Among other things, I spent ten weeks of the summer prior to my Senior year in Albany, New York doing research for the New York State Dept. of Health.  I had a really awesome time and would do it all over again - provided it was in the summer and I could find my earmuffs.

Here's the best way I could come up with to tell you about it all (or "awl" in NY speak):
Who
What
When
Where
Why

Summer Updates

With whom did I spend my time?

During the day I spent my time with my lab mates in the Wadsworth Center.  I did research for Dr. Xinxin Ding and there were about ten people in his group.  Specifically, I worked with Guoyu, who is a grad student there.  Much like the rest of the folks in the lab, he's a M.D. and native Chinese.  It was an interesting summer in that respect because I learned a ton about China and stunned them with my comparatively relaxed GRE study habits and love for doughnuts.

One evening a group of us went to go see a performance of "Oklahoma" in Washington Park.  As a show, it was okay.  If you've never seen it, don't let me ruin it for you but let's just say it's a tad predictable.  The song for which it is known is pretty cool, though.  Anyway, the point was it was free, we had fun, and I wheedled a bag of Skittles off Steve.  L to R: Me, Steve, Eli Sean, Aleck (in back), Megan (in front), Chrysa (great accent!), and Mark.  Dave should be in there too, but he's camera phobic or something.

What did I do this summer?

In more or less random order:
  

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When was I there?

My internship was from June 4 - Aug 10, 2001.

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Where was I?

I lived in the lovely city of Albany, NY.  It's a cute place, right on the Hudson River in a valley.  It has a bunch of historical homes, too.  It's the red star, which is roughly sixteen hours from Charlotte, NC, three hours from NYC, and four hours from Rochester.

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Why was I there?

Well, simply put, I was there to do biological research, thanks to the nice people at NSF who saw fit to pay me.  But then, I know you are far too interested in my facinating summer to be content with that answer.  I can't tell you everything I did because technically it belongs to NYS DOH, but I will show you the introduction to my end-of-internship summary paper.  Don't get too excited.

     Cytochrome P450s have optimal spectral absorbency around 450nm when bound by carbon dioxide in a reduced state and are monooxygenases that oxidatively biotransform a plethora of chemicals, including xenobiotics and steroids.  These proteins are capable of interaction with substrates by either detoxifying harmful chemicals or converting inert compounds to reactive intermediates that cause biochemical and / or physiological alterations that produce toxic effects, such as cellular damage, cell death, or tumorigenesis (1).  P450s are most commonly found in the liver, though they are present throughout the body.  P450s vary from individual to individual, both within and across species.
     One important P450 is CYP2A3, which is found in the olfactory mucosa of rats.  This protein is homologous to CYP2A6 and CYP2A13 in humans and is involved in the bioactivation of nitrosamine compounds commonly found in tobacco, which are carcinogenic. Within the promoter region of this gene is a nasal predominant transcriptional activating (NPTA) element that has a similar sequence to the binding site for The Nuclear Factor proteins (2). The NF1 family is a group of site-specific DNA-binding proteins that are involved in the regulation of transcription of numerous cellular and viral genes due to the common presence of their binding sites in the promoter, enhancer, and silencer regions of the genes.  Though NF1-like factors are found in nearly all organs and tissues (3), the NPTA element within CYP2A3 interacts only with a form of NF1 located in the olfactory mucosa.  NPTA element is considered to play a critical role in the expression of this gene in the nasal tissue and is conserved in rat CYP2A3, mouse Cyp2a5, and human CYP2A6.
     Little is understood about the mechanism of tissue-specific gene expression.  The application of this knowledge to P450s would explain tissue-selective toxicity, which is important in assessing the risk of an individual exposed to exogenous compounds, such as tobacco smoke.  Because of its relevance to public health, CYP2A3 was studied.  In this project, the gene expression of CYP2A3 due to the NPTA element in its promoter region was investigated.  An adenovirus-infected mouse model will be helpful in order to confirm the role of the NPTA element in CYP2A3 transcriptional activation in vivo, as suggested by in vitro data obtained in previous studies (2).  An adenovirus containing a LacZ reporter gene driven by a CYP2A3 promoter with a mutated NPTA element was generated for this purpose.  This was accomplished by constructing a plasmid carrying the mutation, recombining it to an adenoviral shuttle vector, and transfecting mammalian cells to generate the mutant virus.

1.   Cytochromes P450: Metabolic and Toxicological Aspects. ed. Costas Ioannides. 1996. CRC Press, Inc.
2. Zhang, J., and Ding, X. (1998) The Journal of Biological Chemistry. 273, 23454-23462
3. Gronostajski, R. M. (2000) Gene. 249, 31-45

If that was a bit overwhelming, here's the gist: I made a mutant virus so we could see if a DNA sequence did what we thought it did.

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I want to go where the heart is.