The title of the REAL paper that Rob wrote and is getting published is entitled, "Adsorbed Fibrinogen Regulates the Behavior of Human Dendritic Cells in a CD18-Dependent Manner." I'm not sending it out because it's huge. Like 10 MB with the figures and all that.
The idea for sending out the fake paper in an e-mail was spawned late at night a month or so ago. Rob was in a funny mood and was making me laugh giving me a detailed account of why I was a house cat, all in the same manner and set-up as a real paper would be. Materials and methods, all that. I told him then that he'd have to write it out so we could tell people that was his paper. So today he spent a good 2 hours plus writing it, just to make me happy.
We're glad you all enjoyed it. If you didn't read it because you thought it was his real paper, you should read it now that I'm telling you it's not. If you're ACTUALLY interested in reading Rob's paper, e-mail me and let me know. Rob says he has smaller versions of it. But, trust me, it's not near as exciting as the fake paper we sent out.
Rob and Tamra
This is a paragraph on Rob's paper that I found on-line (just so you can see how NON-exciting the paper is):
The involvement of fibrinogen in inflammation has been considered by many, but the roles of the protein in that process have yet to be fully elucidated. The protein readily coats surfaces and is deposited at sites of inflammation. Furthermore, adsorbed fibrinogen influences many cells of the immune system, likely a result of increased receptor recognition upon ligand immobilization. To better understand adsorbed fibrinogen's role in inflammation, we studied the effects of the protein, adsorbed to the surface of microscopic beads, on human dendritic cells. Adsorbed fibrinogen increased dendritic cell expression of IL-6, IL-8, MIP-1beta and MCP-1. In contrast, solution phase fibrinogen had no effect. Importantly, dendritic cells formed complexes with, and subsequently accumulated around, beads in fibrinogen-dependent fashion. Antibodies directed against CD18 significantly decreased cytokine/chemokine expression and bead-cell complexation. Epsilon-aminocaproic acid limited bead-cell complexation, suggesting fibrinogen degradation products modulate dendritic cell activity. In support of this proposal, fibrinogen fragment D also increased MCP-1 expression by human dendritic cells. Taken together our data indicate adsorbed fibrinogen and its degradation products directly influence human dendritic cell operation. We propose a model whereby adsorbed fibrinogen plays a distinct causatory role in inflammation through its beta(2) integrin-mediated interaction with dendritic cells.
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