Immunological Tradeoffs and the Impacts of Urbanization on the Reproductive Ecology and Physiology of the Side-Blotched Lizard (\u3cem\u3eUta stansburiana\u3c/em\u3e)

Investing resources into reproduction can limit energy available to other competing demands, such as fighting off an infection; yet, both processes are necessary for organisms to survive and pass on their genes to the next generation. These strategies often follow patterns associated with lifespan, such that shorter-lived animals are more likely to invest more resources into reproduction over survival, and vice versa in long-lived animals. However, environmental change caused by urbanization can disrupt these relationships, and the within- and transgenerational costs of urbanization on females and offspring are unknown. I address these uncertainties in three research chapters to better understand the effects of urbanization on reproductive investment in female Side-blotched Lizards (Uta stansburiana), a small and abundant species of reptile found throughout the western United States. In my second chapter, I examine general variation in female immunity and stress and how it relates to egg number, egg mass, and egg yolk immunity and stress. I found oxidative stress and immunity vary in females depending on how many eggs they produced, and that larger eggs had lower yolk stress levels. I built upon this by examining how metabolism differs across the reproductive cycle and tested whether simulating an infection in females affected immunity, stress, and metabolism. Metabolism was higher at the onset of reproduction and decreased until ovulation, and females differentially responded to infection depending on their stage in the reproductive cycle, which may suggest limited resources underly these findings. In my final chapter, I investigated the impacts of urbanization on female and egg yolk physiology and tested whether simulating infection altered female investment into egg yolk. I found immunity and stress in females and eggs were only apparent in rural females with ectoparasites, but not in urban females and eggs. Fertilization rates were lower in urban populations, which also influenced egg yolk physiology. Differential physiological investment can drastically alter offspring traits; therefore, it is imperative to develop a better understanding of the transgenerational costs of inhabiting an urban environment

Experimental validation of phase space conduits of transition between potential wells

A phase space boundary between transition and non-transition, similar to those observed in chemical reaction dynamics, is shown experimentally in a macroscopic system. We present a validation of the phase space flux across rank one saddles connecting adjacent potential wells and confirm the underlying phase space conduits that mediate the transition. Experimental regions of transition are found to agree with the theory to within 1\%, suggesting the robustness of phase space conduits of transition in a broad array of two or more degree of freedom experimental systems, despite the presence of small dissipation.Comment: 7 pages, 6 figure

Computing fractal dimension in supertransient systems directly, fast and reliable

Chaotic transients occur in many experiments including those in fluids, in simulations of the plane Couette flow, and in coupled map lattices and they are a common phenomena in dynamical systems. Superlong chaotic transients are caused by the presence of chaotic saddles whose stable sets have fractal dimensions that are close to phase-space dimension. For many physical systems chaotic saddles have a big impact on laboratory measurements, and it is important to compute the dimension of such stable sets including fractal basin boundaries through a direct method. In this work, we present a new method to compute the dimension of stable sets of chaotic saddles directly, fast, and reliable.Comment: 6 pages, 3 figure

What Does the Snake Eat? Breadth, Overlap, and Non-Native Prey in the Diet of Three Sympatric Natricine Snakes

We investigated diet breadth and diet overlap in three sympatric snakes of similar body size: Dekay’s Brownsnakes (Storeria dekayi), Red-bellied Snakes (S. occipitomaculata), and sub-adult Common Gartersnakes (Thamnophis sirtalis), by examining recently consumed prey (n = 388) collected from wild-caught snakes (n = 263) in northern Illinois. Storeria occipitomaculata were dietary specialists, feeding nearly exclusively on slugs. Storeria dekayi fed predominately on slugs but also consumed snails and earthworms. Sub-adult T. sirtalis fed predominately on earthworms but also consumed frogs and small mammals. Diet overlap was extensive between Storeria species but relatively low between Storeria and Thamnophis. It is noteworthy that the two most abundant prey types, slugs and earthworms, are non-native. These non-native prey occur in high numbers, which may ameliorate competitive interactions and influence grassland snake abundance and persistence regionally

Local Entropy Characterization of Correlated Random Microstructures

A rigorous connection is established between the local porosity entropy introduced by Boger et al. (Physica A 187, 55 (1992)) and the configurational entropy of Andraud et al. (Physica A 207, 208 (1994)). These entropies were introduced as morphological descriptors derived from local volume fluctuations in arbitrary correlated microstructures occuring in porous media, composites or other heterogeneous systems. It is found that the entropy lengths at which the entropies assume an extremum become identical for high enough resolution of the underlying configurations. Several examples of porous and heterogeneous media are given which demonstrate the usefulness and importance of this morphological local entropy concept.Comment: 15 pages. please contact [email protected] and have a look at http://www.ica1.uni-stuttgart.de/ . To appear in Physica

Rescaling Relations between Two- and Three-dimensional Local Porosity Distributions for Natural and Artificial Porous Media

Local porosity distributions for a three-dimensional porous medium and local porosity distributions for a two-dimensional plane-section through the medium are generally different. However, for homogeneous and isotropic media having finite correlation-lengths, a good degree of correspondence between the two sets of local porosity distributions can be obtained by rescaling lengths, and the mapping associating corresponding distributions can be found from two-dimensional observations alone. The agreement between associated distributions is good as long as the linear extent of the measurement cells involved is somewhat larger than the correlation length, and it improves as the linear extent increases. A simple application of the central limit theorem shows that there must be a correspondence in the limit of very large measurement cells, because the distributions from both sets approach normal distributions. A normal distribution has two independent parameters: the mean and the variance. If the sample is large enough, LPDs from both sets will have the same mean. Therefore corresponding distributions are found by matching variances of two- and three-dimensional local porosity distributions. The variance can be independently determined from correlation functions. Equating variances leads to a scaling relation for lengths in this limit. Three particular systems are examined in order to show that this scaling behavior persists at smaller length-scales.Comment: 15 PostScript figures, LaTeX, To be published in Physica

Differentiation and Protective Capacity of Virus-Specific CD8

Noroviruses can establish chronic infections with active viral shedding in healthy humans but whether persistence is associated with adaptive immune dysfunction is unknown. We used genetically engineered strains of mouse norovirus (MNV) to investigate CD8+ T cell differentiation during chronic infection. We found that chronic infection drove MNV-specific tissue-resident memory (Trm) CD8+ T cells to a differentiation state resembling inflationary effector responses against latent cytomegalovirus with only limited evidence of exhaustion. These MNV-specific Trm cells remained highly functional yet appeared ignorant of ongoing viral replication. Pre-existing MNV-specific Trm cells provided partial protection against chronic infection but largely ceased to detect virus within 72 hours of challenge, demonstrating rapid sequestration of viral replication away from T cells. Our studies revealed a strategy of immune evasion by MNV via the induction of a CD8+ T cell program normally reserved for latent pathogens and persistence in an immune-privileged enteric niche. Chronic infections often cause T cell dysfunction, but how noroviruses (NV) evade immunity is unknown. Tomov et al. show that gut-resident T cells against NV remain functional but ignorant of chronic viral replication, suggesting that NV persists in an immune-privileged enteric niche. © 2017 Elsevier Inc

Type I interferon receptor deficiency in dendritic cells facilitates systemic murine norovirus persistence despite enhanced adaptive immunity

In order for a virus to persist, there must be a balance between viral replication and immune clearance. It is commonly believed that adaptive immunity drives clearance of viral infections and, thus, dysfunction or viral evasion of adaptive immunity is required for a virus to persist. Type I interferons (IFNs) play pleiotropic roles in the antiviral response, including through innate control of viral replication. Murine norovirus (MNoV) replicates in dendritic cells (DCs) and type I IFN signaling in DCs is important for early control of MNoV replication. We show here that the non-persistent MNoV strain CW3 persists systemically when CD11c positive DCs are unable to respond to type I IFN. Persistence in this setting is associated with increased early viral titers, maintenance of DC numbers, increased expression of DC activation markers and an increase in CD8 T cell and antibody responses. Furthermore, CD8 T cell function is maintained during the persistent phase of infection and adaptive immune cells from persistently infected mice are functional when transferred to Rag1-/- recipients. Finally, increased early replication and persistence are also observed in mixed bone marrow chimeras where only half of the CD11c positive DCs are unable to respond to type I IFN. These findings demonstrate that increased early viral replication due to a cell-intrinsic innate immune deficiency is sufficient for persistence and a functional adaptive immune response is not sufficient for viral clearance

Interferons Regulate the Phenotype of Wild-type and Mutant Herpes Simplex Viruses In Vivo

Mechanisms responsible for neuroattenuation of herpes simplex virus (HSV) have been defined previously by studies of mutant viruses in cultured cells. The hypothesis that null mutations in host genes can override the attenuated phenotype of null mutations in certain viral genes was tested. Mutants such as those in infected cell protein (ICP) 0, thymidine kinase, ribonucleotide reductase, virion host shutoff, and ICP34.5 are reduced in their capacity to replicate in nondividing cells in culture and in vivo. The replication of these viruses was examined in eyes and trigeminal ganglia for 1–7 d after corneal inoculation in mice with null mutations (−/−) in interferon receptors (IFNR) for type I IFNs (IFN-α/βR), type II IFN (IFN-γR), and both type I and type II IFNs (IFN-α/β/γR). Viral titers in eyes and ganglia of IFN-γR−/− mice were not significantly different from congenic controls. However, in IFN-α/βR−/− or IFN-α/β/γR−/− mice, growth of all mutants, including those with significantly impaired growth in cell culture, was enhanced by up to 1,000-fold in eyes and trigeminal ganglia. Blepharitis and clinical signs of infection were evident in IFN-α/βR−/− and IFN-α/β/γR−/− but not control mice for all viruses. Also, IFNs were shown to significantly reduce productive infection of, and spread from intact, but not scarified, corneas. Particularly striking was restoration of near-normal trigeminal ganglion replication and neurovirulence of an ICP34.5 mutant in IFN-α/βR−/− mice. These data show that IFNs play a major role in limiting mutant and wild-type HSV replication in the cornea and in the nervous system. In addition, the in vivo target of ICP34.5 may be host IFN responses. These experiments demonstrate an unsuspected role for host factors in defining the phenotypes of some HSV mutants in vivo. The phenotypes of mutant viruses therefore cannot be interpreted based solely upon studies in cell culture but must be considered carefully in the context of host factors that may define the in vivo phenotype