RBC Fellows Symposium 2017

3rd Annual event hosted by the Regenerative Bioscience Center (RBC)

When

13th of April 2017
Starting at 9am

Promoting excellence in regenerative research and mentorship across multi-disciplines

Speakers

A one-day program,
to recognize the exceptional academic work of RBC fellows and professional trainees

The University of Georgia's Regenerative Bioscience Center, involving more than 175 undergraduate and graduate students supported by 33 faculty mentors

RBC Students

One of the special benefits of a large research collaboration, such as the Regenerative Bioscience Center (RBC), is the opportunity it provides students to engage in applied leadership, self-reflection, constructive hypothesizing, and encountering difference in real-world problems and to work under the personal supervision of nationally recognized researchers.

RBC Mentors

UGA faculty provide guidance in a way that allows their students to learn through independent and unique experiences.

RBC Research

Today, under the direction of Dr. Steven Stice, D.W. Brooks Distinguished Professor and Georgia Research Alliance Eminent Scholar, the RBC is a collaboration geared toward identifying regenerative solutions for numerous medical conditions that affect both animals and people. Through a translational approach to research, the RBC is significantly expanding the perspective of veterinarians, scientists and even clinicians, and eradicating the practice of researching in isolation.

The Speakers

An opportunity to present their work to the scientific university community

Justin
Sharma

Undergraduate, Stice Lab

VIEW abstract

John Newman

John
Newman

Undergraduate, Howerth Lab

VIEW abstract

Meghan Logan

Meghan
Logan

Graduate, Karumbaiah Lab

VIEW abstract

Anna Nichenko

Anna
Nichenko

Graduate, Call Lab

VIEW abstract

Kate
Birdwhistell

DVM Professional, Franklin Lab

VIEW abstract

Michael Southern

Michael
Southern

Graduate, Call Lab

VIEW abstract

Maria Naskou

Maria
Naskou

Graduate, Peroni Lab

VIEW abstract

Ana
Maslesa

Undergraduate, Mortensen Lab

VIEW abstract

Symposium Schedule

Thursday, April 13th.

9:00 - 9:05

ADS Auditorium, RM 101. Opening Remarks, Franklin West, Associate Professor Regenerative Medicine

9:05 - 9:20

Dr. MohanKumar will share his personal stories of hard work and perseverance in becoming a DVM PhD

Puliyur S. MohanKumar
BVSc, PhD. Professor, RBC Mentor

Dr. P. S. MohanKumar was born in Tamil Nadu, India. He received his veterinary degree from the Madras Veterinary College, Chennai, India. He went onto pursue a PhD degree in neuroendocrinology at Kansas State University following it with a stint of postdoctoral fellowship at University of Kansas Medical Center. After a brief period as an assistant professor at Kansas State University, he moved to Michigan State University, where he obtained his tenure and rose through the ranks to full professor. Dr. MohanKumar’s research has been regularly supported by funding from the NIH, NSF and USDA. He serves on NIH study sections and reviews for peer-reviewed journals.

Apart from his interest in research, he has been involved in mentoring graduate students, postdoctoral fellows and young faculty members. Dr. MohanKumar has served as the Graduate Program Coordinator and has directed a NIH-funded T32 training grant. He has also served as the research director for the NIH-funded Building Interdisciplinary Research Collaborations in Women’s Health (BIRCWH) program. For his research efforts, he received the Pfizer Research Excellence Award. MohanKumar Bio

9:20 - 9:35

Mitochondrial Abnormalities May Contribute to Skeletal Muscle Weakness and Poor Regeneration in Fukutin-Deficient Muscular Dystrophy Mice

Michael Southern
Jarrod Call, mentor

The dystrophin-glycoprotein complex (DGC) provides a link between extracellular and intracellular structures of the muscle cell. We have previously demonstrated that muscle-specific deletion of the fukutin gene [Myf5/Fktn KO mice (KO)] causes DGC disruption. KO mice present moderate to severe muscular dystrophy characterized by muscle weakness and delayed regeneration following muscle injury. The objective of this study was to determine the extent to which mitochondrial dysfunction contributes to the muscle weakness and delayed regeneration in these mice. We hypothesized that mitochondrial dysfunction contributes to muscle weakness in KO mice and that improving mitochondrial content would benefit muscle regeneration following muscle injury. We administered daily injections of saline or AICAR (500mg/d/kg), an agent previously shown to improve mitochondrial quality in dystrophic muscle, to both KO(saline n = 9, AICAR n = 6) and littermate (LM) control (saline n = 9, AICAR n = 8) mice. Two weeks after onset of treatment, the left hindlimbs (anterior and posterior compartments) of all mice were injured with cardiotoxin to induce muscle regeneration, while the right hind limbs served as contralateral uninjured controls. Mice were sacrificed 2 weeks post-injury. Body mass and gastrocnemius mass normalized to body mass was 21% and 13% lower in KO mice compared to LM controls (body mass: P< 0.001, gastrocnemius: P< 0.002). Pre-injury peak isometric torque about the ankle joint was 38% lower in KO mice compared to LM (P=0.044). Interestingly, muscle strength was not fully recovered in any group of mice 2 weeks post-injury, but AICAR-treated mice had 25% greater muscle strength following injury compared to salinetreated mice, independent of genotype (P=0.036). Mitochondrial respiration of injured and uninjured permeabilized fibers was also assessed 2 weeks post-injury. Mitochondrial respiration was 23% lower in KO mice compared to LM mice, independent of treatment and injury (P=0.023). Further analysis is required to determine if this is due to lower mitochondrial content or mitochondrial dysfunction. While there was no effect of AICAR on mitochondrial respiration, AICAR-treated mice had ~14% greater levels of COXIV protein content compared to salinetreated mice, independent of genotype and injury (P=0.015). This suggests a longer duration of AICAR treatment may be necessary for gains in mitochondrial protein contents to be realized in terms of mitochondrial respiration. In conclusion, this data suggests that fukutin deficiency is associated with mitochondrial abnormalities that may contribute to skeletal muscle weakness and poor regeneration. AICAR treatment may facilitate strength recovery following muscle injury, although it is unclear the extent to which AICAR affects mitochondrial function following injury.VIEW abstract

9:35 - 9:50

The Effects of Aging on Neuroblast Proliferation in the Lateral Ventricle Region: A Canine Model

John Newman
Elizabeth Howerth, mentor

Through the studies of legendary neuroscientist Santiago Ramón y Cajal, it was previously thought that the adult brain lacks the ability to regenerate neurons. In modern science, adult neurogenesis has been well established in the hippocampal region of rodents. Since this landmark, many studies of adult neurogenesis in the hippocampus of gyrencephalic species, such as bovine, have been conducted. However, the ontogeny of neurogenesis in the canine brain, particularly in the lateral ventricle region, is poorly understood. Data concerning the importance of the lateral ventricle and its accompanying cerebrospinal fluid in trauma repair, nutrient delivery and waste removal is burgeoning. Therefore, it is vital to elucidate the neurogenic properties of this region, and the tissue surrounding it. Here, we evaluate the relationship between age and proliferation of neuroblasts, or immature neuronal precursors, in the Subventricular Zone (SVZ) of the lateral ventricle region of the canine brain. The SVZ is a proven hotspot for robust neuroblast proliferation, and thus an excellent target for evaluation. Also, considering the canine brain is similar to humans in that it contains many gyri, there is ample opportunity for neuroblasts to migrate through the SVZ via the Rostral Migratory Stream (RMS). We hypothesize that as age increases, the robustness of neurogenesis in the canine brain will decrease, as indicated by decreasing numbers of DCX and Ki67 immunopositive cells. To address this, formalin fixed brains from dogs of various ages submitted for postmortem examination and with known pathologies were evaluated. Immunohistochemical staining of transverse sections of forebrain for doublecortin protein (DCX) and Ki67 were performed in order to assess the density of migrating neuroblasts, and general cell proliferation, respectively.VIEW abstract

9:50 - 10:05

Small Molecule GAG-Antagonist Surfen Decreases Glioma Cell Infiltration In Vitro and Attenuates Tumor Growth in Rat Model of Glioma

Meghan Logun
Lohitash Karumbaiah, mentor

Glioblastoma multiforme (GBM) is a stage four astrocytoma comprising the majority of primary malignant brain tumor diagnoses in the United States. Conventional therapies are ineffective, leading to patient death within 15 months of diagnosis. Chondroitin sulfate proteoglycans (CSPGs) and their glycosaminoglycan (GAG) side chains are key components of brain extracellular matrix (ECM) implicated in promoting tumor invasion and spread. We hypothesize that glioma cell invasion is triggered by selective expression of oversulfated CS-GAGs in the tumor microenvironment and that preventing tumor cell interactions with CS-GAGs will dampen glioma invasion and spread. Microfluidics devices with mono- and oversulfated CS-GAG matrices were used to evaluate F98 rat glioblastoma cell infiltration in vitro. Cell infiltration was compared across unsulfated hyaluronic acid (HA) and 4,6-sulfated CS-GAG (CS-E) matrices, and media only controls. The small molecule GAG-antagonist (surfen) was introduced to inhibit cell interaction with sulfated GAGs and evaluate if inhibition subsequently halted cell infiltration within hydrogel matrices. Focal adhesion protein colocalization was quantified within antagonist-containing and control hydrogels to determine influence of CS-GAGs on migratory cell phenotype. In vivo tumor inductions in Sprague Dawley rats were performed stereotactically to induce frontal lobe tumors accurately mimicking human GBM. F98 cells either in media only or media containing surfen were inoculated at a depth of ~3 mm to evaluate effects of surfen on glioma formation and invasion over 21 days in vivo. MR imaging was used to track progress and quantify tumor volume and angiogenesis.

Our results demonstrated enhanced preferential cell migration into hydrogel matrices containing disulfated CS-E compared to unsulfated hydrogels (p< 0.05). F98 cells invading into CS-E hydrogels displayed enhanced colocalization (p< 0.05) of focal adhesion proteins compared to cells within unsulfated hydrogels. This effect was significantly reduced in cells within CS-E hydrogels containing surfen (p< 0.05). F98 cells inoculated within rats developed into diffusely invasive tumors after 14 days, but when inoculated in media containing surfen tumors were contained to more defined margins and smaller gross size after 7 days (p< 0.05). These results suggest that sulfated CS-GAGs may directly induce tumor invasion, and this signaling mechanism can be can be disrupted by surfen to restrict invasion.

Our results suggest that heightened presence of extracellular CS-E induces enhanced cellular migration in a GAG sulfation-dependent manner, and perturbing cellular interactions with CS-E has consequences for gross tumor formation and invasion. Identification of the role of CS-GAGs in glioma behavior would advance our understanding of glioma invasion, and contribute to design of novel therapeutic interventions.VIEW abstract

10:05 - 10:15

Break

10:15 - 10:30

Autophagy Related Ulk1 is Necessary for the Recovery of Mitochondrial Function after Skeletal Muscle Injury

Anna Nichenko
Jarrod Call, mentor

The objective of this study was to determine if autophagy is necessary for the recovery of mitochondrial function after muscle damage. Autophagy is a highly conserved cellular process for the degradation of dysfunctional or damaged organelles (e.g.,mitochondria). We have previously demonstrated that traumatic muscle injury impairs mitochondrial content and is accompanied by an induction of autophagy. However, it is unclear: 1) if only traumatic muscle injury induces autophagy, 2) if autophagy induction is contingent on mitochondrial dysfunction, and 3) if autophagy is necessary for the functional recovery of muscle strength and mitochondrial function. To determine the relationship between muscle damage, mitochondrial function and autophagy induction, ten week old C57Bl/6 mice were randomly assigned to the following groups: eccentric contraction-induced injury (physiological), freeze injury (traumatic), or contractile fatigue (non-damaging control). Injured and contralateral uninjured tibialis anterior and extensor digitorum longus muscles were harvested at 0, 6 hours, 1, 3, and 7 days. Mitochondrial function was assessed via state 3 mitochondrial respiration rates from permeabilized muscle fiber bundles, and autophagy induction was measured via Beclin1, an autophagic protein activated downstream of Ulk1, and total LC3 protein content. Therewas no effect of contractile fatigue on mitochondrial function or autophagy induction at any time point (P>0.19). Eccentric contraction-induced injury did not elicit mitochondrial dysfunction in the injured muscle at any time point (P>0.20), but injured muscle did have greater Beclin1 content at 3 and 7 days (~2 fold, P=0.03). This suggests that physiological muscle damage may induce an autophagy response even in the absence of overt mitochondrial dysfunction. In contrast, freeze injury caused severe mitochondrial dysfunction immediately through 3 days after injury (16-53% of contralateral control, P=0.04), and was accompanied by a robust autophagy response in both Beclin1 and LC3 protein content (peak 7 at days ~40 fold ~14 fold P<0.01, respectively) To determine if this robust autophagy response was necessary for the recovery of mitochondrial function, we subjected skeletal muscle-specific Ulk1 knockouts (Ulk1 KO) and their littermates controls (WT) to freeze injury and assessed the recovery of muscle strength and mitochondrial function at 7 days. There was no difference in muscle strength between Ulk1 KO and WT mice prior to injury (P=0.47), but at 7 days muscle strength in Ulk1 KO mice had recovered to only 12% of preinjury strength, significantly less than WT mice (30%, P<0.01). There was no difference in mitochondrial function in the uninjured muscle from Ulk1 KO and WT mice (P=0.35), although at 7 days, mitochondrial function was an astonishing 32% of uninjured in ULK1 KO mice compared to 64% of uninjured in WT mice (P=0.01). In conclusion, autophagy is induced following both traumatic and physiological muscle injury and Ulk1 is required for the recovery of mitochondrial function after traumatic muscle injury.VIEW abstract

10:30 - 10:45

Sustained Release of Transforming Growth Factor-β1 from Platelet-Rich Chondroitin Sulfate-Glycosaminoglycan Gels

Kate Birdwhistell
Samuel Franklin, mentor

Focal cartilage lesions of the knee are common and can be a source of significant pain and dysfunction for patients. Current clinical therapies result in a substandard cartilage with poor long-term performance. Augmentation of these therapies with biologics such as platelet-rich plasma (PRP) may improve their efficacy. The objective of this study was to compare the release of transforming growth factor (TGF)-1 PRP in autologous fibrin and chondroitin sulfate-glycosaminoglycan (CS-GAG) gels. PRP was prepared from nine healthy dogs using a commercially available device. Each PRP was split into 2 aliquots; one activated with bovine thrombin and CaCl2 to form a platelet-rich fibrin (PRF) gel, and the other was used to rehydrate a lyophilized CS-GAG gel. Both gels were incubated in media for 13 days. Media was collected, saved, and replaced after 24 hours and then every 48 hours through day 13. Media samples were frozen at -80C until assayed for TGF-1 concentrations by ELISA. Overall differences between groups were compared using a 2-way ANOVA and a Wilcoxon paired samples test was used to compare treatment groups on individual days. The type of gel had a significant effect on TGF-1 release (p <0.001) with significantly (p<0.05) greater concentrations of TGF-1 released from the CS-GAG gels than the PRF gels on days 3, 5, 7, 9 and 13. TGF-1 concentrations were up to 365% more with use of the CS-GAG gels than the PRF gels on an individual day. Use of the negatively charged CS-GAG hydrogels significantly increased the duration and amount of TGF-1 eluted from canine PRPs in vitro. PRP’s regenerative potential is likely dependent on provision of anabolic growth factors. Therefore, a delivery method that provides sustained release of such growth factors, such as the CS-GAG gels investigated in this study, may improve efficacy in vivo.VIEW abstract

10:45 - 11:00

Platelet Lysate as a Novel Serum Free Media Supplement for the Culture of Equine Bone Marrow Derived Mesenchymal Stem Cells

Maria Naskou
John Peroni, mentor

Mesenchymal Stem Cells (MSCs) produced for clinical purposes rely on culture media that includes fetal bovine serum (FBS). FBS unfortunately is xenogeneic, and thus has the potential to significantly alter the MSCs phenotype, rendering these cells immunogenic. This may result in the rejection of MSCs by the host immune system following administration, even when autologous MSCs are used. Platelet lysate (PL) is considered a possible alternative to FBS that has shown promising results in human and equine medicine. Our goal was to evaluate the use of equine platelet lysate pooled (ePL) from donor horses in place of FBS to culture and expand equine MSCs. We hypothesized that ePL, produced following apheresis, will function as the sole media supplement to accelerate the culture and expansion of equine bone marrow derived MSCs without altering their phenotype and their immunomodulatory capacity. Platelet concentrate was obtained from five equine blood donors via plateletpheresis and ePL was produced via freeze-thaw and centrifugation cycles. Population doublings (PD) and doubling time (DT) of bone marrow derived MSCs (n=3) at P2 to P5 cultured with media supplemented with either 10% FBS or ePL, was calculated using established mathematical equations. Cell viability was assessed via a Live/dead assay and immunophenotypic analysis for the expression levels of MHC-II, CD90, CD105, CD45, CD34 and CD44 markers was performed with flow cytometry. To assess the ability MSCs to modulate inflammatory responses, equine monocytes were stimulated with LPS E.Coli and co-incubated with MSCs cultured in the two different media formulations. Following eighteen hours of incubation, cell culture supernatants were collected and assayed for the production of the pro-inflammatory cytokine tumor necrosis factors-alpha (TNF-α). Our results revealed that MSCs cultured in ePL media exhibited increased PDs and decreased DT compared to those in FBS. Moreover, MSCs cultured in ePL showed comparable viability and expressed similar levels of MSCs markers compared to FBS. MSCs cultured in ePL expressed lower levels of CD34 and CD45. Finally, MSCs cultured in ePL efficiently suppressed the release of TNF-α when exposed to LPS stimulated monocytes. Our data demonstrate that ePL supports the proliferation, viability and immunomodulatory capacity of MSCs without altering their phenotypic profile. Thus, ePL has the potential to be used for the expansion of MSCs before clinical application, avoiding the concerns associated with the use of FBS.VIEW abstract

11:00 - 11:15

Bone characterization in the treatment of Hypophosphatasia with mesenchymal stem cells

Ana Maslesa
Luke Mortensen, mentor

We present the use of second-harmonic generation (SHG) images to characterize bone morphology using Hypophosphatasia (HPP) as a disease model. Hypophosphatasia (HPP) is a rare genetic disorder caused by mutations to the tissue-non-specific alkaline phosphatase (ALP) gene. Diminished ALP activity prevents the enzyme from dephosphorylating inorganic pyrophosphate (PPi), a potent inhibitor of mineralization, resulting in disarticulated collagen and porous bones. Current treatments only alleviate symptoms in the long bones of patients with HPP and do not address premature loss of teeth and craniosynostosis. A promising treatment is mesenchymal stem cell (MSC) therapy, which has been used in clinical studies along with myeloablation and full bone marrow transplants. However, many patients in need do not qualify for bone marrow transplants as they are too sick for such a harsh, risky procedure. While it is established that HPP reduces mineralization in bone, the effect of HPP on other parameters of bone formation, such as bone microarchitecture, is unknown. First, a method for describing pores had to be established. SHG images were used to examine the collagen microstructure in cranial bones of both healthy and HPP mice. Image J was then used to analyze characteristics of bone such as pore size, number, and spacing. As the surface of the skull is curved, the image was first flattened by removing tilt. Next, a sub-region of interest was selected and a projection was created. This image was processed using several different methods and then various thresholds were added to each processed image. Automated pore counts on a small subset of data were compared to manual counts to optimize the way pores are analyzed. The percentage of manually counted pores that was automatically counted and their standard deviation were both factors in choosing a method. It was determined that using sequential image processing was the best protocol for describing pores.In future studies, this method of describing pores will be used to assess the impact of MSCs in their local environment. We predict that bones will have smaller, fewer pores and denser collagen fibers when a mouse is treated with MSC therapy. This data will be used to determine the effectiveness of MSC therapy for HPP and will establish SHG as a means for characterizing bone morphology for bone diseases.VIEW abstract

11:15 - 11:30

Production and scale up of human neural stem cell derived exosomes for pre- clinical trials in porcine middle cerebral artery occlusion models.

Justin Sharma
Steven Stice, mentor

Stroke is currently the second most fatal cause of death globally, and the leading cause of physical disability. Several potential stem cell therapies are in consideration to address the urgent need for stroke treatment, but only one therapeutic has received FDA approval for clinical trials.Standard small molecule pharmaceuticals can bypass the blood brain barrier to deliver treatment to damaged cerebral tissues, but these drugs are limited in their protective and regenerative properties. Although stem cells offer restorative abilities, whole cells cannot bypass the blood brain barrier. Recent studies suggest stem cell derived vesicles, termed exosomes, possess beneficial properties and deliver their contents directly to the site of injury. Exosomes are small lipid vesicles containing proteins and RNA that are actively secreted by several cell types and circulate in all body fluids to communicate with other cells. Via a simple intravenous injection, exosomes can deliver therapeutics in the form of proteins or RNA for the purpose of treating brain injury. The lipid bilayer capsule of the exosomes facilitates the movement of contents from the blood stream to damaged tissues. The objective was to collect neural stem cell (NSC) exosomes for evaluation in a porcine middle cerebral artery occlusion model. Gathering information on vesicle concentration and average exosome output by human NSCs in a controlled environment enables the scale up of production necessary for the sale of a biopharmaceutical. The success of exosome products demands optimization of more efficient purification methods. By examining shortcomings in conventional methods of cell culture, ArunA Biomedical can improve yield and minimize costs of NSC exosome production. The success of a production run supports the large-scale manufacturing processes of exosomes in quantities relevant for large animal studies. These processes will be critical as these new technologies are transferred to biomanufacturing under quality control systems required for human clinical trials of exosome therapeutics.VIEW abstract

11:30 - 11:40

Break, Walk to Poster Session

11:40 - 2:00

Poster Session Review, RM: 142, Dan Daniels

Testimonials

Being an RBC Undergraduate Fellow, grants us the unique opportunity to interact directly, through the symposium, collaboration, and other means, with a more diverse faculty and students from all over campus. Hannah Mason
Karumbaiah Lab
I’m so impressed at how articulate, accomplished, and gifted these students are. The ones I spoke to today will most definitely place us at the top of the line for students seeking a career in research. Derek Eberhart
Director of University of Georgia Innovation Gateway
Getting to talk with other undergraduates at today's event, who are researching different areas of regeneration, encourages me to look at my own research differently. Karishma Sriram
Stice Lab
Every time I present, I feel like I become a better student, communicator and scientist, which is a pretty special experience. Caroline Coleman
West Lab

RBC Fellows Program

About

Empowering students. The program is sponsored and administered by the Regenerative Bioscience Center at the University of Georgia. The Fellows Program incorporates faculty from the Departments of Animal and Dairy Sciences, Engineering, and Veterinary Medicine, as well as faculty from Georgia Tech and Emory University.

Program Overview

An exciting experience for any UGA students seeking direct experience working with faculty, conducting research that leads to new discoveries, treatments, and new cures for the devastating diseases that touch all of our lives. The framework of the concentration takes advantage of faculty strength in both the Animal and Dairy Sciences, Biochemistry, Engineering and Veterinary Medicine within a multi-campus infrastructure. As a student you will gain research experience under the mentorship of internationally recognized academic scientists, while working with graduate students, postdoctoral researchers, and industrial collaborators. Thus, our students will be uniquely positioned to apply for graduate and professional schools with the opportunity to have a very strong foundation on which to build a successful career.

Who is the RBC?

The Regenerative Bioscience Center (RBC) based in Athens, Georgia at the University of Georgia, serves as a vehicle for stimulating growth and productivity of diverse collaborative research efforts amongst the work of veterinarians, toxicologists, biochemists, medicinal chemists and pharmacologists. Through experimentation and analysis, our primary goals are to bridge the gap between basic science and clinical medicine, moving translation research from laboratory science into real therapies and treatments. As a collaborative translational research team we do more — by adding ideas, questions and new experiments and discoveries not yet discovered by traditional basic research.

Leader of the Fellows, Franklin West

Dr. Franklin West, named one of the nation's top scholars under 40 by Diverse: Issues in Higher Education magazine 2010, received a bachelor of science degree in biology from Morehouse College and a doctorate in stem cell biology from the University of Georgia, where he now holds position as an associate professor of animal and dairy science in the College of Agricultural and Environmental Sciences. Dr. West was a MARC (Minority Access to Research Careers) U-Star Research Fellow and a David and Lucille Packard Research Fellow at Morehouse College. He has been published in several national and international scientific peer-reviewed journals for cellular biology, and featured on CNN and NPR. West has the only swine stroke model currently in the USA, which was R01 funded from NIH.

Poster Presentations

An opportunity to meet and speak informally with the student author

Lily Francis
Undergraduate, West Lab

Austin Passaro
Graduate, Stice Lab

Forrest Goodfellow
Graduate, Stice Lab

Anita Qualls
Undergraduate, Call Lab

VIEW ALL Abstracts

Alexandra Flemington
Undergraduate, Call Lab

Emily Pendleton
Graduate, Mortensen Lab

Adir Mohaban
Undergraduate, Mortensen Lab

Guiqian Chen
PostDoc, Lui Lab

VIEW ALL Abstracts

Olivia Fuller
Undergraduate, West Lab

VIEW ALL ABSTRACTS

listed in alphabetical order

Kelly Scheulin
Undergraduate, West Lab

Marie McKenzie
Graduate, Stice Lab

Samantha Spellicy
Graduate, Stice Lab

Madelaine Wendzik
Graduate, West Lab

VIEW ALL Abstracts

Trey Powell
Undergraduate, Mortensen Lab

Mohamed Ishan
Graduate, Liu Lab

Zhonghou Wang
Graduate, Liu Lab

Madison Fagan
Graduate, Duberstein Lab

VIEW ALL Abstracts

Wenxin Yu
Graduate, Liu Lab

Brian Jurgielewicz
Graduate, Stice Lab

Xiaogang Cui
PostDoc, Liu Lab

Sunny Patel
Undergraduate, Liu Lab

VIEW ALL Abstracts

Min Sun
Graduate, Karumbaiah Lab

Seth Andrews
Graduate, Stice Lab

Raymond Swetenburg
Graduate, Stice Lab

Brett Marshall
Tech, Liu Lab

VIEW ALL Abstracts

Pavan Suryadevara
Undergraduate, MohanKumar Lab

Arnav Cherian
Undergraduate, Liu Lab

Aditya Sood
Undergraduate, Stice Lab

LaDonya Jackson
Graduate, Karumbaiah Lab

VIEW ALL Abstracts

Sponsors & Partners

Interested in becoming a sponsor? Get in touch

Location and Venue

on the eastside of the University of Georgia campus.

The RBC Fellows Symposium provides academically ambitious, intellectually curious academic students the opportunity to present and defend their original research. We encourage colleagues, faculty, family, and friends to attend this free event.
Venue

The Edgar L. Rhodes Center for Animal and Dairy Science (ADS)

425 River Road

Athens, GA 30602

Location information
Directions

Exit on College Station Road and turn left at the traffic light. Turn right or left, depending which direction you are coming, onto River Rd & at the first entrance turn right (4 story building). During normal business hours, all surface parking lots surrounding ADS are by permit only. PARKING: USE THE EAST CAMPUS PARKING DECK. Drive past the ADS complex and the parking garage is further down second left (you can see the 3 level deck)

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