2016 Glassman Symposium Abstracts

Academics / Majors and Minors / Neuroscience / Glassman Symposium / 2016 Glassman Symposium Abstracts

Alumni Presenters

Hippocampal neuronal loss and impaired neurogenesis following repeated closed-head concussive impacts

G. Chiren¹, E. Reisenbigler¹, N. Jamnia², N. Kapecki³, G. DeJoseph², J. H. Urban², R. A. Marr³, G. E. Stutzmann³, D. A. Kozlowski⁴, D. A. Peterson¹.
¹Ctr. for Stem Cell & Regenerative Med., ²Dept. of Physiol. and Biophysics, ³Dept. of Neurosci., Rosalind Franklin Univ. Med. Sci., North Chicago, IL;
⁴Biol. Sci., DePaul Univ., Chicago, IL

Head impact and/or acceleration-deceleration can produce traumatic brain injury (TBI) that can be categorized as severe or mild, with concussions categorized typically as mild TBI. There is emerging evidence that the accumulation of concussive injuries, frequently encountered in sports or combat, contributes to the development of chronic traumatic encephalopathy (CTE). To assess the sequence of degenerative and regenerative responses following repeated concussions, we utilized a closed-head model of controlled cortical impact to deliver injury to rats. All procedures were approved by IACUC. Young adult Long Evans rats received a sham procedure (anesthetic) or the addition of impact on the surface of the head by a modified Leica CCI device at a location overlying the sensorimotor cortex. Experimental groups received a single impact or three successive impacts separated by 48 hour intervals. After 30 days, animals were deeply anesthetized, transcardially perfused, and the brains were collected and sectioned at 40 μm. There was no evidence of skull fracture and no macroscopic deformation of the cerebral cortex underlying the impacted skull. Closed head impact produced neuronal disorganization in the underlying cerebral cortex and the volume of cerebral cortex and corpus callosum was reduced in experimental groups. Hippocampal volume was also reduced and we investigated further the effect of impact on this more distant structure. Repeated concussive impact produced no noticeable alteration in Iba1+ microglial or Olig2+ oligodendrocyte progenitor cell populations in the hippocampus. However, repeat concussion produced astrocytic (GFAP+) hypertrophy throughout the hippocampus that was pronounced at the hippocampal fissure. The population of DCX+ neuroblasts was reduced in the dentate gyrus following repeat concussions with more severe loss in the buried blade of the dentate gyrus. Repeated concussion also resulted in neuronal (NeuN+) loss in Area CA1. Despite the distance of the hippocampus from impact, repeated mild impact results in an injury response, reduced neurogenesis, and neuronal loss in the hippocampus. Thus repeated concussion may contribute to long-term disruption of hippocampal circuitry.

Changes in Group I mGluR Surface Expression in the Nucleus Accumbens During Withdrawal from Methamphetamine Self-Administration

Yusuf Ismail¹^,2, Jessica A. Loweth², Mike Milovanovic², Alyssa B. Smith², Marina E. Wolf²

¹Department of Biology, Lake Forest College, 555 N. Sheridan Road, Lake Forest, IL 60045

²Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064

Methamphetamine addicts remain susceptible to relapse long after achieving abstinence. Studies suggest that addictive drugs produce synaptic adaptations in the nucleus accumbens (NAc) that play a critical role in craving and relapse. Therefore, it is important to understand the cellular properties of the NAc during drug taking and drug withdrawal to understand the physiological basis of vulnerability to relapse. We have recently shown that calcium-permeable AMPA receptors (CP-AMPARs) accumulate at NAc synapses during withdrawal from methamphetamine self-administration and mediate the expression of enhanced or incubated cue-induced methamphetamine craving (Scheyer et al., 2016). We have also shown that metabotropic glutamate receptor 1 (mGluR1) exerts an inhibitory influence on CP-AMPAR levels in the NAc (Scheyer et al., 2016; Loweth et al., 2014). A decrease in mGluR1 surface expression, which would be expected to reduce that inhibitory influence, is hypothesized to occur during methamphetamine withdrawal and thereby enable CP-AMPARs to accumulate on medium spiny neurons in the NAc. Another similar receptor, mGluR5, is expressed in the NAc and may also play a role in incubation. The purpose of these studies is to test our hypothesis about mGluR1 and gain insight into mGluR5. To this end, rats will be trained to self-administer methamphetamine or saline and, following specific withdrawal periods (early, middle and late—WD3, WD21 and WD48), the NAc will be dissected and the tissue biotinylated to selectively label and isolate all surface receptors. Immunoblotting will be used to measure levels of surface expressed mGluR1 and mGluR5. So far, we have collected tissue on withdrawal day 3 (WD3). Analysis of this tissue indicated no changes in mGluR1 or mGluR5 surface expression in methamphetamine-exposed rats compared to saline-exposed controls. Studies are currently underway to determine potential changes in mGluR1 and mGluR5 surface expression on WD21 and WD48. Investigating methamphetamine-induced alterations in glutamate receptor expression in the NAc and the time-course of such effects may ultimately help to contribute to the development of medications to reduce cue-induced craving in abstinent methamphetamine addicts.

Mediators in quality of life for individuals with brain injury

Kristina Johnson, B.A. and N. Ditchman Ph.D., CRC, LPCP.

Department of Psychology, Illinois Institute of Technology, Chicago, IL

Individuals with brain injury may suffer from both physical and cognitive impairments that may negatively contribute to the quality of life following injury. Rehabilitation psychology focuses on strengths and psychosocial factors in a person’s life. Recent research suggests that these psychosocial factors may act as mediators to aid in improving quality of life across rehabilitation populations. Two of the previously researched psychosocial constructs include social support and mastery over the disability. Understanding how these constructs may act to mediate the relationship between symptom severity and quality of life in hopes of optimizing rehabilitation is the ultimate goal of this study. This study has a nationwide sample of 172 individuals with brain injury to model how symptom severity, social support, mastery, and quality of life all impact each other utilizing Structural Equation Modeling (SEM). Results demonstrated a good fit in the predicted model suggesting that social support and mastery both mediate the relationship between symptom severity and quality of life (χ²_{(15, n = 172)} = 13.68). Normed Bentler-Bonnet fit index (NFI) was 0.973; Goodness-of-Fit statistic (GFI) was 0.981; and Comparative fit index (CFI) was 1.00. The Root Mean Square Error of Approximation (RMSEA) was 0.00. Examination of the direct effects show that social support increases as a function of decrease in symptom severity (-0.22), and the sense of mastery decreases as severity increases (-0.65) and as social support decreases (0.28). Both mastery and social support were moderately related to quality of life. (0.46 & 0.53). These results support the research model and hypothesized mediating effects of social support and mastery.

Choriocapillaris Non-Perfusion is Associated with Poor Visual Acuity in Eyes with Reticular Pseudodrusen

Peter L. Nesper, B. T. Soetikno, and A. A. Fawzi

Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss among the elderly in the United States and Europe. While drusen deposits in early AMD generally have mild impact on visual function, late stages of AMD are associated with significant visual impairment. Reticular pseudodrusen (RPD) represent a distinct AMD phenotype associated with worse visual function and a higher likelihood of progression to late AMD compared to eyes with regular drusen. The purpose of our study was to use optical coherence tomography angiography (OCTA) to study choriocapillaris blood flow and its correlation to visual acuity (VA) in eyes with RPD versus eyes with regular drusen. In this prospective, cross-sectional study, patients with either drusen or RPD in early AMD underwent OCTA imaging of the superior, inferior, and/or nasal macula. We quantified “percent choriocapillaris area of non-perfusion” (PCAN) in eyes with RPD versus those with drusen. We assessed the repeatability of PCAN and its correlations with VA. Twenty-nine eyes of 26 patients with RPD and 21 eyes of 16 age-matched AMD patients with drusen were included. Qualitatively, the choriocapillaris in areas with RPD showed focal dark regions without flow signal on OCTA (non-perfusion). The repeatability coefficient of PCAN was 0.49%. Eyes with RPD had significantly greater PCAN compared to eyes with drusen (7.31% and 3.88%, respectively; P < 0.001). We found a significant correlation between PCAN and VA for the entire dataset (r = 0.394, P = 0.005). When considering eyes with RPD and eyes with combined RPD and drusen separately, this correlation was stronger (r = 0.474, P = 0.009) but lost significance when considering eyes with drusen separately (r = 0.175, P = 0.45). We concluded that eyes with RPD have significantly larger areas of choriocapillaris non-perfusion compared to eyes with drusen and no RPD. The correlation between PCAN and VA in this RPD population provides a potential mechanistic explanation for vision compromise in RPD compared to other forms of drusen in AMD.

Using [SWI+] to Study Protein Misfolding, Aggregation and Amyloid Formation

Stephanie Valtierra, Zhiqiang Du, Liming Li

Northwestern University, Biochemistry and Molecular Genetics, Chicago,

Current knowledge of prion biology has been greatly enhanced by studies in Saccharomyces cerevisiae, which contains several self-perpetuating misfolded protein elements known as yeast prions. Our laboratory discovered the yeast prion [SWI⁺], whose protein determinant is Swi1, a subunit of an evolutionarily conserved ATP-dependent chromatin-remodeling complex SWI/SNF. The formation of [SWI⁺] results in the transmission of several heritable phenotypes in an epigenetic manner. In addition to the partial loss of function in utilization of non-glucose carbon sources, the conformational change of Swi1 leads to a complete loss of multicellularity. This complete loss of multicellular features, including flocullation, pseudohyphal formation, invasive and adhesive growth, was found to be a result of the tight regulation of the FLO1 gene, which encodes key regulators required for multicellularity in yeast, by [SWI⁺]. Additional work showed that other proteins in the same biological pathway were also misfolded and sequestered, providing convincing evidence that formation of one prion, [SWI⁺], can have an effect on multiple pathways in yeast.

Based on our recent finding that [SWI⁺] tightly regulates FLO1, our laboratory recently designed a novel reporter system that can faithfully report the prion status of Swi1. We conducted high-throughput screens to identify compounds that can eliminate or inhibit [SWI⁺] and obtained a number of promising anti-[SWI⁺] compounds. We are currently elucidating the hit compounds’ mechanism of action and investigating their ability to antagonize PrP^Sc and inhibit Aβ-induced toxicity in a mammalian cell culture system.

In addition to the previous studies, we also aim to obtain a deeper understanding of the sequence and structural requirements for amyloidogenesis and prionogenesis. To this end, a series of Swi1 truncation experiments were carried out. We showed that the first 38 amino acids of Swi1 were able to aggregate, and maintain and propagate [SWI⁺]. However, further deletion to the first 26 amino acids resulted in a loss of aggregation, indicating that the minimal prion domain (PrD) of Swi1 lies between residues 26 to 38. Further analysis showed that the first 30 amino acids of Swi1 are able to aggregate, and maintain a prion conformation in the absence of full-length Swi1, suggesting that this region is likely the minimal PrD of Swi1. These Swi1 based studies will shed light on the mechanisms of protein misfolding, aggregation, and amyloid fiber formation and their effect on multiple biological pathways – all of which are relevant to prion diseases and other amyloid-based neurological disorders.

Abnormal Bone Phenotypes in Dicer Deficient Mice

Atsawasuwan, M. Ouibaidin, A. Mohammed, C. Vivirito, B. Dalal, H. Khan, C. Evans.

Department of Orthodontics, College of Dentistry, UIC, Chicago, IL

Dicer, an endoribonuclease, plays a critical role in microRNA (miRNA) biogenesis because it cleaves the miRNA precursor during the process of miRNA maturation. Mature miRNAs are important for osteoclast/blast differentiation and functions during bone homeostasis and remodeling. This process requires strict regulation at post-transcriptional and post-translational stages. Deletion of Dicer in both osteoclasts and osteoblasts in mice have been shown to exhibit the same phenotype. Here we investigate the effect of Dicer deficiency in long bones under a different bone specific promoter Sp7 promoter. The objective of this study was to evaluate whether postnatal lack of mature miRNAs in a mouse model would lead to dysregulation of bone maturation and remodeling in vivo. A Tet-off conditional Dicer deficient under Sp7 promoter mouse was employed in this study. R26R carrying Sp7 promoter mice were used and femurs were stained with β-galactosidase staining to verify the expression of Sp7 promoter in postnatal femurs. Femurs from mice aged 10 weeks were studied using Faxitron® radiography and microcomputed tomography. In addition, fluorescence bone labeling of the mouse femurs were employed to determine bone remodeling activity. Dicer deficient mice exhibited faster rate of mineral apposition but decreased cortical bone density and high porosity. The male mice exhibited significant phenotypes while the female mice showed a milder phenotype.

Wnt7A Skews Macrophage Phenotype

Jennillee Wallace, Lena Al-Harthi

Dept. Immunology/Microbiology, Rush University Medical Center, Chicago, IL

Monocytes in response to specific signals differentiate into pro-inflammatory macrophages (M1), alternative or anti-inflammatory macrophages (M2), or an intermediate phenotype. An M1 phenotype is linked to a number of pathological conditions including the size of HIV encephalitic lesion in neuroAIDS, while an M2 phenotype is linked to tumor progression and metastasis. Given that Wnts, a family of 19 morphogenic glycoproteins which initiate -catenin-dependent or independent signaling, are responsible for many cellular events including cellular differentiation; we evaluated their impact on macrophage differentiation and function. We show that culturing human monocytes with recombinant human Wnt7A protein inhibited the expression of CD14+CD16- by 10- folds relative to M0 and M2 monocyte derived macrophages (MDMs), and 25- folds relative to M1 MDMs. Wnt7A also inhibited CD14+CD16+ expression by 3-, 5- and 12- folds relative to M0, M2 and M1 MDMs, respectively. Further, Wnt 7A inhibited expression of CD163 by 3-, 4-, and 7- folds relative to M0, M2 and M1 MDMs, respectively. Wnt 5A, on the other hand, had no impact on these macrophage markers. Additionally, Wnt 7A inhibited secretion of two inflammatory mediators (IL1β and DKK1), and increased secretion of the anti-inflammatory cytokine IL-10 compared to M0, M1 and M2 MDMs. Finally, phagocytic ability was reduced in Wnt7A treated MDMs. Together; these studies demonstrate that Wnt7A can be harnessed to generate an anti-inflammatory phenotype of macrophages.

Student Presenters

Drug Inhibition by Quaternary Ammonium Inhibitors in KcsA Potassium Channels

Gross, D. Burdette, and T. Aldaas

Department of Biochemistry and Molecular Biology, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60064

KcsA is a potassium channel found in Streptomyces lividans and contributes to the cell’s potassium flux by gating in response to intracellular pH levels. KcsA is a well characterized potassium channel due to the ease of production and purification. The pore structure of KcsA is shared by many potassium channels throughout multiple kingdoms of life.

The goal of the experiments was to determine binding affinities of triethylhexlyammonium (TEHA), triethyloctylammonium (TEOA), and triethyldecylammonium (TEDA). These would be useful in scientific research because in conjuction with structural data it could aid in the design of drugs that block specific potassium channels. The hypothesis was that an increase in asymmetrical QA concentration would cause an increase in potassium channel blockage with affinity increasing as hydrophobic area increased as in symmetrical QAs. Tests were run to find the maximal inhibition concentrations, but the results were inconclusive. Future studies could address the hypothesis.

The 5-HT1B Serotonin Receptor Mediates Fluoxetine Effects on Methylphenidate-Induced Gene Regulation in the Striatum

Acharya, J. A. Beverley and H. Steiner

Dept. of Cellular & Molecular Pharmacology, Chicago Medical School/Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Psychostimulants such as cocaine alter gene regulation in the striatum, which is critical for addiction. Cocaine blocks dopamine and serotonin reuptake, and both transmitters contribute to cocaine-induced gene regulation. Methylphenidate (Ritalin, MP) is a psychostimulant that is widely used to treat attention-deficit hyperactivity disorder (ADHD) and is also abused as a cognitive enhancer. MP blocks dopamine, but not serotonin, reuptake and has more moderate effects on gene regulation than cocaine. We previously showed that increasing serotonin action in conjunction with MP treatment, by adding a selective serotonin reuptake inhibitor (SSRI) antidepressant, fluoxetine (FLX), potentiates MP-induced gene regulation, thus mimicking cocaine effects. The 5-HT1B serotonin receptor subtype is implicated in cocaine-induced gene regulation. Current research investigated a role for 5-HT1B in MP+FLX-induced gene regulation. MP+FLX-induced expression of the gene marker Zif268 in the striatum was attenuated by the 5-HT1B receptor antagonist SB224289. This effect was maximal in the lateral (sensorimotor) striatum, indicating that sensorimotor corticostriatal circuits are mostly affected. These circuits mediate compulsion in addiction. MP+SSRI combinations are often used to treat ADHD/depression comorbidity and other disorders. Co-exposure to these drugs also occurs in patients on SSRI antidepressants who abuse MP as a cognitive enhancer or party drug. Our previous studies show that this drug combination potentiates addiction-related gene regulation, and may thus increase the addiction liability. Our present findings suggest that the 5-HT1B receptor participates in the SSRI-induced potentiation of gene regulation. The 5-HT1B receptor may thus serve as a pharmacological target to prevent these effects.

Sex differences in the neuronal activity of the basolateral amygdala and the impacts of stress.

Avonts, J. Vantrease, A. Rosenkranz

Department of Cellular and Molecular Pharmacology, Rosalind Franklin University, North Chicago, 60064

Neuroscience Program, Lake Forest College, Lake Forest, IL, 60045

Anxiety disorders affect 1 in 5 adults and can interfere with daily activities including job performance, school work, and relationships. Half of individuals with anxiety or depressive order episodes also suffer from a second comorbidity of depressive or anxiety disorder. Anxiety disorders are also more prevalent in females, such that women are twice as likely to be diagnosed than males, however, the mechanisms contributing to the susceptibility in sex differences remains poorly understood. The basolateral amygdala (BLA) is known to play a role in fear and anxiety such that in human studies using fMRI and PET shows neural activity of humans diagnosed with anxiety greater amygdala activity than control subjects. In other prior studies, BLA activity was seen to be greater in female rats compared to male rats. Previous research has also shown a small conductance Ca2+ activated K+ channel (SK) inhibits neuron excitability and the overexpression of the SK2 isoform can protect against anxiety. To induce anxiety we used a repeated restraint stress model because it has been shown chronic restraint stress causes anxiety like behavior, quantitatively measured by cortisol activity. Therefore, we are interested to see how stress impacts BLA activity because if females exhibit higher neuronal BLA activity we think they will have less SK channels. Results supported no difference in SK2 channel at the mRNA levelmeasured by quantitative real time PCR but differences occurred at the translational level measured by western blot analysis. We found that in naïve rats SK2 channel was reduced compared to males and that stress reduced SK2 channels in male rats, but not females.

Evaluation of the P300 Event- Related Brain Potential Using a 3-Stimulus Auditory Oddball Paradigm

Blumfelt, J. Berg, K.Meuli, & N. Wentworth

Department of Psychology and Neuroscience Program, Lake Forest College, Lake Forest, IL 60045

An interesting component in the pathophysiology of Schizophrenia is the delayed latency and impaired amplitude of the P300 event-related brain potential (ERP). The P300 is a positive deflection in the EEG waveform present around 350 ms after stimulus presentation. Past literature has implicated P300 in attentional processes and working memory, skills both attributed to the frontal lobe. Frontal lobe dysfunction is a characteristic of Schizophrenia, and as such impairments of attention and working memory are present in the disease. This study employs a 3-stimuli auditory oddball paradigm to evaluate the P300 waveform in a control group consisting of healthy college students with no familial history of Schizophrenia as well as an experimental group with a familial history of the disorder. This between groups design involves the use of three auditory tones: a frequent tone, an infrequent distractor tone, and an infrequent target tone. Tones will be presented in a random order with the participants being asked to mentally count the number of target tones they hear. The latency and amplitude of the P300 response will be measured in both groups. Statistical analysis with SPSS will compare group means for amplitude and latency. Consistent with the results of past literature, we expect to see increased latency and decreased amplitude in the familial history group.

An evaluation of viral prevalence and activity in patients with multiple sclerosis.

Brittain, M. Sorenson, D. Everly, and J. Reynolds

Lake Forest College, Lake Forest, IL; DePaul University, Chicago, IL; Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Multiple sclerosis is a demyelinating autoimmune disease of the central nervous system and represents the most common neurological disease of young adults. There has been a general consensus that the pathogenic process of multiple sclerosis involves a pattern of interaction between genetic predisposition and environmental factors that act in concert to initiate the development of auto reactive T cell. Genetic predisposition to MS is believed to center around immune system variability, especially in MHC genes. Several genes of the human leukocyte antigen (HLA) loci have been associated with MS, including the susceptible HLA-DR15, HLA-DQ6, and HLA-DRB1*1501 genes as well as the protective HLA-C55A and HLA-DRB1*11 genes. Viral infection is one of the leading environmental factor triggers for MS. Studies have suggested a number of different viruses that may trigger the immune system to mediate development, progression, and relapse of MS. Our long-term goal is to understand the relationship between viral infection, immune activation, and the development of multiple sclerosis (MS) as a means to designing innovative new approaches to treat MS. The aims of our project are: 1) To determine the viral prevalence and viral immune activity in MS patients compared to normal individuals and 2) to determine the HLA type of control individuals and MS patients using next generation sequencing. The results of these studies will provide correlations between viral immune activity and encephalitogenic T cell activation in order to better understand the relationship between viral infection and MS. In addition, these experiments will provide the conceptual framework for future experiments to identify the critical reactive cells in MS patients that are correlated with specific viral exposure. Long-term, determining specific viruses or virus/host interactions that induce MS pathology will help determine the mechanisms that underlie MS development and lead to the development of new and novel personalized therapies for MS patients.

Cellular Reprogramming: Applications in Disease Modeling

Clark Briggs¹, Deeana Brinks¹, Virginie Bottero¹, Trevor Buhr², Melissa Hoshizaki¹, Robert Marr¹, John McDaid¹, Dan Peterson¹, Grace E. Stutzmann¹

¹Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

²Lake Forest College, Lake Forest, IL 60045

Cellular reprogramming has a wide range of applications. Here we use viral vector technology to manipulate cell fate to model disease and allow for large scale drug screenings. Previous research has modeled Alzheimer’s disease in mice yet little has been done in analyzing living human neurons from individuals that were diagnosed with Alzheimer’s disease. Our approach intends to improve generalizability of results by avoiding animal models and discover new drug treatments that antagonize ryanodine (RyR) receptors which are overabundant in neurons with the presenilin 1 (PSEN1) mutation, a known genetic marker of early onset Alzhiemer’s disease. We used induced pluripotent stem cells (iPSCs) derived from fibroblasts from deceased healthy donors and donors who tested positive for the PSEN1 mutation, a genetic marker for early onset Alzheimer’s disease. These groups of iPSCs were then reprogrammed via neurogenin-2 lentiviral vector into induced neurons (iNs) and overexpression of RyR was confirmed in diseased iNs. Electrophysiological data revealed that diseased iNs exhibited larger calcium responses to administration of an RyR agonist than healthy iNs.

Starved of Oxygen: The insulin regulation of growth in response to hypoxia in Drosophila

Olivia Dellomodarme¹, Jeanne M.C. McDonald¹, Lilly S. Thorsen, Pegah Nabili, Alexander W. Shingleton. ¹Joint first authors.

Department of Biology, Lake Forest College, Lake Forest, IL 60045

In almost all animals, hypoxia during development – a deficiency in physiological levels of oxygen – slows growth and reduces final body size. Despite the ubiquity of this phenomenon, however, the developmental mechanisms by which oxygen levels affect growth are largely unknown. We have previously shown that a rise in the hormone ecdysone is necessary to suppress growth in hypoxia. Previous studies have demonstrated that elevated ecdysone can suppress growth by inhibiting the insulin-signaling pathway, a pathway primarily utilized to regulate growth with respect to nutrition. We therefore tested whether insulin-signaling activity is also suppressed in response to oxygen deprivation using a GFP reporter construct for Pi3K activity, and by measuring the expression of key insulin-regulated genes using qPCR. Both assays show that insulin-signaling is robustly inhibited in hypoxic conditions. Collectively, our data indicate that the effects of hypoxia on body size may occur as a programmed inhibition of growth via the insulin-signaling pathway, by very similar mechanisms used to inhibit growth in response to starvation.

Increasing Physical Activity in Adults at Risk for a Diabetic Foot Ulcer

Domijancic, R. Crews, V. Subramanian, K. Schneider, S. Hwang, E. Moxley

DePaul University, Chicago, IL 60614; Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Diabetes is an increasing public health problem currently affecting 29.1 million adults in the U.S. Since 25% of adults with diabetes will develop a diabetic foot ulcer (DFU) within their lifetime, prevention of DFUs is critical to curbing amputations, decreasing healthcare expenditures, and preserving quality of life. Regular physical activity is critical to glycemic control and can help prevent DFUs. However, at risk patients present with barriers to increasing physical activity given the challenge of finding an appropriate amount of physical activity that balances the benefits of physical activity for glycemic control, with the potential risk of a DFU. Research shows that employing supervised physical activity sessions has increased physical activity in adults at risk for a DFU. However, supervised physical activity programs are typically not reimbursable and can be burdensome to patients. The present study assessed the feasibility of low-cost physical activity strategies (behavioral strategies, Fitbit, private Fitbit online social network, text-messaging, GPS) for adults at risk for DFUs to determine which components could be used to increase physical activity and improve glycemic control. With six participants enrolled to date, this study is still on going. Initial results suggest that this study is feasible for patients with diabetes who are at risk for developing a DFU and that four supervised activity visits appears manageable. FitBit use and goal achievement are high in participants to date.

Effects of Sexualized Media on Attention

Domijancic, A. Khan, K. Meuli, N. Wentworth

Psychology Department, Lake Forest College

The prominence of sexual images and themes in almost all forms of media,commercials, magazines, music videos, et cetera., has received lots of attention and concern. This has lead to a great deal of research on the potential outcomes of heightened exposure to sexual material. While the effects of sexualized media on attention in particular have been investigated, this research has been limited to the effects of erotic videos. The present study examined the effect of sexualized media on attention and ability to detect sexual cues in college students. A convenience sample (N= 42) of males (N=25) and females (N=17) was gathered using an online survey. Participants were randomly assigned to watch a sexually explicit music video or a control music video. Both videos focused on one male and female with equal prominence and sexual explicitness from both genders. Then, participants completed a dot detection task to test reaction time and a word search containing sexually cued and control words. A significant effect on reaction time (P<.05) was obtained based on video type. Participants who viewed the sexually explicit video had slower reaction times compared to controls, as expected. The ratio of sexually cued to control words in the word search showed a significant interaction (P<.05) based on video type and gender. This interaction suggested a significant effect (P<.05) of video type on the word ratio found for females only. The word ratio was higher for females who watched the sexually explicit video than female controls.

Inner Doors to Faërie: Edwardian Mysticism and the Cosmology of A.E. Waite

Fobert and C. Arnell

Richter Scholar Program, Lake Forest College, IL 60045

The combination of the new rationalist, scientific movement with the failing of Christianity in the wake of the Victorian spiritualist movement led to the advent of the mystical and occult revivals in the Edwardian period. One key figure of this literary movement was Arthur Edward Waite. Waite provided the most comprehensive scholarly work on occult texts available in his time, and perhaps even today. The goal of my research was to investigate Waite’s cosmological worldview and the scheme of his influence upon the literary movement as a whole. Reading primary texts by authors of the mystical and occult revivals, as well as delving into the history of the organizations of which these authors were a part, revealed significant influences on the majority of these authors to include Hermeticism, mystical Kabbalah, tarot symbolism, and Catholicism. The cosmological structure of Waite’s The Quest of the Golden Stairs also aligned heavily withMedieval cosmology. In the future, work could be done to compose a comprehensive bibliography of all of Waite’s works, to determine the extent of his influence on the literary world beyond the occult, and possibly to create a critical edition of The Quest of the Golden Stairs.

Insight into Parkinson’s Disease from Yeasts: Growing evidence for sumoylation as a protective factor against a-synuclein toxicity

Yoan Ganev, Rosemary Thomas, Alexandra Roman, Morgan Marshall, Galina Lipkin, and Shubhik K. DebBurman

Neuroscience Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Parkinson’s disease (PD) is a neurodegenerative disorder linked to the loss of dopaminergic neurons in the midbrain. A key pathological marker of PD is the presence of Lewy bodies, which are mainly composed of misfolded alpha-synuclein protein. Alpha-synuclein is a highly post-translationally modified protein. While phosphorylation and nitration of alpha-synuclein are well studied as contributors to PD pathology, less is known about sumoylation, which is proposed to be neuroprotective based on limited studies. The majority of sumoylation takes place on the lysine-96 and lysine-102 sites of alpha-synuclein and it increases the protein’s solubility. The first goal of this project was to complete a tool kit to be used in investigations of the interaction between sumoylation and phosphorylation in our fission yeast model of PD. Second, we began functional assays testing the effects of blocking sumoylation on alpha-synuclein in both budding and fission yeast. Finally, we asked how altering the phosphorylation of alpha-synuclein would affect sumoylation’s protective role and found that blocking phosphorylation reduced alpha-synuclein’s toxicity in the absence of sumoylation. In the future, we will conduct studies to further understand how sumoylation affects other variants of alpha-synuclein and other modifications on it.

Antisense Oligonucleotides Delivered to the Amniotic Cavity in Utero Modulate Gene Expression in the Postnatal Mouse
Viktoriya Georgieva¹^,2 ,Frederic F. Depreux², Lingyan Wang³ , Han Jiang³, Francine M. Jodelka², Jennifer J. Lentz⁴,Frank Rigo⁵, John V. Brigande³, Michelle L. Hastings¹

¹Biology Department and Neuroscience Program, Lake Forest College, Lake Forest, IL 60045 ²Department of Cell Biology and

Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA;

³Department of Speech Education and Communication Disorders, University of Nebraska-Lincoln, Nebraska, USA;⁴Department of Otorhinolaryngology and the Neuroscience Center of Excellence, Louisiana State University Health Science Center, New Orleans, LA, USA; ⁵Ionis Pharmaceuticals, Carlsbad, CA, USA

Congenital diseases account for a large portion of pediatric illness. Prenatal screening and diagnosis allow for the detection of many genetic diseases early in gestation. Fetal therapeutic strategies aimed at managing disease processes as early as possible represent a powerful new approach for clinical care. A safe and effective in uteropharmacotherapy designed to modulate gene expression should avoid direct mechanical engagement of the fetus while presenting an external reservoir of drug. The amniotic cavity could serve as an ideal reservoir. Antisense oligonucleotides (ASOs) are an established tool for the therapeutic modulation of gene expression and are also an ideal clinical drug, because they are specific, stable, easily delivered, and have low toxicity. We hypothesize that ASOs administered to the amniotic cavity will gain entry to the fetus and modulate gene expression. Here, we show that transuterine microinjection of an ASO targeting MALAT1 RNA into the amniotic cavity of mouse embryos at embryonic day 13-13.5 significantly decreased MALAT1 RNA in postnatal tissues. This reduction was sustained for up to one month in the liver. We have previously shown that an antisense oligonucleotide (ASO) can correct the splicing defect associated with an Usher mutation in the Ush1C gene encoding harmonin and effectively improve vestibular and hearing deficits in a mouse model of the disease (Lentz, Jodelka et al. 2013). Therefore, we wanted to determine whether ASO delivered to the amniotic cavity could effectively correct abnormal splicing in the Ush1C.216A mouse model. As hypothesized, intra-amniotic injection rescued splicing in treated mice. Therefore, we found that intra-amniotic ASO delivery is well tolerated and produces a lasting effect on postnatal gene expression. This delivery paradigm introduces new opportunities for the fetal treatment of conditions where prenatal intervention can maximize therapeutic efficacy .

Transport and degradation of the SLO-1 BK channel in C. elegans

James J. Haney^1,2 and Dr. Hongkyun Kim¹¹Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064
²Lake Forest College, Lake Forest, Illinois 60045

Neurons and muscle cells are activated by calcium influx. However, uncontrolled calcium influx can be detrimental to these cells. One of the important feedback negative regulators is a calcium-activated potassium SLO-1 BK channel. The SLO-1 channel is conserved across species, including the nematode, C. elegans. Research has also shown that SLO-1 can also be activated by ethanol, leading to inhibitory effects. In C. elegans the protein ERG-28 has been identified as the molecule responsible for transporting SLO-1 from its synthesis in the endoplasmic reticulum to the plasma membrane. erg-28 mutants show greatly reduced SLO-1 signaling, suggesting ER associated degradation of the potassium channel via the ubiquitin-proteasome system. To confirm this, we will identify a ubiquitin ligase responsible for the degradation of the SLO-1 channel using both fluorescent microscopy and behavioral studies in C. elegans. We will also perform mutagenesis tests on C. elegans with RFP tagged ERG-28 in order to better elucidate the erg-28 and slo-1 pathways.

PMCT Synthesis Trials Using a Cell-Free System

Malia Hansen and Ronald Kaplan

Department of Biochemistry and Molecular Biology, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60085

What if you could extend your life with a simple drug, and what if the side effect was loosing weight? Inhibition of the citrate transporter INDY (I’m Not Dead Yet) extended the lives of several Drosophilia in a similar way to caloric restriction. By inhibiting the same pathway in humans (shown below), the cell is converting less cytosolic citrate into lipids and other fatty acids. The human version of INDY is named PMCT (plasma membrane citrate transporter), and finding the right inhibitor can only be done after expressing enough PMCT to be tested. Because membrane proteins are notoriously difficult to express, several methods were examined. The following work focused on determining if cell free translation can efficiently produce functioning PMCT.

Stressful journey to the extended amygdala: Characterization of CRF neurons in the bed nucleus of stria terminalis (BNST) in transgenic CRF-Cre rat model

Janeček and J. Dabrowska

Department of Cell and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Bed nucleus of the stria terminalis (BNST), a part of the extended amygdala, has been found to play an integrative and modulatory function in the affective component of the stress response. Of particular importance are the corticotropin-releasing factor (CRF)-containing neurons, which mediate autonomic and sustained behavioral responses to stress. Within the extended amygdala circuitry, CRF functions as a hormone regulating the affective response to stress whose dysfunction has been consistently associated with addiction, depression, anxiety, and PTSD. Because detecting immunoreactivity of CRF is challenging, CRF neurons within the BNST have been mapped with limited success. Here, we employ a transgenic CRF-Cre rat developed by Pomrenze et al. (2015), in which CRF neurons express Cre-recombinase. The rats (N = 4), of which 2 were subjected to acute restraint stress (RS) and 2 served as naive controls (CTRL), were injected with DIO-mCherry-AAV to the BNST to specifically label CRF-expressing neurons in the oval nucleus of the BNST (BNSTov). Our objective was to determine the location of cellular markers previously described in the BNSTov, including striatal-enriched protein tyrosine phosphatase (STEP) and protein kinase C delta (PKCd) relative to CRF neurons, and to qualitatively characterize the CRF neuron signal using fluorescent immunohistochemistry and confocal microscopy. In addition, a neuronal activation marker, c-Fos, was used to compare CRF neuron activation in the BNSTov in RS and CTRL rats. Previously, STEP was detected in the CRF neurons of the BNSTov using immunohistochemistry and PCR approaches. In this study, we report that mCherry positive neurons in the BNSTov also co-express STEP. Furthermore, we report little to no co-localization of PKCd with CRF, which is consistent with previous studies showing that CRF does not co-localize with PKCd in the extended amygdala. Because atypical c-Fos signal was observed in the BNSTov, CRF neuron activation between RS and CTRL rats was not compared. Although a larger tissue sample should be used in the future to investigate the full potential of the Tg CRF-Cre rat model, our study provides initial validation of the Tg CRF-Cre rat model and confirms some of the previously described CRF neuronal markers found using traditional approaches.

The effect of nutritional variation on genital size in Drosophila: Females match males.

Sonia M. Messar ¹, Chirsten, K. Mirth ², Alexander W. Shingleton

¹ Department of Biology, Lake Forest College, Lake Forest, IL 60045

² School of Biological Science, Monash University, Melbourne, Australia

Among arthropods, the male genitalia show a pattern of being highly variable between species, but highly invariable within species. The intraspecific pattern is most obvious as the relative insensitivity of the male genitalia to environmental factors that affect size, particularly developmental nutrition. This phenomenon is hypothesized to arise due to selection for male genital size to match female genital size. If this were true, it follows that female genital size should also be resistant to environmental change. To test this, we reared female D.suzukii on diets that varied in the amount and ratio of protein and carbohydrates, and measured the size of several adult morphological traits, including the ovipositor. We found that the ovipositor was relatively resistant to changes in both food quality (protein:carbohydrate ratio) and food quantity (total caloric value). Thus the selection pressures that result in male genital invariance may also generate female genital invariance.

Understanding Parkinson’s Disease in Yeast Models: Role of Amino Acid Charge and Polarity in New Familial Mutants of α-synuclein

Mwale, E. Ong, M. Buabeng, S.K. DebBurman

Neuroscience Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Parkinson’s Disease (PD) is a neurodegenerative disease that results from the loss of midbrain dopamine neurons, an area in the brain essential for movement. This cell death is caused by the misfolding of the protein, α-synuclein. 10% of PD is genetic and linked to mutations in at least seven genes, including α-synuclein. Six α-synuclein mutations cause PD; three of them (H50Q, G51D, and A53E) were recently discovered and less is known about them. Our lab has already discovered that each mutation has unique properties (Tembo et al., manuscript in preparation). Despite this progress, we still do not know what causes pathological characteristics to arise from these new mutants. Is it the loss of the original amino acid or the gain of the new amino acid that is responsible for disease? Our lab plans to test the hypothesis that the loss of the original amino acid in each familial mutant is key to PD pathology. For my Richter project, I focused on the H50Q mutant, while my mentor (Emily Ong ’17) focused on the other two mutants. For all mutants, four substitutions were made that represent each of the four functional classes of amino acids (polar, hydrophobic, acidic, basic). I sought to make four substitution mutants for H50Q (H50A, H50D, H50R, H50N). My mentor did the same for G51D (G51A, G51E, G51Q, G51R) and A53E (A53D, A53G, A53R, A53N). If our hypothesis is true, then substitution mutants which conserve the property of the original amino acid should behave like wild-type and all other substitution mutants that change the properties of the original amino acid should behave like the familial mutant. For example, we would expect all but H50R would exhibit pathological properties similar to disease-causing H50Q, as H and R are functionally similar. If property of Q is key, only H50N will be similar to H50Q, as Q and N are functionally similar. Here, I demonstrate our progress towards making all of the substitution mutants and assessing them in budding and fission yeast model systems.

Exploring an anti-inflammatory drug, Lipoxin to treat Kaposi’s sarcoma associated herpesvirus (KSHV) infection

B. Najibi, J. Chandrasekhran, and N. Walia-Sharma

Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, Chicago, IL

Lipoxins are host anti-inflammatory molecules that play a vital role in restoring tissue homeostasis. The efficacy of lipoxins and their analog epilipoxins in treating inflammation and related diseases has been well documented. Kaposi’s Sarcoma (KS) and Primary Effusion Lymphoma (PEL) are two well-known inflammation related diseases caused by Kaposi’s Sarcoma-Associated Herpesvirus (KSHV). Controlling inflammation is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evaluating the therapeutic potential of using lipoxins. Recently published work (Chandrasekharan, 2016) showed that KSHV infected cells downregulated lipoxin secretion via its miRNA cluster. Treating KSHV infected endothelial cells with lipoxin downregulated key inflammatory molecules such as NFKB, ERK and AKT (Chandrasekharan, 2016). This study documents the influence of lipoxin treatment on KSHV lifecycle, and its mechanism. Several host transcription factors including EGR-1, SP-1, AP-1, and PPARs, have known to influence KSHV life cycle. Lipoxin alters the level of these host transcription factors to modulate KSHV life cycle. Treating PEL cells with lipoxin has shown to decrease cell proliferation and enhance cell death. This study provides a new insight into the treatment of KS and PEL using nature’s own anti-inflammatory molecule, lipoxin.

Eye Movements and Analysis of Artwork

Penn-Francis and N. Wentworth

Richter Project, Psychology Department, Lake Forest College, IL, 60045

Measuring attention can be determined by studying eye movements and how people fixate on images or aspects of the image itself. Analyzing fixation patterns of participants is a way to determine which part of the image held the most attention. This lead to the question of whether or not the influence of background information could affect where the participant’s attention was held. This study used four discreetly religious images and manipulated the background information participants received before viewing the images. The background information either explained the religious context of the image or described background about art types. The results showed that background type did not directly influence the patterns of fixation. The study showed that it is possibly the artist’s technique that influences the pattern of fixations.

Studying Traumatic Brain Injury and Alzheimer’s Disease in Animal Models

Shylanski, N. Kapecki, A. Littlefield, A. Perrit, and G. Stutzmann

Neuroscience Program, Lake Forest College, IL 60045, and Rosalind Franklin University of Medicine and Science, IL 60088.

Alzheimer’s disease (AD) is a chronic neurodegenerative disease commonly associated with old age. Common symptoms include memory loss, mood swings, and disorientation. AD-like neurodegeneration can also occur in patients that have suffered from traumatic brain injury (TBI). To study the effects of TBI, we have devised an animal model that uses rats to study neurodegeneration following both single and repeated TBI. After being euthanized, blood and neural tissue samples will be collected. Plasma will be isolated from the blood and used to investigate possible biomarkers for neurodegeneration, while neural tissue will be used to observe differences in pathology between groups.

Identifying Ryanodine Receptor Types Expressed by N2A Neuronal Cells by Western Blotting

Smith¹ and J. K. Buolamwini²

Neuroscience Program, Lake Forest College, IL 60065
Department of Medicinal Chemistry, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Alzheimer’s Disease (AD) is an incurable neurodegenerative disorder characterized by late-stage markers of amyloid plaques, neurofibrillary tangles, and cognitive decline. However, it is unclear how effective these markers are as targets for treatment as they are late-stage and are diagnostic of AD, not necessarily the cause. Recent studies in AD models have identified dysregulation in calcium signaling and related downstream pathways, which occur long before the diagnostic histopathological or cognitive changes. Increased calcium levels are functionally linked to the major features and risk factors of AD. Ryanodine Receptors (RyR1, RyR2, and RyR3), specifically RyR2, have been shown to be involved in this dysregulation. Stabilization of Endoplasmic Reticulum (ER) RyR2 Ca2+ channel function is being focused on as an early preventative strategy for Alzheimer’s Disease. Small molecule compounds have been developed based on the RyR inhibitor, Dantrolene, to modulate RyR2 and reduce the amount of calcium released from the ER. In order to evaluate the effectiveness of the compounds created, the inhibition of calcium release is evaluated using a calcium release assay in neuronal N2a cells. However, the presence of RyR2 channels in N2A cells must first be confirmed to be sure that the compounds are affecting the desired channel. Through western blotting, this study confirms the presence of RyR2 type receptors in N2a neuronal cells. Further testing using a calcium detection assay will be performed so that the most effective compounds may be selected for further evaluation and development.

The effect of dietary composition on insulin-signaling gene expression in Drosophila larvae

Lily S Thorsen, Jeanne M.C. McDonald, Olivia Dellomodarme, Pegah Nabili, Alexander W. Shingleton

Department of Biology, Lake Forest College, Lake Forest, IL 60045

A major regulator of body size in animals is developmental nutrition, which acts through the insulin-signaling pathway to regulate growth rate and duration. Whilst we know much of how dietary quantity affects body size and insulin-signaling, we know very little of the impact of diet quality. Here we compare and contrast the effect of changes in dietary caloric value versus protein-to-carbohydrate ratio on the genetic mechanisms that regulate body size in Drosophila melanogaster. We reared flies from first to third larval instar on one of 24 diets that varied in their concentration and ratio of proteins and carbohydrates, and measured the expression of genes that activate or are activated by the insulin-signaling pathway. Our data indicate that activity of the insulin-signaling pathway responds primarily to changes in protein level but not carbohydrate level. These data suggest that diet quality impacts body size primarily through changes in the quantity of a single macronutrient: protein.

The Functional Maturation of the Female Prefrontal Cortex through Ventral Hippocampal Stimulation

Lily Veldran¹ and Kuei Y. Tseng²

¹Department of Neuroscience, Lake Forest College, Lake Forest, Illinois, 60045

²Department of Cellular and Molecular Pharmacology, The Chicago Medical School at Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, 60064

The prefrontal cortex (PFC) is the last brain region to develop. In humans, complete development stops in the early 20s. During this period of maturation, the GABAergic system in the prefrontal region undergoes significant functional and structural changes. From a functional perspective, these changes underlie a balance of excitatory and inhibitory transmission, that allow a higher cognitive function to occur (e.g. decision making and impulse control). Previous research has shown that during this developmental period, from pre-adolescence to start of adulthood, there is an increase in inhibitory control in the PFC from afferent signals from the ventral hippocampus (vHipp). These results have been done primarily in male subjects, without female comparison. The goal of this study is to investigate the functional maturation of the female PFC through afferent mechanisms from the vHipp. The measure of maturation was done using local field potential recordings in the PFC and ventral hippocampal stimulation in vivo. Stimulation at a frequency of 20 Hz (beta waves) in adolescent rats postnatal days (P) 30-35 showed facilitation, while adolescents at age P40-45 showed no overall facilitation or suppression. However, in adulthood (P50-110), the females showed an overall suppression response of the vHipp signal. At a 40 Hz frequency (gamma waves) both P30-35 and P40-45 groups showed suppression of the signal, but not as much as the P50-110 group. Together these results show a pattern of increasing inhibitory control in the PFC from the vHipp as the female rodents age from P30-110.

Inhibition of GLUT5 Protein Transporter for Cancer Treatment

Verma, A.G. Thompson, & J. Choe

Department of Biochemistry and Molecular Biology

Chicago Medical School/Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

In humans, the transport across the cell membrane of glucose and related hexoses along concentration gradients is facilitated by members of the glucose transporter (GLUT) family. GLUT5 is a transporter of fructose that is overexpressed in breast cancer cells and involved in obesity and diabetes. The goal of this research was to find inhibitors of GLUT5 as a starting platform for potential cancer and diabetes drug treatment options. This study used hexose transporter knock-out yeast cells for GLUT5 transport assay. First, the plasmids containing GLUT5 were introduced in yeast cells (a process known as ‘cell transformation’) and then grown in YPM (yeast-peptone maltose) solid media, in Petri dishes. Throughout the study, a pilot cell sample had to be freshly prepared before any supplemental experiments since yeast cells lose activity quickly. The pilot cultures were grown in YPM media, as these cells grow well in maltose. When the density of cells was appropriate, cells were separated from the YPM media by centrifugation, resuspended in YPF (yeast-peptone fructose) media, and grown overnight. For GLUT5 transport activity assay, we used 10 ml of yeast cell solution at a cell density that corresponded to O.D.600nm of 6.0. Cells were incubated with various chemicals and 10 mM radioactive 14C fructose for 20 mins. To determine GLUT5 fructose uptake in cells, we measured the radioactivity accumulated inside cells with a Scintillation Counter, and analyzed data with non-linear algorithm plots supplied by Prism (GraphPad Software). Out of 180 chemical inhibitors, only 8 chemicals showed a decrease in GLUT5 transport activity (i.e. inhibition) (IC50~ 100 μM to 500 μM).

FIYS106 Medical Mysteries of the Mind

Medical Mysteries of Memory

Niam Abeysiriwardena, Danielle Berninzoni, Alexsandra Biel, Lauren Guirini, and Joseph Mountain

First-Year Studies Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Students of FIYS106 Medical Mysteries of the Mind will present the neuroscience underlying how we sleep and stay awake and they will delve into several current medical mysteries that are the cutting of scientific research. They will educate the audience using posters, models and interactive activities.

Medical Mysteries of Thought

Ariane Balaram, Fillip Komornik, Brett Palmero, Jacqureline Rogers, Anna Sandler

First-Year Studies Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Students of FIYS106 Medical Mysteries of the Mind will present he neuroscience underlying how engage in thought processes and they will delve into several current medical mysteries that are the cutting of scientific research. They will educate the audience using posters, models and interactive activities.

Medical Mysteries of Sleep

Blake Becker, Anna Denslow, Nena Fasbenber, Emma Kuhr, and Sara Tallen

First-Year Studies Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Medical Mysteries of Emotions

Sam Gascoigne, Katelyn Harris, Brooke Ingram, Zala Rutar, and Noah Vanderhyde

First-Year Studies Program and Biology Department, Lake Forest College, Lake Forest, IL 60045

Students of FIYS106 Medical Mysteries of the Mind will present the neuroscience underlying how we express emotions and why we do it and will delve into several current medical mysteries that are the cutting of scientific research. They will educate the audience using posters, models and interactive activities.