Welcome to the UA Campus Repository, a service of the University of Arizona Libraries. The repository shares, archives and preserves unique digital materials from faculty, staff, students and affiliated contributors. Contact us at firstname.lastname@example.org with any questions.
- The UA Campus Repository team is thrilled about the launch of our sister repository, ReDATA. To deposit research datasets and code, please use the newly created UA Research Data Repository (ReDATA). ReDATA will curate the data and provide a DOI upon publication. Access is currently by request only. To obtain access, please contact email@example.com.
- Doctoral posters and theses from Spring 2020 graduates are now available in the College of Medicine - Phoenix Scholarly Projects collection.
- Have you heard about the site Aguada Fénix, a monument discovered by an international team led by Professors Takeshi Inomata and Daniela Triadan from the UA School of Anthropology? Learn more about their discovery in this UA News article and explore related reports and data in the Middle Usumacinta Archaeological Project collection.
- Master's reports from Spring 2020 graduates are now available in the MS-GIST Master's Reports collection.
- Theses and posters from Spring 2020 graduates are now available in the Sustainable Built Environments Senior Capstones collection.
- The Archive and the Guide Series, published by the Center for Creative Photography (CCP), are now available in the repository. The volumes highlight materials in the CCP's research collections.
- Rangelands Volumes 1-38 (1979-2016) are now available in the Campus Repository. These publically available journal archives are made available by the University of Arizona Libraries in partnership with the Society for Range Management.
- Are you interested in women's history and agriculture in Arizona? Special Collections at the University of Arizona Libraries has digitized Reports of the Home Demonstration Agents. These documents provide a window into Arizona life from 1918-1958.
- The Arizona Geological Survey continues to add new content, from reports and maps to geospatial data, to the Campus Repository. Explore the latest materials in the AZGS Document Repository.
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Simple Paper-based Liver Cell Model for Drug ScreeningInvestigation of the potential adverse effects of chemicals and drugs is essential during the drug development process.In vitrocell model systems have been developed over the past years towards such toxicity investigation. 96-well plate is the common platform for screening drug toxicity due to its simplicity. However, this platform only offers 2D cell culture environment and lacks the flow of solutions, which fails to provide the suitable environment for the cells to adequately metabolize the drugs, for the media to replenish, and for the metabolites and wastes to be removed. Microfluidic chips populated with human or animal cells, known as organ-on-a-chip (OOC), can reconcile many issues ofin vitrocell models, such as the lack of extracellular matrix and flow as well as the species difference. However, OOC can be complicated to fabricate and operate. To bridge this gap, we utilized paper as a primary substrate for OOC, considering its fibrous structure that can mimic natural extracellular matrix, as well as a syringe pump and filter that are commonly available in most laboratories. Paper microfluidic model was designed and fabricated by wax printing on nitrocellulose paper, seeded and proliferated with liver cells (primary rat hepatocytes and HepG2 cells), and two paper substrates were stacked together to complete the paper model. To this paper-based liver cell model, the following drugs were added: Phenacetin (pain reliever and fever reducer), Bupropion (antidepressant), Dextromethorphan (antidepressant), and phosphate-buffered saline (PBS) as a control, all under a physiologically relevant flow rate. The combination of these drugs with Fluconazole (antifungal drug) was also investigated. Cell count, cell morphology, protein production, and urea secretion after drug treatment confirmed that the model successfully predicted toxicity within 40 minutes. This simple, paper-based liver cell model provided enhanced and faster cell response to drug toxicity and showed comparable or better behavior than the cells cultured in conventional 2Din vitromodels.
Using Continuous Glucose Monitoring to Motivate Physical Activity in Overweight and Obese Adults: A Pilot StudyBackground: Regular physical activity (PA) is associated with a lower risk of several types of cancers. However, two-thirds of overweight/obese adults are not sufficiently active; this, in combination with the unfavorable effect of excess body weight, puts them at a greater risk for cancer. One reason that these individuals do not engage in enough PA may be their lack of motivation to change their current behavior due to the perception of putting in effort for possible future gain without obvious short-term benefits. There is a need for innovative ways to help individuals recognize the immediate health benefits of PA and thus increase their motivation. Methods: This pilot intervention tested a PA education module that included a one-on-one counseling session highlighting the acute effects of PA on glucose patterns, followed by a 10-day self-monitoring period with a continuous glucose monitor (CGM) and a Fitbit tracker. Participants rated the acceptability of the education module on a 5-point Likert scale and completed surveys assessing stages of change for motivational readiness. Results: Nineteen overweight/obese adults (84% female) completed the study. Participants gave high ratings to the counseling session for improving their PA-related knowledge (mean 4.22), increasing motivation (mean 4.29), and providing personally relevant information (mean 4.35). The summary acceptability scores for the self-monitoring period were 4.46 for CGM and 4.51 -for Fitbit. Participants reported a significant decrease in the precontemplation stage and an increase in the action stage (P < 0.05). Conclusions: CGM is a feasible tool for PA interventions. Impact: Information from CGM could be used as biologicalbased feedback to motivate PA.
Monte Carlo simulations of electron-sample interactions at phase boundaries and implications for automated mineralogyAutomated mineralogy instrumentation (QEMSCAN, MLA, TIMA) is routinely used for materials characterization in the mining industry. All current techniques identify minerals based on a combination of backscattered electron and chemical (energy-dispersive spectroscopy) signals read from the sample. Boundary zones, where two or more minerals are touching, yield signals that reflect a mix of the characteristics of multiple minerals and that may or may not match anything in the mineral database. These phase boundaries, varying in width, are known to cause errors in automated mineralogy analyses, but what mineral and boundary characteristics affect phase boundary width and how much error phase boundaries can cause remain poorly understood. New Monte Carlo modeling of electron-sample interactions at and near phase boundaries shows that the width of the zone of mixed signals, and hence the amount of error, depends on the grain size and texture of the sample; the densities of the minerals and the ionization potentials of their constituent elements; and the position and orientation of the boundary between the minerals, as well as various instrumental factors such as beam accelerating voltage. Error induced by phase boundaries is high when a high accelerating voltage is used to examine fine-grained samples with complex (intergrowth, exsolution) textures that involve low-density minerals with low-ionization-potential elements. Error is low when the sample is coarse-grained, lacks complex textural relationships that create boundary area, and consists of high-density minerals with high-ionization-potential elements, which have a higher electron stopping power and prevent the beam from spreading out as much. Where low- and high-density minerals are in contact at an angled boundary, the width of the boundary zone is low when the high-density mineral is on top and high when the low-density phase is on top. Calculations based on these simulations indicate that the amount of area that could fall within phase boundary zones depends strongly on grain size, shape, and width of boundary zone. Boundary phases may contribute significantly to overall analytical error for fine-grained minerals with low densities and composed of elements with low ionization potentials, but for most samples the boundary phase area is likely to be < 5% of the total surface area and the error relatively small. Errors induced by boundary phases will probably continue to annoy geometallurgists for some time, but with proper laboratory procedures for validating and cross-checking automated mineralogy results, they should not be a major component of error for most samples.
Formoterol, a β-adrenoreceptor agonist, induces mitochondrial biogenesis and promotes cognitive recovery after traumatic brain injuryTraumatic brain injury (TBI) leads to acute necrosis at the site of injury followed by a sequence of secondary events lasting from hours to weeks and often years. Targeting mitochondrial impairment following TBI has shown improvements in brain mitochondrial bioenergetics and neuronal function. Recently formoterol, a highly selective β2-adrenoreceptor agonist, was found to induce mitochondrial biogenesis (MB) via Gβγ-Akt-eNOS-sGC pathway. Activation of MB is a novel approach that has been shown to restore mitochondrial function in several disease and injury models. We hypothesized that activation of MB as a target of formoterol after TBI would mitigate mitochondrial dysfunction, enhance neuronal function and improve behavioral outcomes. TBI-injured C57BL/6 male mice were injected (i.p.) with vehicle (normal saline) or formoterol (0.3 mg/kg) at 15 min, 8 h, 16 h, 24 h and then daily after controlled cortical impact (CCI) until euthanasia. After CCI, mitochondrial copy number and bioenergetic function were decreased in the ipsilateral cortex of the CCI-vehicle group. Compared to CCI-vehicle, cortical and hippocampal mitochondrial respiration rates as well as cortical mitochondrial DNA copy number were increased in the CCI-formoterol group. Mitochondrial Ca2+ buffering capacity in the hippocampus was higher in the CCI-formoterol group compared to CCI-vehicle group. Both assessments of cognitive performance, novel object recognition (NOR) and Morris water maze (MWM), decreased following CCI and were restored in the CCI-formoterol group. Although no changes were seen in the amount of cortical tissue spared between CCI-formoterol and CCI-vehicle groups, elevated levels of hippocampal neurons and improved white matter sparing in the corpus callosum were observed in CCI-formoterol group. Collectively, these results indicate that formoterol-mediated MB activation may be a potential therapeutic target to restore mitochondrial bioenergetics and promote functional recovery after TBI.
β-adrenergic receptor-mediated mitochondrial biogenesis improves skeletal muscle recovery following spinal cord injuryIn addition to local spinal cord dysfunction, spinal cord injury (SCI) can result in decreased skeletal muscle mitochondrial activity and muscle atrophy. Treatment with the FDA-approved β2-adrenergic receptor (ADRB2) agonist formoterol has been shown to induce mitochondrial biogenesis (MB) in both the spinal cord and skeletal muscle and, therefore, has the potential to address comprehensive mitochondrial and organ dysfunction following SCI. Female C57BL/6 mice were subjected to moderate contusion SCI (80 Kdyn) followed by daily administration of vehicle or formoterol beginning 8 h after injury, a clinically relevant time-point characterized by a 50% decrease in mtDNA content in the injury site. As measured by the Basso Mouse Scale, formoterol treatment improved locomotor recovery in SCI mice compared to vehicle treatment by 7 DPI, with continued recovery observed through 21 DPI (3.5 v. 2). SCI resulted in 15% body weight loss in all mice by 3 DPI. Mice treated with formoterol returned to pre-surgery weight by 13 DPI, while no weight gain occurred in vehicle-treated SCI mice. Remarkably, formoterol-treated mice exhibited a 30% increase in skeletal muscle mass compared to those treated with vehicle 21 DPI (0.93 v. 0.72% BW), corresponding with increased MB and decreased skeletal muscle atrophy. These effects were not observed in ADRB2 knockout mice subjected to SCI, indicating that formoterol is acting via the ADRB2 receptor. Furthermore, knockout mice exhibited decreased basal spinal cord and skeletal muscle PGC-1α expression, suggesting that ADRB2 may play a role in mitochondrial homeostasis under physiological conditions. These data provide evidence for systemic ADRB2-mediated MB as a therapeutic avenue for the treatment of SCI.