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- Creators: Barrett, The Honors College
Non-native consumers can significantly alter processes at the population, community, and ecosystem level, and they are a major concern in many aquatic systems. Although the community-level effects of non-native anuran tadpoles are well understood, their ecosystem-level effects have been less studied. Here, I tested the hypothesis that natural densities of non-native bullfrog tadpoles (Lithobates catesbeianus) and native Woodhouse's toad tadpoles (Anaxyrus woodhousii) have dissimilar effects on aquatic ecosystem processes because of differences in grazing and nutrient recycling (excretion and egestion). I measured bullfrog and Woodhouse's carbon, nitrogen, and phosphorus nutrient recycling rates. Then, I determined the impact of tadpole grazing on periphyton biomass (chlorophyll a) during a 39-day mesocosm experiment. Using the same experiment, I also quantified the effect of tadpole grazing and nutrient excretion on periphyton net primary production (NPP). Lastly I measured how dissolved and particulate nutrient concentrations and respiration rates changed in the presence of the two tadpole species. Per unit biomass, I found that bullfrog and Woodhouse's tadpoles excreted nitrogen and phosphorus at similar rates, though Woodhouse's tadpoles egested more carbon, nitrogen, and phosphorus. However, bullfrogs recycled nutrients at higher N:C and N:P ratios. Tadpole excretion did not cause a detectable change in dissolved nutrient concentrations. However, the percent phosphorus in mesocosm detritus was significantly higher in both tadpole treatments, compared to a tadpole-free control. Neither tadpole species decreased periphyton biomass through grazing, although bullfrog nutrient excretion increased areal NPP. This result was due to higher biomass, not higher biomass-specific productivity. Woodhouse's tadpoles significantly decreased respiration in the mesocosm detritus, while bullfrog tadpoles had no effect. This research highlights functional differences between species by showing non-native bullfrog tadpoles and native Woodhouse's tadpoles may have different effects on arid, aquatic ecosystems. Specifically, it indicates bullfrog introductions may alter primary productivity and particulate nutrient dynamics.
AAbs provide value in identifying individuals at risk, stratifying patients with different clinical courses, improving our understanding of autoimmune destructions, identifying antigens for cellular immune response and providing candidates for prevention trials in T1D. A two-stage serological AAb screening against 6,000 human proteins was performed. A dual specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) was validated with 36% sensitivity at 98% specificity by an orthogonal immunoassay. This is the first systematic screening for novel AAbs against large number of human proteins by protein arrays in T1D. A more comprehensive search for novel AAbs was performed using a knowledge-based approach by ELISA and a screening-based approach against 10,000 human proteins by NAPPA. Six AAbs were identified and validated with sensitivities ranged from 16% to 27% at 95% specificity. These two studies enriched the T1D “autoantigenome” and provided insights into T1D pathophysiology in an unprecedented breadth and width.
The rapid rise of T1D incidence suggests the potential involvement of environmental factors including viral infections. Sero-reactivity to 646 viral antigens was assessed in new-onset T1D patients. Antibody positive rate of EBV was significantly higher in cases than controls that suggested a potential role of EBV in T1D development. A high density-NAPPA platform was demonstrated with high reproducibility and sensitivity in profiling anti-viral antibodies.
This dissertation shows the power of a protein-array based immunoproteomics approach to characterize humoral immunoprofile against human and viral proteomes. The identification of novel T1D-specific AAbs and T1D-associated viruses will help to connect the nodes in T1D etiology and provide better understanding of T1D pathophysiology.