About

Jorge Piedrahita is a professor at NC State University within the Department of Molecular Biomedical Sciences. The provided page text does not include specific details about his research focus, background, or key contributions.

Research topics

• Medicine
• Biology
• Chemistry
• Surgery
• Anatomy
• Genetics
• Pathology
• Cell biology
• Anesthesia
• Computational biology
• Chemical engineering
• Biomedical engineering
• Organic chemistry
• Polymer chemistry
• Biochemistry
• Materials science
• Composite material
• Molecular biology
• Pharmacology
• Endocrinology
• Internal medicine

Selected publications

• A preclinical pig model of Angelman syndrome mirrors the early developmental trajectory of the human condition

  Proceedings of the National Academy of Sciences · 2025-07-21 · 4 citations

  articleOpen access

  Angelman syndrome is a neurodevelopmental disorder characterized by severe motor and cognitive deficits. It is caused by the loss of the maternally inherited allele of the imprinted ubiquitin-protein ligase E3A ( UBE3A ) gene. Rodent models of Angelman syndrome do not fully recapitulate all the symptoms associated with the condition and are limited as a preclinical model for therapeutic development. Here, we show that pigs ( Sus scrofa ) with a maternally inherited deletion of UBE3A ( UBE3A -/+ ) have altered postnatal behaviors, impaired vocalizations, reduced brain growth, motor incoordination, and ataxia. Neonatal UBE3A -/+ pigs exhibited several symptoms observed in infants with Angelman syndrome, including hypotonia, suckling deficits, and failure to thrive. Collectively, these findings are consistent with the pathophysiology and developmental trajectory observed in individuals with Angelman syndrome. We anticipate that this pig model will advance our understanding of the pathophysiology of Angelman syndrome and be used as a preclinical large animal model for therapeutic development.

  PublisherDOI

• Clesrovimab for Prevention of RSV Disease in Healthy Infants

  New England Journal of Medicine · 2025-09-17 · 36 citations

  article

  BACKGROUND: Clesrovimab is a long-acting investigational monoclonal antibody against site IV of the respiratory syncytial virus (RSV) fusion protein. Data regarding the safety and efficacy of clesrovimab in healthy infants are needed. METHODS: We randomly assigned healthy preterm and full-term infants entering their first RSV season in a 2:1 ratio to receive one intramuscular 105-mg dose of clesrovimab or placebo. The primary efficacy end point was RSV-associated medically attended lower respiratory infection (including at least one indicator of lower respiratory infection or disease severity) through 150 days after injection. A key secondary efficacy end point was RSV-associated hospitalization during the same period. RESULTS: A total of 3614 infants received an injection: 2412 infants received clesrovimab, and 1202 infants received placebo. Through day 150 after injection, RSV-associated medically attended lower respiratory infection occurred in 60 of 2398 infants in the clesrovimab group (incidence rate over 5-month period, 2.6%) and in 74 of 1201 infants in the placebo group (incidence rate over 5-month period, 6.5%), for an efficacy of 60.4% (95% confidence interval [CI], 44.1 to 71.9; P<0.001). RSV-associated hospitalization within 150 days was reported in 9 of 2398 infants in the clesrovimab group and in 28 of 1201 infants in the placebo group, for an efficacy of 84.2% (95% CI, 66.6 to 92.6; P<0.001). Serious adverse events were reported in 278 of 2409 infants (11.5%) in the clesrovimab group and 149 of 1202 infants (12.4%) in the placebo group. CONCLUSIONS: In healthy preterm and full-term infants, a single dose of clesrovimab reduced the incidence of RSV-associated medically attended lower respiratory infection and RSV-associated hospitalization, with a safety profile similar to that of placebo. (Funded by Merck Sharp and Dohme; CLEVER ClinicalTrials.gov number, NCT04767373.).

  PublisherDOI

• A preclinical pig model of Angelman syndrome mirrors the early developmental trajectory of the human condition

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-11 · 1 citations

  preprintOpen access

  ABSTRACT Angelman syndrome is a neurodevelopmental disorder characterized by severe motor and cognitive deficits. It is caused by the loss of the maternally inherited allele of the imprinted ubiquitin-protein ligase E3A ( UBE3A ) gene. Rodent models of Angelman syndrome do not fully recapitulate all the symptoms associated with the condition and are limited as a preclinical model for therapeutic development. Here, we show that pigs ( Sus scrofa ) with a maternally inherited deletion of UBE3A ( UBE3A −/+ ) have altered postnatal behaviors, impaired vocalizations, reduced brain growth, motor incoordination, and ataxia. Neonatal UBE3A −/+ pigs exhibited several symptoms observed in infants with Angelman syndrome, including hypotonia, suckling deficits, and failure to thrive. Collectively, these findings are consistent with the pathophysiology and developmental trajectory observed in individuals with Angelman syndrome. We anticipate that this pig model will advance our understanding of the pathophysiology of Angelman syndrome and be used as a preclinical large animal model for therapeutic development.

  PublisherOA PDFDOI

• Novel Porcine Model Reveals Two Distinct LGR5 Cell Types During Lung Development and Homeostasis.

  UNC Libraries · 2025-11-06

  articleOpen access

  Cells expressing LGR5 play a pivotal role in homeostasis, repair, and regeneration in multiple organs including skin and gastrointestinal tract, yet little is known about their role in the lung. Findings from mice, a widely used animal model, suggest that lung LGR5 expression differs from that of humans. In this work, using a new transgenic pig model, we identify two main populations of LGR5⁺ cells in the lung that are conserved in human, but not mouse lungs. Using RNA sequencing, 3D imaging and organoid models, we determine that in the fetal lung, epithelial LGR5 expression is transient in a subpopulation of SOX9⁺/ETV⁺/SFTPC⁺ progenitor lung tip cells. In contrast, epithelial LGR5 expression is absent from postnatal lung, but is reactivated in bronchioalveolar organoids derived from basal airway cells. We also describe a separate population of mesenchymal LGR5⁺ cells that surrounds developing and mature airways, lies adjacent to airway basal cells, and is closely associated with nerve fibers. Transcriptionally, mesenchymal LGR5⁺ cells include a subset of peribronchial fibroblasts (PBF) that express unique patterns of <em>SHH, FGF, WNT</em> and <em>TGF-&beta;</em> signaling pathway genes. These results support distinct roles for LGR5⁺ cells in the lung and describe a physiologically relevant animal model for further studies on the function of these cells in repair and regeneration.

  PublisherDOI

• ABS1114 RETENTION OF GOLIMUMAB TREATMENT IN RHEUMATOID ARTHRITIS PATIENTS PRELIMINARY RESULTS OF AN INTERNATIONAL REAL-WORLD LIFE PANLARS REGISTER

  Annals of the Rheumatic Diseases · 2025-06-01

  articleOpen access

  <h2>Abstract</h2><h3>Background:</h3> Golimumab has been widely used in the treatment of rheumatoid arthritis, but its retention rates and factors influencing its discontinuation remain under investigation. <h3>Objectives:</h3> To assess the golimumab retention rate during follow-up and to evaluate associated factors. <h3>Methods:</h3> Clinical, demographic and treatment data from the real-world life PANLAR´s register of consecutive rheumatoid arthritis patients treated with golimumab from Dec 2021 to Nov 2024 were analyzed. Descriptive statistics were used to summarize patients' characteristics. A Kaplan-Meier curve was created to assess drug survival, and a Cox regression analysis was performed to evaluate factors associated with golimumab retention. <h3>Results:</h3> We included 84 patients, predominantly women (84.5%, 95%CI:74.9-91.5), with a median age of 47.2 years (IQR: 37.6-55.5) and a disease duration of 7.4 years (IQR:1.9-12.5). 90.5% (95%CI:82.1-95.8) were seropositive for rheumatoid factor or anti-ACPA antibodies. Most patients had moderate to high disease activity at the initiation of the new treatment (DAS28ers>3.2 and DAS28crp>3.2 were 84.6% and 80.9% respectively) and were receiving corticosteroids (62.7%, 95%CI:50.6-72.3) and cDMARDs (85.7%, 95%CI:76.4-92.4) concomitantly. 56.6% (95%CI: 44.7-66.7) of patients had failed bDMARDs or tsDMARDs, primarily TNFi (80.8%, 95%CI: 66.7-90.8). The remaining variables of interest are summarized in Table 1. The drug retention rates (see Figure 1) were 97.6% (95% CI: 90.7-99.4), 89.1% (95% CI: 79.9-94.1), and 50.1% (95% CI: 38.4-60.6) at 3, 6, and 12 months, respectively. Although in the unadjusted Cox regression analysis, the presence of extra-articular manifestations (HR:1.9, p=0.01) and older age at treatment initiation (HR:1.03, p=0.02) were associated with lower drug survival, only the former variable (HR:2.19, p=0.03) remained significant in the adjusted analysis. The most common reason for discontinuation was loss of efficacy (61.5%, 95% CI: 31.6-86.1). Only one discontinuation due to an adverse event was reported. <h3>Conclusion:</h3> Approximately half of the patients with rheumatoid arthritis treated with golimumab remained on the drug at the end of the first year of follow-up. Only the presence of extra-articular manifestations was significantly associated with a higher risk of discontinuation. <h3>REFERENCES:</h3> <b>NIL</b>. Figure 1Persistence rates with golimumab treatment through 12 months for RA patients. Table 1Baseline characteristics and treatment patterns of RA patients.Golimumab (n=84)Prescription line, median (IQR)2 (1-3)-First line, n, % (95%CI)34, 40.4% (29.9-51.7)-Second line, n, % (95%CI)28, 33.3% (23.4-44.5)-Third line, n, % (95%CI)15, 17.9% (10.3-27.7)-Fourth line or beyond, n, % (95%CI)7, 8.4% (3.4-16.4)At least 1 cDMARD failure n, % (95%CI)83, 98.8% (93.5-99.9)At least 1 bDMARD failure n, % (95%CI)47, 56.6% (44.6-66.7)-TNFi, n, % (95%CI)38, 80.9% (66.7-90.8)-IL6i, n, % (95%CI)10, 21.3% (10.7-35.6)-CD80-86i, n, % (95%CI)17, 36.2% (22.6-51.4)-CD20i, n, % (95%CI)3, 6.4% (1.3-17.5)JAKi failure, n, % (95%CI)10, 11.9% (58.6-20.8)Extra-articular disease, n, % (95%CI)21, 25% (16.2-35.6)Bone erosión, n, % (95%CI)50, 59.5% (48.2-60.1)HAQ, mean (SD)1.13 (0.66)IQR: Interquartile range; SD: Standard deviation: CI: Confidence interval. <h3>Acknowledgements:</h3> This register received a irrestricted grant of Abbvie, Pfizer and Janssen. <h3>Disclosure of Interests:</h3> <b>None declared</b>. © The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.

  PublisherDOI

• 166. A Phase 2b/3 Study to Evaluate the Efficacy and Safety of an Investigational Respiratory Syncytial Virus (RSV) Antibody, Clesrovimab, in Healthy Preterm and Full-Term Infants

  Open Forum Infectious Diseases · 2025-01-29 · 18 citations

  articleOpen access

  Abstract Background Clesrovimab is an investigational, long-acting monoclonal antibody (mAb) targeting site IV of the fusion protein for the prevention of RSV lower respiratory tract infection in infants. Methods This phase 2b/3 double-blind, randomized, placebo-controlled pivotal study enrolled healthy preterm and full-term infants birth to 1 year of age entering their first RSV season. Participants (pts) were randomized 2:1 to receive clesrovimab (105 mg IM) or placebo on day 1. Safety and tolerability were a primary endpoint. There were two hypothesis-tested endpoints: the efficacy of clesrovimab against RSV-associated medically attended lower respiratory tract infection (MALRI) through day 150 (primary) and against RSV-associated hospitalization through day 150 (secondary). The MALRI definition required ≥1 indicators of lower respiratory tract infection (LRI) or severity. To facilitate comparison across RSV mAb trials, a definition of RSV-associated MALRI that required ≥2 indicators of LRI/severity (≥1 indicator of LRI and ≥1 indicator of severity) was assessed post hoc. Results There were 3,632 pts randomized across 22 countries; &amp;gt;99% received study intervention. RSV-associated efficacy endpoints through day 150 and day 180 are shown in Table 1. Clesrovimab reduced the incidence of RSV-associated MALRI requiring ≥1 indicator of LRI/severity (60.4% [95% CI: 44.1, 71.9], p&amp;lt; 0.001) and ≥2 indicators of LRI/severity (88.0% [95% CI:76.1, 94.0]), RSV hospitalization (84.2% [95% CI: 66.6, 92.6], p&amp;lt; 0.001), and severe MALRI (91.7% [95% CI:62.9, 98.1]) through day 150 postdose compared to placebo. Efficacy increased with increasing RSV-associated disease severity and was similar from days 1-180 compared to days 1-150 across endpoints. The proportions of pts with adverse events (AEs), including injection-site and systemic AEs, drug-related AEs, and serious AEs were comparable between the clesrovimab and placebo groups (Table 2). There were no treatment-related deaths or deaths attributed to RSV disease. Conclusion A single dose of clesrovimab given before or during the first RSV season was efficacious in reducing RSV-associated MALRI and RSV-associated hospitalization in healthy preterm and full-term infants and was generally well tolerated with a safety profile comparable to placebo. Disclosures Heather J. Zar, PhD, MSD, Pfizer, AstraZeneca, Moderna (DSMB): Advisor/Consultant|MSD, Pfizer, AstraZeneca, Moderna (DSMB): Grant/Research Support|MSD, Pfizer, AstraZeneca, Moderna (DSMB): Honoraria|MSD, Pfizer, AstraZeneca, Moderna (DSMB): MSD Principal Investigator for the study and on MSD Advisory Board Eric Simoes, MD DCH, Pfizer, Sanofi, Merck, Icosavax, Enanta Cidara, Adiagio, Nuance, Shionogi, GIlead,: Advisor/Consultant|Pfizer, Sanofi, Merck, Icosavax, Enanta Cidara, Adiagio, Nuance, Shionogi, GIlead,: Grant/Research Support|Pfizer, Sanofi, Merck, Icosavax, Enanta Cidara, Adiagio, Nuance, Shionogi, GIlead,: Honoraria|Pfizer, Sanofi, Merck, Icosavax, Enanta Cidara, Adiagio, Nuance, Shionogi, GIlead,: MSD - PI for this study; DSMB Abbvie, Moderna, GSK Sabhir Madhi, MD, Pfizer, GSK, Medimmune, Merck &amp; Co., Inc., Rahway, NJ, USA: Grant/Research Support|Pfizer, GSK, Medimmune, Merck &amp; Co., Inc., Rahway, NJ, USA: Honoraria Octavio Ramilo, MD, Pfizer, Sanofi, Gates Foundation, NIH, and Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Advisor/Consultant|Pfizer, Sanofi, Gates Foundation, NIH, and Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Grant/Research Support|Pfizer, Sanofi, Gates Foundation, NIH, and Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Honoraria|Pfizer, Sanofi, Gates Foundation, NIH, and Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): SAC member for MSD Shelly Senders, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Julie S. Shepard, MD, MPH, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Kamolwish Laoprasopwattana, MD, Merck &amp; Co., Inc., Rahway, NJ, USA: Grant/Research Support|Merck &amp; Co., Inc., Rahway, NJ, USA: MSD - PI for this study Jorge Piedrahita, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Jose M. Novoa Pizarro, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Principal Investigator for the study for MSD Sergio L. Vargas, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Marc Dionne, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Teresa Jackowska, MD, MSD Poland, Merck &amp; Co., Inc, Rahway, NJ, USA: Advisor/Consultant|MSD Poland, Merck &amp; Co., Inc, Rahway, NJ, USA: Grant/Research Support|MSD Poland, Merck &amp; Co., Inc, Rahway, NJ, USA: Honoraria|MSD Poland, Merck &amp; Co., Inc, Rahway, NJ, USA: MSD - PI for this study Enmei Liu, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Yasunori Ishihara, MD, PhD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Kazushige Ikeda, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Principal Investigator Ying Zhang, PhD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Employee|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Stocks/Bonds (Public Company) Radha A. Railkar, PhD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, US (MSD): Employee|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, US (MSD): Stocks/Bonds (Public Company) Jeannine Lutkiewicz, BS, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Employee|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Stocks/Bonds (Public Company) Andrew W. Lee, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Employee at the time of study|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Stocks/Bonds (Public Company) Andrea Guerra, MD, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Employee|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA: Stocks/Bonds (Public Company) Anushua Sinha, MD, MPH, Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Employee|Merck Sharp &amp; Dohme LLC, a subsidiary of Merck &amp; Co., Inc., Rahway, NJ, USA (MSD): Stocks/Bonds (Public Company)

  PublisherOA PDFDOI

• Novel Porcine Model Reveals Two Distinct LGR5 Cell Types during Lung Development and Homeostasis

  American Journal of Respiratory Cell and Molecular Biology · 2024-11-05 · 1 citations

  articleOpen accessSenior author

  Abstract Cells expressing leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) play a pivotal role in homeostasis, repair, and regeneration in multiple organs, including skin and gastrointestinal tract, but little is known about their role in the lung. Findings from mice, a widely used animal model, suggest that lung LGR5 expression differs from that of humans. In this work, using a new transgenic pig model, we identify two main populations of LGR5+ cells in the lung that are conserved in human but not mouse lungs. Using RNA sequencing, three-dimensional imaging, and organoid models, we determine that in the fetal lung, epithelial LGR5 expression is transient in a subpopulation of SOX9+/ETV5+/SFTPC+ progenitor lung tip cells. In contrast, epithelial LGR5 expression is absent from postnatal lung but is reactivated in bronchioalveolar organoids derived from basal airway cells. We also describe a separate population of mesenchymal LGR5+ cells that surrounds developing and mature airways, lies adjacent to airway basal cells, and is closely associated with nerve fibers. Transcriptionally, mesenchymal LGR5+ cells include a subset of peribronchial fibroblasts that express unique patterns of SHH, FGF, WNT, and TGF-β signaling pathway genes. These results support distinct roles for LGR5+ cells in the lung and describe a physiologically relevant animal model for further studies on the function of these cells in repair and regeneration.

  PublisherOA PDFDOI

• A gene edited pig model for studying LGR5+ stem cells: implications for future applications in tissue regeneration and biomedical research

  Frontiers in Genome Editing · 2024-06-06 · 2 citations

  reviewOpen accessSenior authorCorresponding

  Recent advancements in genome editing techniques, notably CRISPR-Cas9 and TALENs, have marked a transformative era in biomedical research, significantly enhancing our understanding of disease mechanisms and helping develop novel therapies. These technologies have been instrumental in creating precise animal models for use in stem cell research and regenerative medicine. For instance, we have developed a transgenic pig model to enable the investigation of LGR5-expressing cells. The model was designed to induce the expression of H2B-GFP under the regulatory control of the LGR5 promoter via CRISPR/Cas9-mediated gene knock-in. Notably, advancements in stem cell research have identified distinct subpopulations of LGR5-expressing cells within adult human, mouse, and pig tissues. LGR5, a leucine-rich repeat-containing G protein-coupled receptor, enhances WNT signaling and these LGR5 + subpopulations demonstrate varied roles and anatomical distributions, underscoring the necessity for suitable translational models. This transgenic pig model facilitates the tracking of LGR5-expressing cells and has provided valuable insights into the roles of these cells across different tissues and species. For instance, in pulmonary tissue, Lgr5 + cells in mice are predominantly located in alveolar compartments, driving alveolar differentiation of epithelial progenitors via Wnt pathway activation. In contrast, in pigs and humans, these cells are situated in a unique sub-basal position adjacent to the airway epithelium. In fetal stages a pattern of LGR5 expression during lung bud tip formation is evident in humans and pigs but is lacking in mice. Species differences with respect to LGR5 expression have also been observed in the skin, intestines, and cochlea further reinforcing the need for careful selection of appropriate translational animal models. This paper discusses the potential utility of the LGR5 + pig model in exploring the role of LGR5 + cells in tissue development and regeneration with the goal of translating these findings into human and animal clinical applications.

  PublisherOA PDFDOI

• Organogenesis and related approaches for organ replacement

  Elsevier eBooks · 2024-01-01

  book-chapter
  PublisherDOI

• A LGR5 reporter pig model closely resembles human intestine for improved study of stem cells in disease

  The FASEB Journal · 2023 · 18 citations

  • Biology
  • Molecular biology
  • Cell biology

  ISCs are reproducibly isolated in LGR5-H2B-GFP pigs and used to model CRC in an organoid platform. The known anatomical and physiologic similarities between pig and human, and those shown by crypt-base FISH, underscore the significance of this novel LGR5-H2B-GFP pig to translational ISC research.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01HD048510

  NIH · $1.5M · 2012

• NIH Grant R21OD010553

  NIH · $213k · 2014

• NIH Grant R01HL051587

  NIH · $4.6M · 2015

• NIH Grant R21OD01055301A1

  NIH · $186k · 2014

• Improved large animal model for the study of adult stem cells

  NIH · $413k · 2014–2017

Frequent coauthors

• Shengdar Q. Tsai

  St. Jude Children's Research Hospital

  28 shared

• Steve Bischoff

  Helix (United States)

  21 shared

• Matthew B. Fisher

  North Carolina State University

  20 shared

• Stephanie G. Cone

  University of Wisconsin–Madison

  19 shared

• Kathryn M. Polkoff

  North Carolina State University

  18 shared

• Nicholas E. Hardison

  17 shared

• Sean Simpson

  16 shared

• Alon Greenbaum

  University of North Carolina at Chapel Hill

  14 shared

Education

• Ph.D., Comparative Biomedical Sciences

  North Carolina State University

  2008

• M.S., Comparative Biomedical Sciences

  North Carolina State University

  2004

• B.S., Animal Science

  North Carolina State University

  2002