Research Opportunities for Residents and Fellows
Labs with Research Projects
HUDNALL LAB
PI: David Hudnall, BML 116B
david.hudnall@yale.edu
The Hudnall Lab is involved in a number of studies focused upon the functional significance of tumor-infiltrating inflammatory cells in human cancer. In particular, the lab is studying the reactive infiltrate in Hodgkin lymphoma. Methods used include immunohistochemistry with novel markers, RT-PCR, DNA sequencing, Western blotting, cell culture, and laser capture microdissection.
Potential resident projects:
1. Development and application of two-color immunohistochemistry to define specific inflammatory cells (Th1, Th2, Th3, Treg, M1 and M2) in Hodgkin lymphoma biopsies.
2. Laser capture microdissection and molecular analysis of Reed-Sternberg cells from EBV+ and EBV- cases of Hodgkin lymphoma.
3. Laser capture microdissection and molecular analysis of T-cell rosettes in Hodgkin lymphoma.
KYRIAKIDES LAB
PI: Themis Kyriakides, Amistad Research Building 301C
themis.kyriakides@yale.edu
Research Project: Thrombospondin-2 and diabetic wound healing.
Project Description: Investigation of TSP2 levels in skin and wounds of diabetic patients and analysis of wound healing in wild type and TSP2-null mice made diabetic via streptozoticin treatment. Analyses include immunohistochemisty, quantitative PCR, and western blot.
Required background: Experience with immunohistochemistry or western blots is desired but not essential. Residents that can provide assistance with histological evaluations are encouraged to contact the lab.
Time Requirement: 4-6 hours per week (2-3 hours per day; two consecutive days per week). Completion of the project is anticipated within in 4-6 months, but has the potential to expand.
MADRI LAB
PI: Joseph A. Madri, Lauder Hall LH115
joseph.madri@yale.edu
Research Project: Early identification of very low birth weight premature infants at risk for developing significant neurodevelopmental handicaps.
Project Description: Over 60,000 very low birth weight premature infants are born in the USA every year having a survival of approx. 85%. Many (up to 50%) suffer significant intellectual disability and cerebral palsy. This condition has been successfully modeled in mice, with the mice mimicking the morphological, biochemical and behavioral pathologies observed in this human population. Using this murine model and transcriptome analysis we have identified many dysregulated genes. We have used neural stem cells and microvascular endothelial cells isolated from murine pup brains in 2- and 3-dimensional co-culture to mimic the subventricular neurovascular niche. Using these co-culture models, we have elucidated several signaling pathways affected by specific gene dysregulations. Using this information, we have utilized selected ELISA assays and selected SNP analyses to validate our in vitro findings in our murine models and in cord blood samples of premature infants with the goal of developing a rapid diagnostic test to identify premature infants “at risk” for developing significant neurodevelopmental handicaps and ultimately to monitor future therapies developed from our mechanistic studies.
A resident would utilize ELISA assays to determine cord blood levels of BDNF, SDF-1 and VEGF (which we know to be depressed in mice experiencing behavioral pathologies and in a 30 patient training set). In addition, a resident could also perform selected SNP analysis, identifying specific BDNF, SDF-1 and VEGF polymorphisms (which we also know to be expressed in mice experiencing behavioral pathologies and in a 30 patient training set).
Drs. C. & I. Buhimuschi in Maternal and Fetal Medicine have collected and made available 400 well-annotated samples of premature infant cord blood obtained from patients displaying a range of risk factors associated with neurodevelopmental handicaps). Testing these samples for these proteins and their selected polymorphisms is expected to result in a reliable test (in conjunction with established clinical parameters) for early detection of at risk infants and facilitate the development of novel therapies designed to beneficially affect neurogenesis.
MOECKEL LAB
PI: Gilbert Moeckel, LB 20
gilbert.moeckel@yale.edu
Please contact Dr. Moeckel for available projects.
MORROW LAB
PI: Jon Morrow, BML 140
jon.morrow@yale.edu
Please contact Dr. Morrow for available projects.
POLITI LAB
PI: Katerina Politi, SHM I 242A
katerina.politi@yale.edu
Please contact Dr. Politi for available projects.
ROBEK LAB
PI: Michael Robek, LH315
michael.robek@yale.edu
Research Project: Development of HBV therapeutic vaccine vectors.
Project Description: The HBV-specific immune response is weak in individuals who become chronically infected with the virus. Therapeutic vaccination to boost the immune response in chronically infected people is a potential new way to treat the infection. We are developing vaccine vectors based on the vesicular stomatitis virus as potential improved prophylactic and novel therapeutic vaccines for HBV infection. Analyses include histological evaluation of liver disease in immunized mice.
Required background: Experience with cell culture and mice is preferred but not required.
Time Requirement: 4-6 hours per week.
SHADEL LAB
PI: Gerald Shadel, BML 371
gerald.shadel@yale.edu
Research Project 1. Mitochondrial signaling in deafness pathology.
Project Description: We recently have developed a mouse model of hearing loss that we hypthesize recapitulates the pathology of deafness-associated mtDNA mutations. The project would be to determine the underying cochlear pathology, which ultimately involves death of the hairs cells. The project could occur over the period of a few months and could be done and would involve collaborators that have expertise in measuring hearing loss and looking for specific pathology. Finally, we want to treat the animals with aminoglycosides, which we predict will exacerbate the hearing loss and cross these animals to other trasgenic and knock-out mice to achieve therapeutic endpoints.
Research Project 2. Mitochondrial involvement in neurdegeneration and Ataxia-Telangiectasia Pathology.
Project Description: We are studying two mouse models of neurdegeneration and testing the hypothesis that mitochondrial damage and dysfunction underlie Pathology. We are also in a collaboration involving a potentially therapeutic drug. The project would involve examining tissues for mitochondria defects in mouse tissues +/- the drug (already in hand) and would involve some assay development, for example a PCR-based assay for mtDNA damage. We are also studying muscle and bone pathology in ATM null mouse models of A-T.
These projects could occur over a span of a few months.
STERN LAB
PI: David Stern, BML 348A
dfstern@yale.edu
Please contact Dr. Stern for available projects.