Biology and Bio-Engineering

Dr. Shane Burch, MD, is an orthopaedic surgeon who specializes in spinal disorders. He is a Professor in Residence in the UCSF Dept. of Orthopaedic Surgery and cross appointed to the Department of Neurological Surgery.

Dr. Burch’s clinical practice focuses on the surgical treatment of the cervical, thoracic, lumbar and sacral regions of the spine. He is an international leader in computer assisted and robotic surgery and uses these techniques to perform both highly complex procedures and minimally invasive procedures of the spine.

Matthew Bucknor, MD, is an Associate Professor in Residence in the Musculoskeletal Imaging subspecialty section, and the Inaugural Associate Chair for Wellbeing and Professional Climate in the UCSF Department of Radiology and Biomedical Imaging. He is also the Chair of the Radiology and Biomedical Imaging Diversity Committee in the Department of Radiology and Biomedical Imaging at the University of California, San Francisco.

Originally from Liverpool, England, Andrew graduated with a PhD in Molecular Biology and Biophysics from King’s College London. He did two postdoctoral fellowships, the first with Simon Hughes at King’s College London and the second with Tom Rando at Stanford University. Andrew started his own lab at the Center for Regenerative Medicine, MGH, Harvard University in 2008. In 2015 he moved to UCSF to begin the next phase of his lab's journey.

Dr. Stefano Bini, MD was born in Italy, raised in Australia (he still has a slight Aussie accent) and finished high school in San Francisco. He received his BA from Stanford University, his MD from Columbia University’s College of Physician and Surgeons, and completed Residency training at UCSF. Subsequently, he completed a Fellowship at the Rizzoli Orthopaedic Institute in Italy and obtained a second MD from the University of Florence (and ate lots of great food!). Prior to joining the faculty at UCSF, Dr. Bini worked at Kaiser Permanente as a joint replacement surgeon.

My research is focused on the hormonal regulation of calcium metabolism, and includes projects involving the classic target tissue of bone as well as non classic tissues such as the skin. The projects  with bone focus on the mechanisms by which parathyroid hormone and insulin like growth factor-1 regulate bone formation and differentiation, the response of bone to mechanical loading and unloading, and the ability of bone to heal fractures. We use a number of cell specific gene deletion models in different cells in the skeleton to address these questions.

The long-term goal of my research is to understand the role of tissue secretory senescent cells in aging, autoimmunity and metabolic diseases. Our recent discovery shows that pancreatic beta cells acquire a secretome during T1D in mice and human and exhibit many non-cell autonomous properties. Senescent beta cells can remodel the islet environment in a paracrine manner by promoting bystander senescence and immune surveillance. We have identified key immune cells that can selectively eliminated senescent beta cells to halted progression of beta cell destruction prevent T1D in mouse models.

Dr. Sigurd H. Berven has a strong clinical interest in spinal disorders of children and adults. He is interested in pediatric and adult deformity, degenerative conditions of the spine, spinal tumors and spinal trauma. His research interests include assessment of clinical outcomes of surgery, and minimally invasive techniques in spine surgery.  Berven also is studying cellular and molecular techniques for the biological regeneration of components of the spine including the intervertebral disc.

The Ahituv lab is focused on understanding the role of regulatory sequences in human biology and disease. Through a combination of comparative genomic strategies, biochemical assays, regulatory element analysis, human patient samples, mouse and fish genetic engineering technologies, and massively parallel reporter assays they are working to elucidate mechanisms whereby genetic variation within these sequences lead to changes in human phenotypes.