Academic Title: Assistant Professor
Primary Appointment: Department of Obstetrics and Gynecology
3005 Smith East, MS-2028
Kansas City, Kansas, 66160
I completed my undergraduate and graduate studies and received my Ph.D. through Department of Physiology at Xian Medical University, China. Postdoctoral training was obtained in the laboratory of Dr. Marc Simard and Dr. Loren Thompson at University of Maryland School of Medicine. In 2006, I joined the faculty of the Department of Obstetrics and Gynecology at University of Kansas School of Medicine.
The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary. The most common underlying cause of perinatal brain injury is hypoxia/ischemia. Intrauterine hypoxia and birth asphyxia induced brain damage are associated with increased perinatal mortality and long term sequelae of neurodevelopmental compromise, seizures disorders and cerebral palsy. The roles of ROS, Ca2+, NMDA receptors, excitatory amino acids, and apoptotic genes on fetal brain injury have been studied exclusively. These works have led to substantial conceptual agreement on a general outline of how fetal brain injury triggers and evolves to produce neuropathologic lesions and neurodevelopmental disabilities. However, the precise etiological factors for the development of the majority of fetal hypoxic brain injury have not been identified satisfactorily. We initially indicated that multiple pathways involved in the fetal brain injury mediated by chronic hypoxia.
Role of proinflammation cytokine in fetal brain injury during chronic hypoxia: Our studies reveal an association between fetal hypoxemia damage and a marked inflammatory reaction that contributes to the tissue injury. With the approach of gene microarray and quantitation PCR techniques, we indicated that degrees of hypoxia induced stress created fetal organ damage via up regulation fetal pro-inflammatory cytokines; pro-inflammatory cytokines play a central role in the causation of fetal organ damage in hypoxia condition. However, the specific mechanism underlying these processes is poorly understood. The ultimate goal of our lab is to study the molecular mechanism of pro-inflammatory cytokine regulation in hypoxemia fetus.
Proteomic identification of specific proteins by chronic hypoxia in fetal organ damage: By utilizing advanced proteomic techniques, we found, a new novel protein, phosphorylated cofilin-1 dramatically down regulated in hypoxic fetal brain, and cofilin-1 post translational modification (phosphorylation), mediated by reactive oxygen species(ROS), involved in the novel mechanism of the fetal hypoxic brain damage. We hypothesize that chronic hypoxia induces the cofilin gene modification mediated by ROS. Dephosphorylated cofilin may evoke activation of apoptotic genes leading to neuronal damage in the preterm hypoxic fetal brain. Further studies will be performed, we hope the findings may provide a new concept resulting in the development of a pharmacological inhibitor to inactivate cofilin and prevent chronic hypoxia, which would have a major impact and implication on brain injuries in the fetus.
The laboratory has several openings for technicians, and postdoctoral fellows. Please email your CV/resume.