Our experiment is about diabetes and Humalog synthetic insulin crystallization in a microgravity environment. We feel like this is a good experiment to design because we could find out if there is a way to prevent crystallization of insulin, especially if we understand how it happens in microgravity. When insulin crystallizes, the bacteria that usually makes it viable stops working. This would cause it to be ineffective for patients in dire need of this medication. To complete this experiment we are going to keep the insulin in a type 1 FME at the International space station (ISS) at above 65℉ to see if it crystallizes within a certain amount time. We will keep the experiment refrigerated at or below 40℉ during transportation to the ISS and again on arrival back to Earth’s gravity. Refrigeration slows the crystallization growth and this is how it is stored on Earth. Keeping our experiment refrigerated during transportation is an important step because the insulin crystallization growth should only be measured while in microgravity. We will be conducting the same experiment, using the same time frame and refrigeration needs before and after, for our earth bound experiment.

Our experiment is how well will a hornwort plant purify polluted water in microgravity. We will see how it will purify at the same rate as it does in full gravity. We chose this plant because they can purify water and they grow at a fast rate. This will help astronauts because if they run out of water they can grow hornwort even if the only water they have is polluted. Also, it will help them to have purified water if their water system breaks down. The hornwort plant will be growing on the way from Earth to the ISS. The experiment will be purifying the polluted water in microgravity for 5-6 days. Then the formalin will be added to the plant to stop its growth and preserve the sample. We are polluting the water with Cyanobacteria, which is more commonly known as blue green algae. We will know it has worked if the polluted water has become purified after it has been tested.

Previous studies, including those in the Jeffries lab, have shown that female animals are able to fight and survive infection better than males. However, the underlying cause of this difference remains unclear. Because many differences between males and females are due to differences in sex steroid hormone (e.g., estrogen, testosterone, etc.) concentrations, it is possible that differences in immune function are also due to such differences in hormone levels. The objective of this study is to uncover the role of sex steroid hormones in the immune response of fathead minnows (Pimephales promelas). Because females exhibit better pathogen resistance than males, it is hypothesized that estrogen (a “female” hormone) enhances immune system function. The results of this study provides insight into the potential crosstalk between the reproductive and immune systems, as well as a better understanding of the role of sex hormones in the organism.

The fathead minnow (Pimephales promelas), a small fish model often used to screen for reproductive endocrine disrupting compounds, has recently been used by some investigators to screen for chemicals with thyroid disrupting capabilities. However, it is uncertain how known thyroid disruptors affect various markers of thyroid disruption in this species. This study aimed to fill this gap in knowledge by assessing the sensitivity of endpoints known to be responsive to thyroid disruption in other closely-related species in larval fathead minnows. In addition, we sought to uncover how the timing and length of exposure influenced the response of these endpoints. To accomplish these objectives, larval fathead minnows were exposed to various doses of propylthiouracil (PTU; a known thyroid disruptor) and thyroxine (T4; a known thyroid stimulant) for 35 days. Several metrics indicative of alterations in thyroid hormone status (e.g., thyroid related gene expression, growth, thyroid cell follicular height, etc.) were measured on day 7, 21, and 35. The results of this study provide valuable information that can be utilized in developing fathead minnow thyroid disrupting chemical screening assays.

Cancer is the second leading cause of death and will directly affect approximately 40% of the people in the United States over the course of their life. Chemotherapy has been shown to be an effective therapeutic strategy, but it lacks specificity, resulting in a multitude of negative side effects. Targeted therapies such as Herceptin, Iressa, and Nivolumab have shown increased effectiveness against cancer by attacking specific molecules in the target cell. For example, Herceptin inhibits the HER2 protein, which is overproduced in some breast cancer cells, and stops cell division. Biotin is an innate coenzyme for carbohydrate, lipid and protein metabolism. Certain cancer types overexpress biotin transporters on the surface of each cancer cell in order to increase biotin absorption necessary for metabolic processes. Furthermore, the intracellular environment in cancer cells is more reducing compared to non-cancer cells due to increased metabolism. Ferrocene is an iron-based organometallic molecule that has been shown to generate reactive oxygen species (ROS) in the reducing environment of cancer cells. Given that certain cancer cells absorb biotin with a higher efficiency, we hypothesize that linking biotin to ferrocene will increase the efficiency of ferrocene entering the cell and result in selective cancer cell death. Therefore, we have produced a library of biotin-ferrocene conjugates to selectively target cancer cell lines that over express biotin receptor sites. Experiments were conducted utilizing ferrocene and a variety of ferrocene-biotin conjugates (C1, C2, 2) in both cancer (MCF-7) and noncancer (HEK 293) cell lines in order to compare the relative toxicity between compounds.