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Summer Research Opportunities

The Molecular Medicine and Translational Science program participates in the SROP (Summer Research Opportunities) program sponsored by the Wake Forest University Graduate School of Arts and Sciences. The following is a list of recent research projects for the Molecular Medicine and Translational Science Graduate program participants.  For information on how to apply, follow this SROP Graduate School link.  MMTS opportunities for the summer of 2011 will be announced in January-February of 2011.

Cristina Furdui, PhD 
Internal Medicine/Molecular Medicine

Research in our laboratory is directed towards applying advanced systems biology methodologies to i) investigate the timing of signaling events in the propagation of receptor tyrosine kinases signaling, ii) quantify the effect of oncogenic mutations or oxidation on the re-wiring of these signaling networks under pathogenic conditions, iii) apply clinical proteomics to identify molecular predictors of response to different  cancer therapies in an effort to create personalized therapies; and iv) interface time-resolved mass spectrometry with microfluidics technology and develop new nanokinetics platforms for quantitative monitoring of rapid enzyme kinetics/drug screening assays to further our understanding of potential drug targets at molecular level. To accomplish our goals, we are taking a cross-disciplinary approach based on:

  • proteomics methodologies
  • specific instrumentation for cellular stimulation with growth factors with millisecond time resolution,
  • highly specific molecular probes for the detection of sulfenic acid containing proteins as key intermediates in redox signaling, and
  • computational methods to integrate and evaluate the massive amount of data generated by the proteomics approach.    

Mark Van Dyke, PhD
Regenerative Medicine

Using keratin biomaterials to treat spinal cord injury.

Michael Seeds, PhD  & Duncan Hite, M.D.
Internal Medicine/Molecular Medicine/Pulmonary, Critical Care, Allergic and Immunologic Disease

Our laboratories have several projects on the inflammatory biochemistry of lung diseases and acute lung injury.  Secretory Phospholipase A2 (sPLA2) proteins are elevated in a variety of lung diseases, including Acute Respiratory Distress Syndrome (ARDS), and asthma.  Although much is known about the 10 human genes coding different sPLA2 proteins, the identity of the specific sPLA2 proteins in the injured lung and the mechanisms by which injury occurs is largely unknown. 

Specific tasks, suitable for a summer project, are given here.  More information can be gathered clicking either faculty link.

Project 1.  Develop novel antibody based assays to identify specific phospholipase A2 proteins.  Using antibodies raised by our laboratory, the student will develop immunoassays for use in analyzing inflammatory proteins in archived ARDS patient samples from our studies.  These assays may include ELISAs, immuno-histochemistry, and Western blotting.

Project 2.  sPLA2 hydrolyze pulmonary surfactant phospholipids causing surfactant dysfunction.  ARDS patient surfactant samples will be analyzed to determine surfactant composition and function that occurred in the lung during the disease.  The nature of the surfactant injury will be confirmed by treating purified surfactant components with recombinant sPLA2 in the laboratory, comparing the findings to the analysis of the ARDS patient samples to determine mechanisms of injury.

Cristin Ferguson, M.D.  
Orthopaedics

Title: Impact of oxygen tension, growth factor, and HIF-1a signaling on human adipose derived stem cell differentiation into fibrochondrocytes

This project will investigate the impact of hypoxia, growth factor supplementation, and HIF-1a signaling on the differentiation of human adipose derived stem cells toward the fibrochondrocyte phenotype compared with normal human meniscus tissue standards. These cell culture based studies will improve our understanding of human meniscus biology and will lay the foundation for effective bioreactor cultivation approaches for meniscus tissue regeneration.

Donald Bowden, PhD 
Center for Genomics and Personalized Medicine Research

My laboratory carries out research on the genetic basis of common diseases with specific emphasis on type 2 diabetes and the complications of type 2 diabetes. Multiple studies are underway which use modern molecular genetic techniques to identify genes contributing to diabetes and its components of insulin sensitivity and beta cell dysfunction, diabetic nephropathy, cardiovascular and cerebrovascular disease.

April E. Ronca, PhD  
Professor, Obstetrics & Gynecology
Women's Health Center of Excellence for Research, Leadership, Education

Research in our lab focusses on animal models of obstetric complications (birth asphyxia; prenatal stress), perinatal epigenetic programming of neurodevelopmental disorders, and phenotypic developmental profiling of genetically and/or environmentally altered rodent models combining molecular and cellular neurobiological, biochemical, behavioral and neuroimaging approaches.

Studies underway include: 

1) Analyses of the birth program as a key, organizing event in the transition from prenatal to postnatal life

2) Establishing neurometabolic biomarkers for enduring consequences of obstetric complications using In Vivo Proton Magnetic Resonance Spectroscopy (MRS) and In Vitro Nuclear Magnetic Resonance (NMR)

3) Translational analyses of prenatal movement in mice and rats following genetic and/or environmental manipulations

4) Developmental of adult body weight regulation, HPAA activity and behavior following moderate, variable prenatal stress

George Kulik, D.V.M., PhD
Associate Professor, Cancer Biology
Comprehensive Cancer Center

Animals, whole, cancer/oncogenesis, drugs/therapeutic agents pharm, human, cells only, reproductive system, basic mechanisms

Projects:

  1. Loss of Mcl-1 is necessary to induce rapid apoptosis in cells with dephosphorylated BAD
    a. does Mcl-1 knockout sensitize cells to BAD dephoshorylation?
    b. cooperation between BAD and Mcl-1 r in other cell lines.

  2. Is BAD phosphorylation necessary for prostate cancer development in vivo?
    PTENp-/-BAD3SA mice

  3. Prostate-selective inhibitors of anti-apoptotic pathways.

  4. Monitoring activity of survival signaling pathways in tumors in vivo.
    a. luminescent reporters of PKA/CREB/CRE pathway
    b. luminescent reporter of Mcl-1 expression.

  5. Stress/epinephrine; role in therapy resistance and cancer progression
    a. anti-apoptotic signaling in prostate tumors
    b. effects on therapy resistance
    c. prostate cancer patients; epinephrine levels and PKA/BAD/Mcl-1 in tumors
Last Updated 11/28/2011
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