Chemodynamics of dwarf galaxies under ram-pressure

By implementing a dynamic wind-tunnel model in a smoothed-particle chemodynamic/hydrodynamic simulation suite, we have investigated the effects of ram pressure and tidal forces on dwarf galaxies similar to the Magellanic Clouds, within host galaxies with gas and dark matter halos that are varied, to compare the relative effects of tides and ram pressure. We concentrate on how the distributions of metals are affected by interactions. We find that while ram pressure and tidal forces have some effect on dwarf galaxy outflows, these effects do not produce large differences in the metal distributions of the dwarf disks other than truncation in the outer regions in some cases, and that confinement from the host galaxy gas halo appears to be more significant than ram pressure stripping. We find that stochastic variations in the star formation rate can explain the remaining variations in disk metal properties. This raises questions on the cause of low metallicities in dwarf galaxies.Comment: Submitted to ApJ, under 2nd review (very minor revisions

Chemodynamic evolution of dwarf galaxies in tidal fields

The mass-metallicity relation shows that the galaxies with the lowest mass have the lowest metallicities. As most dwarf galaxies are in group environments, interaction effects such as tides could contribute to this trend. We perform a series of smoothed particle hydrodynamics (SPH) simulations of dwarf galaxies in external tidal fields to examine the effects of tides on their metallicities and metallicity gradients. In our simulated galaxies, gravitational instabilities drive gas inwards and produce centralized star formation and a significant metallicity gradient. Strong tides can contribute to these instabilities, but their primary effect is to strip the outer low-metallicity gas, producing a truncated gas disk with a large metallicity. This suggests that the role of tides on the mass-metallicity relation is to move dwarf galaxies to higher metallicities.Comment: Accepted to Ap

Role of the Cochlear Nucleus Circuitry in Tinnitus and Hyperacusis

Tinnitus is the disorder of phantom sound perception, while hyperacusis is abnormally increased loudness growth. Tinnitus and hyperacusis are both associated with hearing loss, but hearing loss does not always occur with either condition, implicating central neural activity as the basis for each disorder. Furthermore, while tinnitus and hyperacusis can co-occur, either can occur exclusively, suggesting that separate pathological neural processes underlie each disorder. Mounting evidence suggests that pathological neural activity in the cochlear nucleus, the first central nucleus in the auditory pathway, underpins hyperacusis and tinnitus. The cochlear nucleus is comprised of a ventral and dorsal subdivision, which have separate principal output neurons with distinct targets. Previous studies have shown that dorsal cochlear nucleus fusiform cells show tinnitus-related increases in spontaneous firing with minimal alterations to sound-evoked responses. In contrast, sound-evoked activity in ventral cochlear nucleus bushy cells is enhanced following noise-overexposure, putatively underlying hyperacusis. While the fusiform-cell contribution to tinnitus has been well characterized with behavioral and electrophysiological studies, the bushy-cell contribution to tinnitus or hyperacusis has been understudied. This dissertation examines how pathological neural activity in cochlear nucleus circuitry relates to tinnitus and hyperacusis in the following three chapters. In the first chapter, I characterize the development of a high-throughput tinnitus behavioral model, which combines and optimizes existing paradigms. With this model, I show that animals administered salicylate, a drug that reliably induces tinnitus at high doses in both humans and animals, show behavioral evidence of tinnitus in two separate behavioral tests. Moreover, in these same animals, I show that dorsal-cochlear-nucleus fusiform cells exhibit frequency-specific increases in spontaneous firing activity, consistent with the increased spontaneous firing observed in animal models of noise-induced tinnitus. In the second chapter, I show that following noise-overexposure, ventral-cochlear-nucleus bushy cells demonstrate hyperacusis-like neural firing patterns, but not tinnitus-specific increases in spontaneous activity. I contrast the bushy-cell neural activity with established fusiform-cell neural signatures of tinnitus, to highlight the bushy-cell, but not fusiform-cell contribution to hyperacusis. These analyses suggest that tinnitus and hyperacusis likely arise from distinct neural substrates. In the third chapter, I use computational modelling of the auditory periphery and bushy-cell circuitry to examine potential mechanisms that underlie hyperacusis-like neural firing patterns demonstrated in the second chapter. I then relate enhanced bushy-cell firing patterns to alterations in the auditory brainstem response, a sound-evoked electrical potential generated primarily by bushy cells. Findings in this chapter suggest that there are multiple hyperacusis subtypes, arising from separate mechanisms, which could be diagnosed through fine-tuned alterations to the auditory brainstem response.PHDBiomedical EngineeringUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/163087/1/damartel_1.pd

Star Formation History in Barred Spiral Galaxies. AGN Feedback

We present a numerical study of the impact of AGN accretion and feedback on the star formation history of barred disc galaxies. Our goal is to determine whether the effect of feedback is positive (enhanced star formation) or negative (quenched star formation), and to what extent. We performed a series of 12 hydrodynamical simulations of disc galaxies, 10 barred and 2 unbarred, with various initial gas fractions and AGN feedback prescriptions. In barred galaxies, gas is driven toward the centre of the galaxy and causes a starburst, followed by a slow decay, while in unbarred galaxies the SFR increases slowly and steadily. AGN feedback suppresses star formation near the central black hole. Gas is pushed away from the black hole, and collides head-on with inflowing gas, forming a dense ring at a finite radius where star formation is enhanced. We conclude that both negative and positive feedback are present, and these effects mostly cancel out. There is no net quenching or enhancement in star formation, but rather a displacement of the star formation sites to larger radii. In unbarred galaxies, where the density of the central gas is lower, quenching of star formation near the black hole is more efficient, and enhancement of star formation at larger radii is less efficient. As a result, negative feedback dominates. Lowering the gas fraction reduces the star formation rate at all radii, whether or not there is a bar or an AGN.Comment: 18 pages, 17 figures. Accepted for publication in MNRA

Poultry as a host for the zoonotic pathogen Campylobacter jejuni

Campylobacteriosis is the most reported foodborne gastroenteritic disease and poses a serious health burden in industrialized countries. Disease in humans is mainly caused by the zoonotic pathogen Campylobacter jejuni. Due to its wide-spread occurrence in the environment, the epidemiology of Campylobacter remains poorly understood. It is generally accepted, however, that chickens are a natural host for Campylobacter jejuni, and for Campylobacter spp. in general, and that colonized broiler chicks are the primary vector for transmitting this pathogen to humans. Several potential sources and vectors for transmitting C. jejuni to broiler flocks have been identified. Initially, one or a few broilers can become colonized at an age of >2 weeks until the end of rearing, after which the infection will rapidly spread throughout the entire flock. Such a flock is generally colonized until slaughter and infected birds carry a very high C. jejuni load in their gastrointestinal tract, especially the ceca. This eventually results in contaminated carcasses during processing, which can transmit this pathogen to humans. Recent genetic typing studies showed that chicken isolates can frequently be linked to human clinical cases of Campylobacter enteritis. However, despite the increasing evidence that the chicken reservoir is the number one risk factor for disease in humans, no effective strategy exists to reduce Campylobachter prevalence in poultry flocks, which can in part be explained by the incomplete understanding of the epidemiology of C. jejuni in broiler flocks. As a result, the number of human campylobacteriosis cases associated with the chicken vector remains strikingly high