Undergraduate Medical Education

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    Common Molecular Alterations in Canine Oligodendroglioma and Human Malignant Gliomas and Potential Novel Therapeutic Targets
    (Frontiers, 2019-08-14) Mitchell, Dana; Chintala, Sreenivasulu; Fetcko, Kaleigh; Henriquez, Mario; Tewari, Brij N.; Ahmed, Atique; Bentley, R. Timothy; Dey, Mahua; Neurological Surgery, School of Medicine
    Spontaneous canine (Canis lupus) oligodendroglioma (ODG) holds tremendous potential as an immunocompetent large animal model of human malignant gliomas (MG). However, the feasibility of utilizing this model in pre-clinical studies depends on a thorough understanding of the similarities and differences of the molecular pathways associated with gliomas between the two species. We have previously shown that canine ODG has an immune landscape and expression pattern of commonly described oncogenes similar to that of human MG. In the current study, we performed a comprehensive analysis of canine ODG RNAseq data from 4 dogs with ODG and 2 normal controls to identify highly dysregulated genes in canine tumors. We then evaluated the expression of these genes in human MG using Xena Browser, a publicly available database. STRING-database inquiry was used in order to determine the suggested protein associations of these differentially expressed genes as well as the dysregulated pathways commonly enriched by the protein products of these genes in both canine ODG and human MG. Our results revealed that 3,712 (23%) of the 15,895 differentially expressed genes demonstrated significant up- or downregulation (log2-fold change > 2.0). Of the 3,712 altered genes, ~50% were upregulated (n = 1858) and ~50% were downregulated (n = 1854). Most of these genes were also found to have altered expression in human MG. Protein association and pathway analysis revealed common pathways enriched by members of the up- and downregulated gene categories in both species. In summary, we demonstrate that a similar pattern of gene dysregulation characterizes both human MG and canine ODG and provide additional support for the use of the canine model in order to therapeutically target these common genes. The results of such therapeutic targeting in the canine model can serve to more accurately predict the efficacy of anti-glioma therapies in human patients.
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    Unique Molecular Features in High-Risk Histology Endometrial Cancers
    (MDPI, 2019-10-27) Pandita, Pooja; Wang, Xiyin; Jones, Devin E.; Collins, Kaitlyn; Hawkins, Shannon M.; Obstetrics and Gynecology, School of Medicine
    Endometrial cancer is the most common gynecologic malignancy in the United States and the sixth most common cancer in women worldwide. Fortunately, most women who develop endometrial cancer have low-grade early-stage endometrioid carcinomas, and simple hysterectomy is curative. Unfortunately, 15% of women with endometrial cancer will develop high-risk histologic tumors including uterine carcinosarcoma or high-grade endometrioid, clear cell, or serous carcinomas. These high-risk histologic tumors account for more than 50% of deaths from this disease. In this review, we will highlight the biologic differences between low- and high-risk carcinomas with a focus on the cell of origin, early precursor lesions including atrophic and proliferative endometrium, and the potential role of stem cells. We will discuss treatment, including standard of care therapy, hormonal therapy, and precision medicine-based or targeted molecular therapies. We will also discuss the impact and need for model systems. The molecular underpinnings behind this high death to incidence ratio are important to understand and improve outcomes.
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    Seeing With Sound: Educational Insights of the 200th Anniversary of Laennec's Magnum Opus
    (Elsevier, 2019) Mohiuddin, Amer M.; Gunderman, Richard B.; Radiology and Imaging Sciences, School of Medicine
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    Cell Cycle–Mediated Cardiac Regeneration in the Mouse Heart
    (Springer, 2019) Eghbali, Arash; Dukes, Austin; Toischer, Karl; Hasenfuss, Gerd; Field, Loren J.; Medicine, School of Medicine
    Purpose of Review Many forms of heart disease result in the essentially irreversible loss of cardiomyocytes. The ability to promote cardiomyocyte renewal may be a promising approach to reverse injury in diseased hearts. The purpose of this review is to describe the impact of cardiomyocyte cell cycle activation on cardiac function and structure in several different models of myocardial disease. Recent Findings Transgenic mice expressing cyclin D2 (D2 mice) exhibit sustained cardiomyocyte renewal in the adult heart. Earlier studies demonstrated that D2 mice exhibited progressive myocardial regeneration in experimental models of myocardial infarction, and that cardiac function was normalized to values seen in sham-operated litter mates by 180 days post-injury. D2 mice also exhibited markedly improved atrial structure in a genetic model of atrial fibrosis. More recent studies revealed that D2 mice were remarkably resistant to heart failure induced by chronic elevated afterload as compared with their wild type (WT siblings), with a 6-fold increase in median survival as well as retention of relatively normal cardiac function. Finally, D2 mice exhibited a progressive recovery in cardiac function to normal levels and a concomitant reduction in adverse myocardial remodeling in an anthracycline cardiotoxicity model. Summary The studies reviewed here make a strong case for the potential utility of inducing cardiomyocyte renewal as a means to treat injured hearts. Several challenges which must be met to develop a viable therapeutic intervention based on these observations are discussed.
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    The Impact of Covid-19 on Inmate Trust in Health Care and Willingness to Seek Treatment - A Qualitative Investigation
    (Indiana Medical Student Program for Research and Scholarship (IMPRS), 2020-12-15) Kumalo, Valarie; Nelson, Alexander; Messmore, Niki; IU School of Medicine
    Background and Objective: The coronavirus has disproportionately impacted vulnerable members of society. With the U.S. as the global leader in incarceration and the difficulties prison systems face implementing many of the mitigation strategies employed by the general population, the incarcerated population is in a uniquely vulnerable position particularly within an already strained prison healthcare system. Given the nature of prisons as total institutions, negative experiences with the virus coupled with a lack of autonomy could lead to a loss of trust in the healthcare system which has the potential to impact health-seeking behaviors. In this study, we aim to examine the effect of Covid-19 on Indiana inmates’ trust in healthcare.  Project Methods: Data from 380 surveys distributed across Indiana’s prison system will be collected and analyzed. These results will be used to develop an interview protocol to conduct at least 25 in-depth interviews which will then be coded using NVivo to identify any emerging themes regarding their experiences with Covid-19. Prior to this, in-depth literature reviews were done on health care in prison populations and trust in healthcare. Results: The surveys and interview protocol will be developed in the ensuing months and thus no data has yet been collected. The literature review revealed that the quality and accessibility of care in prisons is lacking, an issue exacerbated by the pandemic. Because of the disproportionate number of preexisting issues, inmates worried about the ability of prison administrators to properly protect inmates from contracting the virus. Additionally, it was found that trust likely does have an effect on health, and that many commonalities of inmates are poor predictors for trust. Potential Impact: This study aims to identify potential loss of trust in healthcare systems to inform community reentry programs in developing strategies that prioritize inmate health needs and perceptions.  
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    Possible Neuroinflammatory Mechanisms Which May Lead to Long-Term Neurological Disorders in COVID-19 Patients
    (Indiana Medical Student Program for Research and Scholarship (IMPRS), 2020-12-15) Lange, Michael; Shi, Riyi; IU School of Medicine
    This review aims to provide insight into the possible long-term neurological complications that COVID-19 patients may experience after the resolution of intense acute inflammation characterized as “cytokine storm.” Neurological symptoms such as fatigue, headache, dizziness, nausea, confusion, dyspnea, anorexia, malaise, myalgia, ataxia, seizure, hypogeusia, and hyposmia are commonly seen in these patients. COVID-19 related encephalitis is also seen sporadically. However, some researchers believe neuroinflammation is more common than what is reported. Neurological abnormalities that are linked to neuroinflammation are of particular concern because neuroinflammation is hypothesized to cause neurological diseases such as Alzheimer’s Disease, Parkinson’s Disease, and Schizophrenia. Many potential routes can lead to inflammation in the nervous system and elicit neuron cell death in COVID-19 patients. These include the potential neurotropic pathway of the novel coronavirus, CNS parenchymal infectability, thrombotic ischemic stroke, cytokine storm, and blood-brain barrier breakdown. Past pandemics of similar neurotropic viruses could also offer insights regarding the long-term neurological effects of COVID-19. In support of our hypothesis, the Spanish Flu pandemic of 1918-1919 saw an increased incidence of neurodegenerative disease, Parkinson’s disease, and schizophrenia. We do not know exactly what the future will hold for COVID-19 however, it is of paramount importance to attempt to anticipate and prepare for the possible chronic neurological sequelae and mitigate or prevent their effects.
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    Symptoms of Anxiety and Depression Among Community Dwelling Older Adults: Impact of Covid-19
    (Indiana University, 2020) Seibert, Tara; Perkins, Anthony J.; Fowler, Nicole R.; Medicine, School of Medicine
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    Exploratory Analysis of COVID-19 Case Demographics in Gary, Indiana
    (Indiana University, 2020) Snapp, Cameron; Trimoski, Bill; Brown, Martin; Han, Amy; Kostrominova, Tatiana; Psychiatry, School of Medicine
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    A Case of Aceruloplasminemia Which Was Not Wilson Disease
    (2021-03-26) Williams, Cody; Clemens, Joseph; Wu, Joey; Zimmerman, Michelle
    Case: A 58 year old woman presented with 5+ years of fatigue and joint pain as well as recent short term memory concerns. She was evaluated for Lyme disease and was found to have mild anemia with elevated iron and persistently elevated ferritin as high as 2100 ng/ml. An unrelated cardiac scan had the incidental finding of hepatic iron accumulation. No fibrosis was noted on MRI. Liver biopsy was significant for 3-4+ hemochromatosis with sinusoidal dilation and congestion. Labs showed aceruloplasminemia with low urine and serum copper. Eye exam was negative for Kayser Fleischer rings but did show retinal iron deposits and early macular degeneration not supporting Wilson disease. Later genetic testing for CP (ceruloplasmin) gene showed heterozygosity for sequence variant c.2342A>C, predicted to cause amino acid substitution p.Lys781Thr. Conclusion: She is currently awaiting MRI to evaluate possible CNS disease in the setting of aceruloplasminemia but was delayed due to significant COVID-19 risk. Otherwise, she is tolerating deferasirox well. Significance: Our patient had a complex path to diagnosis given that low ceruloplasmin is commonly associated with Wilson disease. However, ceruloplasmin is also a key component in regulating ferric iron binding to transferrin and maintaining copper and iron homeostasis. This case was an exemplar of interdisciplinary diagnosis. Clinical evidence of anemia, ophthalmologic findings, and subjective cognitive dysfunction combined with histology and genetic results contributed to accurate characterization of aceruloplasminemia related hemochromatosis rather than Wilson’s disease. Genetic analysis revealed CP gene c.2342A>C (p.Lys781Thr), a novel mutation not reported elsewhere to our knowledge. Given her heterozygous status for the mutation, further investigation is needed. More importantly for our patient, recognition and treatment at this stage could reduce morbidity from neurodegeneration, pancreatic, and hepatic disease.