Master of Science, University of Toledo, 2022, Mechanical Engineering

When the COVID-19 pandemic broke out, dental clinics were asked to suspend due to an elevated risk of airborne viral transmission. Dental professionals and their assistants were thought to be at a significantly high risk due to the nature of dental procedures, which result in a high number of aerosolized particles ejected from the dental equipment and oral cavity. Several recommendations were proposed by the Centers for Disease Control and Prevention (CDC) and others to safeguard dental personnel. In this study, we quantitatively examined the efficacy of those safeguards and proposed testing additional ones. To investigate the effects of mitigation strategies on aerosol control in dental practices, we first had to accurately replicate the production of aerosols under common settings in a dental operatory, and then characterize and map particle concentration under altered standard of care practices. Numerous clinical setting scenarios, including those suggested by the CDC, were executed, and their effectiveness in reducing aerosols was assessed by characterizing the rates of aerosol production procedures. The results suggest that dry drilling generates a huge amount of particles and the use of an extraoral suction unit reduces aerosols significantly. Because the study focused on aerosolized and airborne particles, these results can be used in non-clinical situations involving the spread of airborne particles from a point source in confined spaces.

Committee: Omid Amili Dr. (Committee Co-Chair); George Choueiri Dr. (Committee Chair) Subjects: Biomedical Research; Dental Care; Dentistry; Mechanical Engineering; Particle Physics

PHD, Kent State University, 2020, College of Arts and Sciences / Department of Biological Sciences

Cell shrinkage and dehydration are significant, essential, and most reproducible characteristics of apoptosis, Dehydration and fragmentation are the two general mechanisms which are responsible for apoptotic volume decrease (AVD). However, previous authors have not been able to differentiate between these two very different processes and tended to attribute the entire volume decrease to water loss. Based on some theoretical considerations, we believe that such interpretation cannot be correct in all cases. We are now equipped to quantify dehydration and fragmentation and investigate their regulation separately. But to do that, we had to develop new experimental methods. We first developed a method based on calibrated transport of intensity equation (TIE) microscopy combined with transmission-through dye (TTD) microscopy previously developed in our lab. The combination of TTD and TIE allows us to differentiate dehydration from fragmentation and we have demonstrated in various systems that our method works. Second, because intracellular water balance depends on monovalent ions, we had to improve the existing methods for quantification of intracellular ions. That involved some highly original approaches. We developed a method for intracellular potassium measurement. This approach used to calibrate the potassium sensitive fluorescent probe can be further used to quantify intracellular sodium and chloride. These methods enable us to undertake rigorous and quantitative studies of volume and water behavior in various systems where cells undergo apoptotic or necrotic death. We have been able to uncover and explain new paradoxical features of necrotic membrane blebs. We showed that water measurement reveals new features of long-term volume maintenance in anisosmotic environment. We showed that water loss induced by the same apoptotic agent (staurosporine) depends on cell type and attachment. We have been able to circumvent an inherent limitation of many previous studies (open full item for complete abstract)

Committee: Michael Model (Advisor); Derek Damron (Committee Member); Gail Fraizer (Committee Member); Soumitra Basu (Committee Member); Bansidhar Datta (Committee Member) Subjects: Biochemistry; Biology; Biophysics; Cellular Biology; Molecular Biology; Physiology

Doctor of Philosophy, Case Western Reserve University, 2016, Physiology and Biophysics

This thesis examined the mechanisms of neurotransmission underlying feedback inhibition mediated by somatodendritic G-protein coupled dopamine D2-autoreceptors in the ventral tegmental area (VTA), noradrenaline ¿2-autoreceptors in the locus coeruleus (LC), and serotonin 5-HT1A autoreceptors in the dorsal raphe nucleus (DRN). Local feedback inhibition mediated by these GI-coupled monoamine receptors had been speculated to ubiquitously occur via extended transmitter spillover and obligatory extracellular transmitter pooling. Collectively termed volume transmission, these mechanisms of transmission are presumed to result in a tonic, inhibitory tone that modulates the firing rates of monoaminergic neurons in response to slowly changing extracellular concentrations of monoamines. However, evidence for the volume transmission hypothesis is indirect and relies on measuring bulk extracellular monoamine concentrations and predicting receptor activation based on steady-state affinities and mathematical diffusion modeling. In monoamine neurons, autoreceptors couple to G-protein coupled, inwardly rectifying potassium channels (GIRKs) through the ¿¿-subunits of trimetric G-proteins. Activation of somatodendritic autoreceptors by locally released monoamines generates potassium currents that inhibit neuronal excitability. In this thesis, I directly investigated the synaptic mechanisms controlling autoreceptor activity by using electrophysiological methods to measure GIRK-mediated currents in response to evoked transmitter release in rodent brain slices. After characterizing the calcium dependence and clearance of midbrain dopamine transmission to demonstrate species-dependent differences in dopamine transmission, I tested the contributions of spillover and pooling to shaping autoreceptor activation in the dopamine, noradrenaline, and serotonin systems. While both spillover and transmitter pooling contributed to noradrenergic ¿2-autoreceptor activation, dopamine reuptake (open full item for complete abstract)

Committee: Christopher Ford (Advisor) Subjects: Biophysics; Neurosciences; Physiology

Master of Mathematical Sciences, The Ohio State University, 2013, Mathematics

Sleep inertia is known to cause delayed reaction times and general performance deficits immediately after awakening, but specifics manifested in children are not well defined. This research aims to elucidate the effects of sleep inertia in children aged 5 to 12. Results were that younger children sustained slower reaction times than older children at baseline and upon awakening. All age groups had greater impairment after a second awakening, possibly due to a circadian effect and/or cumulative fatigue. All groups had improved reactions in the final 2 minutes of testing compared to the first 2 minutes after awakening (though reaction times were still slower than at baseline), suggesting partial recovery in sleep inertia with increased time. Recovery from sleep inertia may be due to wake-promoting neuromodulators; the increase in concentration may be responsible for improved performance with extended time awake. The current study constructs a model based on volume transmission of these neuromodulators. The model is capable of producing results similar to those observed in individuals with little variance in reaction time, but the model struggles to produce adequate replications of more variable data. Furthermore, the model cannot produce many of the dynamics found in the observed data, suggesting that the current model, if appropriate at all, requires many alterations.

Committee: Best Janet PhD (Advisor); Splaingard Mark MD (Advisor); Dawes Adriana PhD (Committee Member) Subjects: Mathematics