The rowing study aims to delve into the potential benefits of interval training compared to conventional rowing, particularly concerning its impact on overall muscle fatigue. By scrutinizing this aspect, the study seeks to uncover insights that could ... prove invaluable, especially for individuals with lower muscle fitness levels. Understanding whether interval training induces less muscle fatigue than traditional rowing holds significant promise for enhancing training methodologies and optimizing fitness routines. This investigation holds promise for several reasons. First and foremost, it addresses a critical gap in current understanding regarding the comparative effects of different training modalities on muscle fatigue. By elucidating whether interval training offers a potential advantage in mitigating overall muscle fatigue, the study could pave the way for more tailored and effective exercise prescriptions, particularly for those with lower baseline muscle fitness. Furthermore, the implications extend beyond athletic performance to encompass broader health considerations. Individuals with lower muscle fitness levels, whether due to age, injury, or other factors, often face unique challenges in maintaining an active lifestyle. If interval training indeed proves to be less fatiguing, it could serve as a valuable tool for promoting physical activity and improving overall health outcomes in populations with varying levels of muscle fitness. Overall, the rowing study holds promise not only for advancing scientific knowledge in the realm of exercise physiology but also for offering practical applications that could positively impact the lives of individuals striving to enhance their fitness and well-being. Read more

Retroviruses are a family of RNA viruses that have an enzyme capable of making a DNA copy of the viral RNA, and then infecting it into a host’s cell’s DNA. This virus includes Coronavirus, HIV, Ebola, etc… COVID-19, for example, can enter a host’s ce ... ll by changing Its shape to fit the cell, by binding to the HR2. The main purpose of inhibiting HR2 is to prevent retroviruses from infecting the host using HR2. Read more

The Prevention and Recovery Center for Early Psychosis (PARC) at Eskenazi Hospital works with patients experiencing early psychosis in hopes to identify causes of the disorder, determine best possible treatments, and gain insight into preventing psyc ... hosis from an early age. Dr. Bethany Leonhardt and the PARC team of researchers are involved in an ongoing study aiming to identify the effect of Metacognitive Reflection and Insight Therapy with individuals diagnosed with Early Psychosis (MERIT-EP). MERIT-EP is a therapy approach that allows patients to gain a complex, in-depth understanding of themselves, their diagnosis, and their experiences in order to achieve an individualized definition of recovery. MERIT has previously been used in studies on long-term psychosis patients but has not yet been studied in younger individuals coming to terms with their diagnosis and navigating young adulthood. The MERIT method approach is unique in that it encourages achieving subjective recovery, specific to the individual, rather than its standardized definition. Ultimately, studying this method aims to shift treatment techniques on patients with all levels of psychosis towards a more personalized approach and promote positive long-term outcomes. Read more

In my role at the Sandusky pathology lab, I assist researchers by converting physical slides into digital format, making them accessible on computers. Using specialized software, I analyze specific characteristics like positivity percentages. I also ... support professors by digitizing slides for teaching. I did an independent research project. My focus was on analyzing the impact of chemotherapy using a specific biomarker called p53. This involved examining how clinical treatment affected P53 presence in tumor cells and its impact on patient clinical outcomes. Overall, my experience at the digital pathology lab has been about supporting research and education initiatives while conducting my own investigation into cancer treatment effects. It's been a valuable opportunity to contribute to scientific understanding and enhance my skills in data analysis and interpretation. Read more

Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-secreting pancreatic ?-cells leading to dysregulation of blood glucose levels. Both genetic and environmental factors contribute to T1D pathogenesis, but the triggeri ... ng events for disease onset are still unknown. The Linnemann lab has shown that autophagy, a process to regulate cell survival and maintenance, is defective in islets during human T1D. Therefore, the lab is now focused on understanding how defective autophagy may contribute to the development of T1D. To understand the various influences of these pathways, the lab selectively knocked out the critical autophagy enzyme, ATG7, in the ?-cells of mice (ATG7??-cell mice). Initial characterization of these mice revealed that all ATG7??-cell mice spontaneously developed diabetes. Initial data gathered in the lab suggests involvement of endoplasmic reticulum (ER) stress response and ER associated degradation pathways. Therefore, to determine whether any of the 3 branches of the ER stress response are preferentially upregulated, we performed immunofluorescence staining on pancreas tissue from ATG7??-cell mice to evaluate these pathways. We also evaluated isolated islets under basal and stress conditions to help determine the mechanism of ATG7??-cell islet loss using incucyte live cell imaging. Read more

Stiffening of the liver, better known as liver fibrosis, is caused by the formation of large amounts of scar tissue. This scar tissue is formed as a result of liver injury, which can be caused by metabolic disorders, obesity, alcohol use, drug use, o ... r viral infection. Hepatic stellate cells (HSCs) will become activated due to this injury and drive fibrogenesis in order to heal the wounded liver. In the case of liver fibrosis, the injury is chronic, and HSCs are persistently activated, leading to the buildup of scar tissue and eventually cirrhosis. Because of the limited understanding of the mechanisms driving this, there are no FDA approved treatment options that will limit or reverse fibrosis. Fibrogenesis is driven by an increased transcription and translation of extracellular matrix proteins by HSCs. This increased translational demand places a stress on HSCs, which activates the unfolded protein response (UPR). One branch of the UPR that regulates translation is PERK signaling, and we have found that PERK signaling increases with HSC activation. We are engineering a PERK KO cell line using CRISPR-Cas9 technology in order to determine if PERK signaling is crucial to HSC activation and fibrogenesis. Read more

It is estimated that 14% of the adult US population has chronic kidney disease (CKD). This is approximately 1 in 7 adults. Bone loss is a common side effect of CKD which leads to increased risk of bone fractures. Treatments in CKD are challenging due ... to decreased kidney function, making safe, effective therapies very needed. In the Allen lab, our goal is to explore different factors that can possibly prevent bone loss in those with CKD. This study specifically explored the impact of different dietary fibers on bone health in rats with CKD. We found that all the different fiber types we studied (inulin, pectin, psyllium) protected against bone loss in CKD and mitigated the declines in bone strength. Overall, this study shows that dietary changes may help protect bone and prevent fracture in CKD. Read more

This LHSI internship has allowed me to work within the Center for Biomedical Informatics at the Regenstrief Institute. At this center they are working alongside the CDC, Indiana University, the VA, and Marion County Public Health department in resear ... ch on long COVID-19. During this internship I completed a scoping review that focused on healthcare disparities and long-COVID 19. Healthcare disparities are defined as factors that impact an individual’s access to healthcare, the presence of disease in different populations, or health outcomes. This research is important as 1 in 13 adults who have survived COVID-19 suffer from long term symptoms and the severity differs among different populations. Read more

My internship has focused on analyzing denervation-induced skeletal muscle atrophy in nerve injury and amyotrophic lateral sclerosis (ALS) models. In the nerve injury model, the sciatic nerve in the right hind limb was surgically cut to document how ... sudden nerve damage leads to disconnection of the neuromuscular junction (NMJ) and subsequent skeletal muscle atrophy in mice. The denervation is useful both for comparing how it can mimic progressive skeletal muscle atrophy that occurs in ALS and how a sudden severance of the sciatic nerve can lead to unique characteristics in atrophy progression. Despite multiple causes of denervation skeletal muscle atrophy, the carboxyl-terminal modulator protein (CTMP) is a common contributor. The Walker lab has identified that upregulation of CTMP promotes skeletal muscle atrophy progression in these models, and the involvement of this protein has been a focus of my project. Read more

In our lab we focus on understanding how stress response pathways help prostate cancer (PCa) cells adapt and survive amino acid (AA) limitations. Our lab discovered that the kinase GCN2 is critical for the maintenance of AAs in PCa cells by turning o ... n genes involved in AA synthesis and transport. Blocking GCN2 function in PCa cells results in AA starvation leading to decreased growth of these cancer cells. These results support that GCN2 may be a potential therapeutic target for treating this deadly disease. However, before GCN2 inhibitors can be taken to the clinic, we need to have a better understanding on how inhibition of GCN2 affects different cellular processes. For my LHSI project, my goal was to study how deletion or inhibition of GCN2 in cultured PCa impacts ribosome biogenesis and translation, both cellular processes are dependent on AAs. Using Click-IT-based reactions and immunofluorescence for detection, we found that the amino acid limitations caused by loss of GCN2 function decreased ribosome biogenesis and translation in PCa cells, and this could be reversed by AA supplementation. Furthermore, culturing PCa cells in media depleted of AAs also reduced ribosome biogenesis and translation, suggesting that AA limitations is a major factor leading to the reduction in these cellular processes following GCN2 inhibition. Read more