Bio Dr. Hodges received his B.S. in Biology from Berry College in 1996 and his Ph.D. in Genetics from Case Western Reserve University in 2002. His graduate training was in the laboratory of Dr. Patricia Hunt where his studies focused on the genetics of chromosome segregation during meiosis and infertility using mouse models. Dr. Hodges then undertook postdoctoral training with Dr. Steven Stice at the University of Georgia studying early embryo dysfunction of clones from nuclear transfer using pigs and cows as model systems. Dr. Hodges returned to Case Western Reserve University to train with Dr. Terry Hassold using mouse models to study chromosome segregation and reproduction. In 2005, Dr. Hodges joined the laboratories of Dr. Mitchell Drumm and Dr. Mark Palmert in which he created two conditional Cftr mouse models that are currently being used to study various aspects of the disease Cystic Fibrosis. Dr. Hodges joined the faculty of the Department of Pediatrics at Case Western Reserve University in 2009. Research Interests Cystic Fibrosis (CF) is a systemic disease affecting many parts of the body including pulmonary, gastrointestinal, pancreatic, immune, endocrine and reproductive systems. With this in mind, we are interested in determining the extent to which specific cell types contribute to CF disease characteristics, whether the pathophysiology can be halted or reversed by CFTR functional correction and understanding the molecular mechanisms behind the physiological consequences of CFTR's absence. We are beginning to address these issues through the use of traditional CF mouse models as well as recently created CF mouse models that allow for the conditional inactivation or restoration of Cftr function in specific tissues, cell types as well as at specific developmental time points. My laboratory is particularly interested in how the loss of CFTR leads to the intestinal dysfunction and reduced growth phenotypes associated with CF. Another focus of the lab is to generate new CF mouse models to test therapeutic approaches. We have recently created humanized CFTR mice with specific human mutations as tools to test CFTR-directed therapies in vivo.