Sneak Peak

As you all know, Matthew is defending his dissertation in just a few short weeks. He spends most nights on the computer typing away at the kitchen table. Which is ok, because most nights I'm studying as well, except one night when I gave him my pouty lipped guilt face and used the old, "I feel like I haven't gotten to spend any time with you." Which is passive aggressive for, "I'm really ready to watch the Olympics, let's hurry it up". :)

So, to give you all a little teaser for his big debut. Here is the first paragraph of his paper... I don't even know if I'm allowed to do this. Oh well.... I don't think my own husband would sue me for copyright issues.

Neutrophilic Inflammation

Polymorphonuclear leukocytes (PMNs), or neutrophils, play an important role in the body’s innate immune system’s response to invading pathogens. PMNs originate in the bone marrow and traffic through the blood until such time as they are recruited to a site of infection or inflammation in the tissues. (1) A family of molecules called chemokines are responsible for neutrophil migration of out the blood stream into the periphery. (2) There are several sub-groups of chemokines, but neutrophil specific chemokines are glutamate-leucine-arginine positive CXC chemokines (ELR+CXC). Interleukin-8 (IL-8) or CXCL8, growth related oncogene (GRO) – α (CXCL1), GRO-β (CXCL2), and GRO–γ (CXCL3) are the primary chemokines in humans. In mice they are cytokine induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP2) (3, 4). In humans these ELR+CXC chemokines bind to CXC receptors 1 and 2 (CXCR1 and CXCR1), although there is only CXCR2 in mice. (5) Neutrophils follow a concentration gradient of these chemokines from the circulation into the tissues at sites of inflammation. (6) The CXC receptors are G-protein coupled receptors (GPCRs), they signal rearrangement of the cytoskeleton via a Gβγ subunit. CXCR activation leads to polymerization of the actin-myosin network in a subcellular localization with actin-myosin depolymerization away from the site of receptor ligation, leading to directional movement of the cell. (7) Upon reaching the tissue the PMNs release their anti-microbial enzymes through a process of degranulation, and can perform an oxidative burst, both of which are mechanisms by which the cells phagocytose and destroy the invading pathogen. (1, 8, 9)

This is hilarious to me... considering that I understand about 10-15% of the whole thing.

Neutrophil- ok, I know this. I look those up on my patient's lab work every week. Who knew that polymorphonuclear leukocytes was another name for neutrophil? You learn something new everyday.

Chemokines- I only know that from vaguely knowing what M's research is about

Mice- I know that one!

Actin-myosin- Remember this from Exercise Physiology

Enzyme- If I didn't know this, I should consider a change in profession

Anti-microbial- hand gel, right?!

And that about sums it up. What's even more hilarious is Matthew likes to ask me to proof read his papers after Ed has looked over them. Just to see if I can catch anything... REALLY? Fortunately for him, my Lipscomb High School education prepared me for this... I am a grammar maniac. Give me any sentence, and I will diagram it for you in a matter of seconds. Now having said this, please don't reread my blog to catch me for grammar mistakes (Heather). I don't proof-read when I write for fun!

Back to the dissertation... Thankfully for Matthew, I could pick a comma splice out of a 2,000 lb haystack (which would equal a ton, right?). My hubby loves him a good run-on sentence. Unfortunately for Matthew, I understand hardly anything. Which sort of defeats the purpose.

And just to make sure that I'm not plagiarizing. Here is my reference. :)

Hardison, M.T.,(2010). A Dual Protease Inhibitor/Receptor Antagonist with Therapeutic Implcations in Chronic Inflammatory Lung Disease. Journal- TBD.