October 2011


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Biosciences Graduate Students <[log in to unmask]>
"Diane St. Germain" <[log in to unmask]>
Tue, 25 Oct 2011 09:51:22 -0400
To: Biology Graduate Students <[log in to unmask]>, BINF Students <[log in to unmask]>, SSB Faculty <[log in to unmask]>, Raymond Weinstein <[log in to unmask]> cc: Jacqueline M Houle <[log in to unmask]>, Tiffany Sandstrum <[log in to unmask]>, Taissia Popova <[log in to unmask]>
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Dissertation Defense Announcement
To:  The George Mason University Community

Candidate: Bryan A. Millis
Program:    PhD Biosciences*
Date:   Thursday November 3, 2011
Time:   10:00 a.m. 
Place:  George Mason University
 	     Occoquan Bldg., Room 203
	     Prince William campus <>*
*Dissertation Chair: Dr. Serguei Popov
Committee members: Dr. Charles L. Bailey, Dr. Raymond Weinstein, Dr. Taissia Popova
*Title: "Induction of Host Extracellular Protein Dysfunction by /Bacillus anthracis/
Hemolytic Factors"

*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.


Barrier dysfunction represents one of the most predominant 
manifestations of an anthrax infection.  Massive pleural edema, which is 
classic of inhalational anthrax, is perhaps one of the only consistent 
symptoms among victims of this pathogen.  However, despite much research 
into how the pathogen escapes the initial immune response, there remains 
little treatment option at later symptomatic stages of infection.  This 
work demonstrates that a group of molecules having functions in barrier 
organization, including Syndecan-1, are either shed from the cell 
surface, or dysfunctional in this role.  This dysfunction is co-incident 
with manifestations of hemodynamic imbalance, resulting in both 
accumulation within the liver and induction of disseminated 
intravascular coagulopathy.  Further, we suggest specific secreted 
virulence factors that contribute to this dysfunction through 
acceleration of host cell shedding processes regulated by MAP kinase 
cascades.  The mechanism of action of these virulence factors points 
toward signaling disturbances which result not only in loss of these 
cell surface molecules, but also cytoskeletal disorganization and 
decoupling from adhesion processes.