Damage to the Central Nervous System (CNS), such as traumatic brain injury (TBI) can often lead to a systemic inflammatory response since inflammatory mediators can be carried through the cardiovascular system. Past studies indicate that this inflammatory response that started at the CNS can increase the risk of heart disease. This growing interest in the heart-brain axis led our lab to explore if there is any impact of TBI on cardiac function and remodeling. TBI has been shown to have short-term effects on the heart, but few studies evaluate the long-term impact of TBI on the heart. To analyze any long-term impacts, we extracted hearts from rats 6 months post TBI, or sham that had been treated with vehicle or lipopolysaccharide (LPS) injections. LPS was administered to assess how inflammation could impact protein expression in the heart. Reactive oxygen species (ROS) targets such as NOX2, NOX4, SOD1, SOD2, catalase, and osteopontin were measured as potential indicators of cardiac remodeling. Rats that received vehicle TBI and LPS TBI resulted in no statistically significant differences (p>0.05) when evaluated as fold-change over the vehicle. This trend was consistent when normalizing to LPS sham. Since there were no changes in ROS targets, the hypothesis that there is long-term cardiac remodeling in the heart post-TBI was rejected. Further investigation is warranted since the present design of this study may not be ideal for evaluating long-term impact as histology samples were not obtained nor cardiac function assessments.

Cyanobacteria and microalgae help reduce the environmental impact of human energy consumption by playing a vital role in carbon and nitrogen cycling. They are also used in various applications like biofuel production, food, medicine, and bioremediation. Understanding how these organisms respond to stress is important for efficient recovery strategies and sustainable outcomes. This study investigated the effects of low-level bleaching and thermal stress on cyanobacteria and microalgae, specifically Synechocystis, Chlorella, and Scenedesmus. The role of ferroptosis, an iron-dependent form of cell death, in the degradation of cellular components under these stressors was examined. Flow cytometry and spectrophotometry were used to measure changes in cellular health and viability. The results showed that temperature influences the type of cell death mechanism and can impact photosynthetic organisms. When treated with Liproxstatin-1, an inhibitor of ferroptosis, both Synechocystis and Chlorella experienced a decrease in oxidative damage, suggesting a potential protective role for the compound. Further investigation into ferroptosis and other forms of cell death, as well as identifying additional inhibitory molecules, could lead to strategies for mitigating oxidative stress and enhancing the resilience of cyanobacteria and microalgae.