Neotropical rain frogs serve as an indicator of habitat and ecological disruption in tropical rainforests through species-specific response to environmental stimuli. These responses are reflected in preference of habitat, such as primary or secondary forest, which may provide insights into the health and stability of not only Neotropical rain frogs and amphibians, but also of the surrounding ecosystem. We studied the diversity and abundance of rain frogs at the El Jamaical Field Station in Costa Rica, located in a transition zone between tropical rainforest and premontane rainforest, by overturning leaf litter along previously established trails that passed through both forest types, photographing found individuals, and recording discovery locations on a map. Focusing our study on the primary and secondary forests, we predicted that the diversity and abundance of rain frogs would be greater in the primary forest than in the secondary due to differences in diversity of trees and flora, humidity, temperature, and light levels. Data analysis will include species identification, proximity to dry streams, and comparison between primary and secondary forest.

The Syr Darya, one of the largest rivers in southern Kazakhstan, is a major source of freshwater feeding the Aral Sea. In the 1950s, water was diverted from the Syr Darya to support agricultural production leading to the drying of the Aral Sea, which has been characterized as one of the worst environmental catastrophes in modern day history. Mismanagement of these diverted waters has paved the way for potential surface water contamination in the Aral Sea Basin. While efforts to revive the Aral Sea are underway, few investigations have sought to assess the impacts of potential heavy metal contamination in the Syr Darya Watershed. As such, the goal of this study was to assess the presence and biological effects of heavy metal contaminants in the Syr Darya. This was accomplished by collecting water and sediment samples from five sites and roach (Rutilus rutilus) samples from three sites along the Syr Darya. Water, sediment, and roach muscle tissue samples were analyzed for a suite of contaminants, while roach liver, brain, gonad, and gill tissues were analyzed for the expression of genes considered to be biomarkers of heavy metal exposures (e.g., metallothionein and superoxide dismutase). Water and fish muscle tissue analysis revealed the presence of multiple heavy metals above local regulatory limits. Roach fish from two of the three sites experienced alterations in the expression of genes considered biomarkers of contaminant exposure suggesting that chemical loads at some of the sites in the Syr Darya were sufficient to induce biological effects. Data collected as part of this study will be utilized to complete an ecological risk assessment of the Syr Darya River basin.

Alzheimer’s disease is a neurodegenerative disorder characterized by the presence of amyloid beta (Aβ) plaques. This pathology results in neuronal dysfunction and eventual cell death. Aβ plaques come from the buildup of beta-amyloid protein which clump together and block cell-to-cell signaling at synapses. To stimulate Aβ production, our lab uses an inflammation model utilizing lipopolysaccharide (LPS) injections. When mice are given intraperitoneal LPS injections over the course of one week they show a significant increase of Aβ in the brain. When a second course of LPS is administered following a two-week recovery period, Aβ levels return to baseline levels. The initial exposure to LPS protects the mouse from a second exposure, preventing further increase in the Aβ. One likely explanation is that the initial exposure primes the immune system, enabling the mouse to quickly initiate an antibody response upon subsequent exposure to LPS. The objective of the present study was to investigate the antibodies produced after the second course of LPS in 5xFAD mice. Plasma antibody levels were measured, and co-localization of antibodies around hippocampal Aβ plaques was investigated. We found that mice who received a second course of LPS injections had a significantly higher amount of IgG co-localized around plaques compared to non-treated control animals. This correlated with higher levels of IgG in the plasma. This data suggests that LPS exacerbates the antibody response in 5xFAD mice, and that these antibodies may specifically target Aβ.

Changes in early physiological development due to chemical effluent exposure can be determined by measuring the levels of gene expression. Genes involved in cardiovascular and neurological development, as well as growth, serve as sensitive endpoints in toxicity tests involving the use of larvae. The purpose of this research was to determine when during development the level of gene expression was high enough for contaminant-induced decreases in expression to be detected. A suite of genes involved in growth, cardiovascular and neurological development was examined in embryos and larvae from 0 to 11 days post hatch. This information was used to determine time points at which selected genes were most highly expressed. For the growth-related genes, expression levels of growth hormone (gH) were highest at Days 4-7 and 11, levels of growth hormone receptor (gHR) at Days 1-7 and 11, and levels of insulin-like growth factor (igf1) at Days 4-11. For the thyroid hormone receptors, thyroid hormone receptor-α (TRα) showed highest expression levels at Days 3-11 and thyroid hormone receptor-β (TRβ) showed highest levels at Days 2-5 and 9. For the deiodinase enzymes, deiodinase-1 (Dio1) expression levels were highest at Days 2-3 and 7-11, levels of deiodinase-2 (Dio2) were highest at Days 7-11, and levels of deiodinase-3 (Dio3) were highest at Days 1-5. Vegfa, a gene involved in cardiovascular development, had levels of gene expression that were highest at days 7-11. HuC, a gene involved in neurological development, had the highest level of gene expression at days 7-11. When the level of expression of these genes is highest is when they have the greatest potential to be used in toxicity tests to measure alterations in expression.

Cancer is the second-leading cause of death in the US. Cancer cells are characterized by loss of regulation of the cell cycle that results in uncontrolled proliferation. To drive this high rate of cellular division, cancer cells have mutated to increase uptake of important nutrients including glucose and vitamins by increasing the number of glucose receptors and vitamin transporters, including biotin receptor, on their surface. Due to this difference in expression of biotin receptor between cancer and normal cells, research focusing on the use of biotin-conjugated molecules has gained attention as a method for anticancer drug delivery.
Another characteristic unique to certain cancer cells is that they exhibit dysregulation in normal cellular redox balance, such that the cellular environment becomes more reducing. A more reducing environment favors the generation of reactive oxygen species (ROS). Many metal-based anticancer drugs have taken advantage of this feature of cancer cells in an attempt to increase the levels of ROS to the point that harmful oxidation reactions occur that lead to cell death. Specifically, the iron atom of ferrocene has been shown to lead to the generation of damaging ROS upon oxidation from Fe2+ to Fe3+.
A problem with current cancer treatment is that the chemotherapeutics often are not specific to cancer cells and can lead to negative side effects. As a result, anticancer drugs with high specificity and cytotoxicity are needed to improve treatments. This research project focuses on testing the cytotoxicity of a variety of biotin-ferrocene derivatives on cancer (HeLa) and non-cancer (293HEK) cell lines. HeLa cells are known to express high levels of biotin receptor and are predicted to have more reducing cellular environments; additionally, 293HEK cells express low levels of biotin receptor and are predicted to have less reducing environments. The tested compounds have three main features: a biotin moiety, a ferrocene core, and a variable linker covalently bound to the ferrocene moiety. We hypothesize that the biotin-containing compounds will enter HeLa cells more efficiently than 293HEK cells, allowing for the ferrocene moiety to reduce oxygen, leading to increased ROS generation and cell death.
Here, we demonstrate that ferrocene shows dose-dependent cytotoxicity specific to HeLa cells, while one of the compounds shows dose-dependent cytotoxicity specific to 293HEK cells. Interestingly, two of the compounds show dose-dependent cytotoxicity to both cell lines. These findings are particularly intriguing in that there appears to be a difference in specificity between some of the compounds. However, future studies are required to reveal how these differences in cytotoxicity are related to the differences in chemical moieties and by what mechanisms these compounds are acting to cause specific cytotoxicity.