School of Medicine


Showing 21-30 of 107 Results

  • Harini Chakravarthy

    Harini Chakravarthy

    Postdoctoral Research fellow, Developmental Biology

    Current Research and Scholarly Interests The discovery that insulin-producing ?-cells can be generated from cell sources within and outside the pancreas is of fundamental importance in terms of developing novel treatment strategies for diabetes. A major caveat to this is our relatively poor understanding of the players involved in this process and the lack of molecular characterization of the ?converted? ?-cells. This knowledge is key to our success in enhancing this process to its maximum therapeutic potential and efficiency. In this context, recent work has shown that ?-cells can be used as a source to generate ?-cells under conditions of near-total ?-cell depletion in mice. However the molecular mechanisms regulating ?-cell identity are unknown. This knowledge would allow us to harness the potential of ?-cells to give rise to ?-cells in diabetic patients where pancreatic ?-cells tend to be in abundant supply within the pancreas. My work in the laboratory has elucidated the role of two genes in maintaining ?-cell identity: Dnmt1 and Arx. Dnmt1, a DNA methyltransferase methylates DNA and is involved in gene repression. Arx is a transcription factor that is essential for ?-cell specification during embryogenesis. My work demonstrates that conditional in vivo inactivation of Dnmt1 and Arx in adult ?-cells causes them to convert into insulin producing ?-like-cells demonstrating the necessity of these two factors in maintaining ?-cell fate. Further functional characterization of these ?converted? cells will elucidate the extent to which ?-to- ?-cell conversion has occurred in these animals. I am also assessing the individual contributions of Dnmt1 and Arx in maintaining adult ?-cell identity.

  • Chia Yu Alex Chang

    Chia Yu Alex Chang

    Postdoctoral Research fellow, Microbiology and Immunology

    Current Research and Scholarly Interests Duchenne muscular dystrophy (DMD) is an X-chromosome-linked genetic disease that is caused by a mutation in the dystrophin gene and affects 1 in every 3500 boys. DMD patients suffer progressive muscle wasting and eventual cardiorespiratory failure that results in an early death in the second or third decade of life. Although extensive research effort has been invested, lack of a good mouse model that mimics the cardiac failure hinders research. We have developed a novel mouse model that exhibit all the symptoms found in DMD patients and our research is aimed at understanding the cardiac failure in DMD for future therapeutic interventions. Our mouse model fully recapitulates the DMD symptoms because we also took into account of the size of human protection DNA on chromosomal ends (telomere) compared to mouse. We would like to study the cause of cardiac failure in our mouse model by 1) determine if telomere shortening is specific to cardiomyocytes, 2) evaluate the level of cellular damage caused by oxidative stress and 3) identify the source of oxidative stress. These experiments will help us to better understand cardiac failure in DMD patients and allow testing of therapeutic interventions.

  • Junlei Chang

    Junlei Chang

    Postdoctoral Research fellow, Hematology

    Current Research and Scholarly Interests With various in vitro tools and in vivo mice models, I am focusing on dissecting the roles of GRP124, GPR125 and Wnt signaling in CNS angiogenesis and vascular integrity after stroke from a translational perspective.

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