May 2010


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Biosciences Graduate Students <[log in to unmask]>
Wed, 5 May 2010 17:35:58 -0400
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"Diane St. Germain" <[log in to unmask]>
George Mason University
To: Biology Graduate Students <[log in to unmask]>, Anna Baranova <[log in to unmask]>, Daniel N Cox <[log in to unmask]>, Alan H Christensen <[log in to unmask]>, Chip Petricoin <[log in to unmask]>, Geraldine M Grant <[log in to unmask]>, Karl J Fryxell <[log in to unmask]>, Monique Van Hoek <[log in to unmask]>, Yuntao Wu <[log in to unmask]>, Charles L Bailey <[log in to unmask]>, Jim Willett <[log in to unmask]>, Serguei Popov <[log in to unmask]>, Lance Liotta <[log in to unmask]>, Valery Soyfer <[log in to unmask]>, Kylene Kehn-Hall <[log in to unmask]>, Fatah Kashanchi <[log in to unmask]>, [log in to unmask], [log in to unmask], Timothy Born <[log in to unmask]>, [log in to unmask] cc: "Gail L. Hodges" <[log in to unmask]>
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> *Dissertation Defense Reminder:
> *
> *Margaret C. Emblom-Callahan
> PhD Biosciences Candidate
> *
> *Date:   Thursday May 6, 2010
> Time:   1:00 p.m. 
> Place:  George Mason University
> ** 	     Discovery Hall Auditorium
> 	     Prince William Campus <>
> Dissertation Chair: Dr. Geraldine Grant
> Committee members: Dr. Daniel N. Cox, Dr. Timothy Born, Dr. Steven Nathan*
> A copy of the dissertation is on reserve in the Johnson Center 
> Library, Fairfax campus.  The doctoral project will not be read at the 
> meeting, but should be read in advance.
> All members of the George Mason University community are invited to 
> attend.*
> *
> *
> IPF is a fatal form of interstitial lung disease (ILD) of unknown etiology and for which there is no proven medical therapy.  The median post diagnosis survival time is three years.  While there are an estimated 5 million people affected by IPF world-wide, the prevalence continues to escalate.  In the United States alone the incidence of IPF has increased considerably from a reported 50,000 people in 2000 to current estimates closer to 200,000.  IPF is characterized by extensive parenchymal fibrosis which ultimately destroys the lungs' architecture and function.  This fibrosis results from an unremitting accumulation of fibroblasts concomitant with their relentless deposition of extra cellular matrix, predominantly in the form of type 1 collagen.  In light of this, the fibroblast is arguably the effector cell of the IPF phenotype.  With no effective therapy available and over 40,000 individuals dying annually, as many as die from breast cancer, there is clearly an immediate need to expand our understanding of IPF, and specifically the fibroblast.  This dissertation 1) presents a novel isolation method of the pulmonary fibroblast cell population from IPF and normal lungs derived without long-term tissue culture; 2) comprehensively characterizes the genomic phenotype of these non-cultured isolated pulmonary fibroblasts in IPF in comparison to normal controls, and 3) documents the evolution and /in vitro/ de-differentiation of this fibroblast model system.  This model is then compared to the current /in vitro/ explant-derived fibroblast model system  The insights gleaned from these studies will further our understanding of the contribution of the fibroblast to the pathogenesis of IPF in addition to providing a platform for systematically investigating aberrant pathways.  Moreover, the findings herein will promote and facilitate development of a more strategic approach to our investigations of this aberrant promoter of IPF progression -- the fibroblast.  
> ###