our analysis of variance (ANOVA) of the distribution of benzene air concentrations for select jobs/tasks across all four refineries.

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While petroleum industry studies have indicated low benzene exposure potential for refinery workers, most provide limited data for assessing job or task-related benzene exposures. This study characterizes job and task-specific airborne benzene concentrations and variability over time for the ExxonMobil refinery in Joliet, Illinois from 1977 to 2006. A database of 2289 industrial hygiene air samples, including 1145 non-task (≥180 min) personal samples and 480 task-related (<180 min) personal samples, were analyzed.

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Because crude oil and refined petroleum products can contain benzene and benzene is considered a known carcinogen by numerous independent and governmental agencies, including the International Agency for Cancer Research, the petroleum industry has implemented exposure control programs for decades. As part of the benzene control programs, significant exposure assessments have been performed; both qualitatively and through quantitative measurements. In this study, we evaluated the airborne concentrations of benzene and their variability over time at the ExxonMobil refinery in Beaumont, TX between 1976 and 2007.

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Background: Knowledge of the anatomy of ligaments that bind the craniocervical junction is important for treating patients with lesions of this region. Although the anatomy and function of these ligaments have been well described, those of the transverse occipital ligament (TOL) have remained enigmatic.

Objective: To describe the anatomy and functions of the transverse occipital ligament.

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Background: There is a paucity in the literature regarding the reflected ligament. Therefore, the present study was performed in order to further elucidate this anatomy.

Material And Methods: Eighteen formalin-fixed adult cadavers (35 sides) underwent dissection of the medial inguinal region.

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Although occupational benzene exposure of refinery workers has been studied for decades, no extensive analysis of historical industrial hygiene data has been performed focusing on airborne concentrations at specific refineries and tasks. This study characterizes benzene exposures at the ExxonMobil Baytown, TX, refinery from 1978 to 2006 to understand the variability in workers' exposures over time and during different job tasks. Exposures were grouped by operational status, job title, and tasks.

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Because crude oil contains up to 3% benzene and there is an association between high chronic exposure to appreciable concentrations of benzene and acute myelogenous leukemia, exposure of refinery workers has been studied for many years. To date, no extensive industrial hygiene exposure analyses for historical benzene exposure have been performed, and none have focused on the airborne concentrations in the workplace at specific refineries or for specific tasks. In this study, the authors evaluated the airborne concentrations of benzene and their variability over time at the ExxonMobil refinery in Baton Rouge between 1977 and 2005.

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Administration of peroxisome proliferators to rodents causes proliferation of peroxisomes, induction of beta-oxidation enzymes, hepatocellular hypertrophy and hyperplasia, with chronic exposure ultimately leading to hepatocellular carcinomas. Many responses associated with peroxisome proliferators are nuclear receptor-mediated events involving peroxisome proliferators-activated receptor alpha (PPARalpha). A role for nuclear receptor-independent events has also been shown, with evidence of Kupffer cell-mediated free radical production, presumably through NAPDH oxidase, induction of redox-sensitive transcription factors involved in cytokine production and cytokine-mediated cell replication following acute treatment with peroxisome proliferators in rodents.

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Long-term exposure of rodents to peroxisome proliferators leads to increases in peroxisomes, hepatocellular proliferation, oxidative damage, suppressed apoptosis, and ultimately results in the development of hepatic adenomas and carcinomas. Peroxisome proliferators-activated receptor (PPAR)alpha was shown to be required for these pleiotropic responses; however, Kupffer cells, resident liver macrophages, were also identified as playing a role in peroxisome proliferators-induced effects, independently of PPARalpha. Previous studies showed that oxidants from NADPH (nicotinamide adenine dinucleotide phosphate, reduced) oxidase mediate acute effects of peroxisome proliferators in rodent liver.

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Reactive oxygen species are thought to be crucial for peroxisome proliferator-induced liver carcinogenesis. Free radicals have been shown to mediate the production of mitogenic cytokines by Kupffer cells and cause DNA damage in rodent liver. Previous in vivo experiments demonstrated that acute administration of the peroxisome proliferator di(2-ethylhexyl) phthalate (DEHP) led to an increase in production of alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN) radical adducts in liver, an event that was dependent on Kupffer cell NADPH oxidase, but not peroxisome proliferator-activated receptor (PPAR)alpha.

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Recent work has shown that peroxisome proliferator-activated receptor beta (PPARbeta) attenuates cell proliferation and skin carcinogenesis, and this is due in part to regulation of ubiquitin C expression. In these studies, the role of PPARbeta in modulating ubiquitin-dependent protein kinase Calpha (PKCalpha) levels and phosphorylation signaling pathways was evaluated. Intracellular phosphorylation analysis showed that phosphorylated PKCalpha and other kinases were lower in wild-type mouse skin treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) as compared with PPARbeta-null mouse skin.

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Prolonged administration of peroxisome proliferators to rodents typically leads to hepatocarcinogenesis. Peroxisome proliferator-activated receptor-alpha (PPARalpha) is required to mediate alterations in PPARalpha target gene expression, repress apoptosis, enhance replicative DNA synthesis, oxidative stress to DNA and hepatocarcinogenesis induced by the relatively specific PPARalpha agonist, Wy-14,643. Interestingly, administration of the less specific PPARalpha agonist, bezafibrate, leads to a modest induction of PPARalpha target genes in the absence of PPARalpha expression.

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