School of Medicine


Showing 1-10 of 10 Results

  • Theo Palmer

    Theo Palmer

    Professor of Neurosurgery

    Current Research and Scholarly Interests Members of the Palmer Lab study the biology of neural stem cells in brain development and in the adult. Our primary goal is to understand how genes and environment synergize in influencing stem cell behavior during development and how mild genetic or environmental risk factors for disease may synergize in their detrimental effects on brain development or in the risk of neuronal loss in age-related degenerative disease.

  • Jon Park, MD, FRCSC

    Jon Park, MD, FRCSC

    Saunders Family Professor

    Current Research and Scholarly Interests Non-fusion dynamic spinal stabilization, artificial disc technologies, and regenerative spinal technologies.

  • Josef Parvizi, MD, PhD

    Josef Parvizi, MD, PhD

    Professor of Neurology and, by courtesy, of Neurosurgery at the Stanford University Medical Center

    Bio Dr Parvizi completed his medical internship at Mayo Clinic and Neurology Residency at BIDMC Harvard Medical School before joining the UCLA for fellowship training in clinical neurophysiology and epilepsy. He has worked at Stanford University Medical Center since 2007 and specializes in treating patients with uncontrollable seizures. Dr. Parvizi is the principal investigator in the Laboratory of Behavioral and Cognitive Neuroscience whose research activities have been supported by National Institute of Health, National Science Foundation, and private foundations. To find out more about Dr Parvizi's scholarly activities please visit http://med.stanford.edu/parvizi-lab.html.

  • Zara Patel

    Zara Patel

    Associate Professor of Otolaryngology - Head & Neck Surgery (OHNS) and, by courtesy, of Neurosurgery at the Stanford University Medical Center

    Bio Dr. Zara M. Patel is Director of Endoscopic Skull Base Surgery and an Associate Professor of Otolaryngology and, by courtesy, of Neurosurgery at Stanford. She was born and raised in St. Louis, completed her MD at the Oregon Health and Sciences University in Portland, Oregon and completed her residency training in otolaryngology at Mount Sinai Medical Center in New York, NY. After pursuing fellowship training in rhinology and endoscopic skull base surgery at Stanford University, she was recruited to join the Emory University faculty in Atlanta in 2011. After four years, the rhinology division recruited her back to the West coast to rejoin the department here at Stanford University.

    Dr. Patel is an expert in advanced endoscopic sinus and skull base surgery. She treats patients with a wide variety of rhinologic complaints, including chronic sinus infection or inflammation, sinus disease that has failed medical therapy, sinus disease that has failed prior surgical therapy, cerebrospinal fluid leaks, benign and and malignant sinus and skull base tumors, as well as olfactory disorders.

    She is immediate past-Chair of the Education Committee and now Member of the Board of Directors for the American Rhinologic Society and has developed a multitude of educational materials for both physicians and patients to help them better understand rhinologic disorders. She is passionate about educating patients to allow them to make the best decisions about their own care, leading to better outcomes.

    Dr. Patel has published widely in topics such as avoiding complications in endoscopic sinus surgery, chronic rhinosinusitis in the immunosuppressed patient population, new devices and techniques for endoscopic skull base surgery, and olfactory dysfunction. She continues to perform research in these areas, and is beginning collaborative efforts with neuroscientists and engineers to develop technology that she hopes will eventually help cure patients with olfactory loss.

  • Claudia Katharina Petritsch

    Claudia Katharina Petritsch

    Associate Professor (Research) of Neurosurgery

    Current Research and Scholarly Interests We study cell fate mechanisms to understand intra-tumoral heterogeneity and overcome therapy resistance and immune suppression in brain tumors.

    Excessive proliferation, apoptotic evasion, and migratory spread are all hallmarks of tumorigenesis. However, these defects fail to explain the incredible heterogeneity and immune suppression observed in malignant brain tumors, two major hurdles to their treatment, which remains mostly palliative. Only once we elucidate the underlying biologic causes for heterogeneity and immune suppression, will we develop better treatment options for brain tumor patients and prevent malignant progression and tumor growth.

    In the healthy brain, neural stem cells generate progenitors, which in turn give rise to differentiating cells that will eventually acquire their final functional state. Cell fate decisions within these hierarchical brain cell lineages are tightly controlled and irreversible: e.g. cells in the state of differentiation will not turn into progenitor cells or stem cells. It is known that brain tumor cells, on the other hand, defy many general principles of neurobiology. This is especially true for malignant glioma cells, which simultaneously express markers of different lineages and states exhibiting incomplete differentiation. Tumor cell hierarchies are poorly understood, providing no explanation for why tumor cells with stem-like, progenitor-like, and differentiated features co-exist and interact with normal brain cells and immune-infiltrating cells within a single tumor entity, and how this heterogeneity relates to the lack of active immune infiltration.

    The Petritsch lab broadly investigates underlying causes for the intra-tumoral heterogeneity and immune suppression in brain tumors from a developmental neurobiology perspective. Defects in cell fate control could explain many key defects present in brain tumors and an understanding of how brain cells control the fate of their progeny may identify novel points of vulnerabilities to target with therapeutics. Of special emphasis, we study the establishment of cell fates within normal hierarchical brain lineages for comparison to the dysregulated cell-fate hierarchies seen in brain tumors. Our lab was the first to demonstrate that normal adult oligodendrocyte progenitor cells (OPCs) undergo asymmetric divisions to make cell fate decisions, i.e. to generate OPCs as well as differentiating cells each time they divide. Drawing from these data, we investigate whether brain tumors divide along hierarchical lineages and how oncogenic mutations might affect cell fate decisions within these hierarchies. A major line of investigation in our lab focuses on whether defects in asymmetric division lead to aberrant cell fate decisions that cause the paradigm mixed lineage phenotypes and the intra-tumoral heterogeneity present across tumors.
    To study interactions of tumor cells and the immune system, we have developed and utilized transplantable mouse glioma models. We are tasked to facilitate and coordinate the distribution of fresh tissue from the neurosurgery operating room, and have access to fresh brain tissue from patient surgeries, from which we prepare cell culture models for brain tumors and normal progenitors. We complement our work with human cells with studies in genetically engineered mouse models of gliomagenesis to conduct molecular, cellular and bioinformatic analyses

  • Giles W Plant

    Giles W Plant

    Associate Professor of Neurosurgery

    Current Research and Scholarly Interests Our research focuses on the repair of the injured spinal cord. We investigate the following areas:
    - Spinal cord injury (SCI): Axonal regeneration, myelination and gene therapy
    - Stem cell transplantation (adult, embryonic and iPS)
    - Endogenous stem cell activity after SCI

  • Kathleen Poston, MD, MS

    Kathleen Poston, MD, MS

    Associate Professor of Neurology and, by courtesy, of Neurosurgery, at the Stanford University Medical Center

    Current Research and Scholarly Interests My research addresses one of the most devastating and poorly treated symptoms that can develop in people with Parkinson's disease - Dementia. We use multi-modal neuroimaging along with genetic and biological markers to understand the different underlying causes of dementia and to understand why dementia develops more quickly in some patients, but not others.

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