I REGISTERED FOR MY FIRST MARATHON!
I looked online today to see if registration was opened for the 27th annual wineglass marathon, and with the luck of the irish...it was! So I forked over my 60 dollars checked the box that says if I die its not their problem, and registered myself for 26.2 miles of running bliss...well probably more like running purgatory. As my friend Ang just pointed out - thats $2.37 a mile. It'd be cheaper to drive.
I'm signed up, no stopping me now, this thing is in the making...did i mention i'm scared?
I was supposed to run in this weekends Johnny's running of the Green, but I was so stressed form my talk last weekend (which ps went very well) that I came down with a head cold and was up ALL night on Friday coughing, so alas, i chickened out - instead Marc ran it, and gave me his T shirt. But I took the opportunity to introduce Bailey to the big city. Bailey and I and Ang and her golden retriever Annie went down to watch the race. Bailey was so upset that there were all those people there, and that Everyone wouldn't stop and pet him. He wined a lot. And then, when 1,000+ runners just ran on by and he wasn't allowed to go too, he was a little bummed about that too.
Funny thing that happened is, I was waiting towards the finish line for Marc, and I saw the girls that were in the lead, and wondered to myself, gee I wonder if I could beat them, then it dawned on me, well gee holly, you can't beat marc, so, no, they'd beat you. Oh well, maybe someday I'll be a fast girl :).
I've been feeling better, I ran 5 miles on saturday (much slower than the 5 mile race I would have done trust me) and 9 miles on Sunday, and another 4 really slow ones today. I'll be in shape by October, somehow :)
I've set a date for my qualifying exam April 28th, and in other news my cousin Katie has agreed to do women's nationals with me!!! I think thats news, i don't think that i posted it before. BUT VERY EXCITING! It's going to be a great summer!
Monday, March 17, 2008
Thursday, March 6, 2008
If you don't like the weather in Western New York, just wait a minute
What a week huh? I'm about to go for a run this morning and thought I'd write a little something. I ran on Sunday in just something light, on Monday I wore something very light (it was 52 when I ran!!!) and then had to bundle up the rest of the week. It was a beautiful morning to walk bailey, a beautiful winter looking sky! I've already ran 19 miles this week, 26 after today. That's a scary thought, that I have run 4 times and ran 26 miles and come october, I have to do that all in one day!
Everything else is happening too! I have to give a talk to my fellow students next monday called a 501. I know it sounds like it should be nothing, but it is really nerve racking! It's an hour long presentation where you present your work and also answer questions. Luckily, my field of study is sort of obscure - so hopefully no one will have tough questions!
I am getting ready to take my qualifying exam, which I think I mentioned before - is my thesis proposal. See if my committee (a group of 4 Drs.) think I'm smart enough to go on. I'm sort of finally getting excited about all of this. Just for giggles -and because I'm a giant dork!- I've posted my abstract - so you can see how silly this profession of mine is:
Everything else is happening too! I have to give a talk to my fellow students next monday called a 501. I know it sounds like it should be nothing, but it is really nerve racking! It's an hour long presentation where you present your work and also answer questions. Luckily, my field of study is sort of obscure - so hopefully no one will have tough questions!
I am getting ready to take my qualifying exam, which I think I mentioned before - is my thesis proposal. See if my committee (a group of 4 Drs.) think I'm smart enough to go on. I'm sort of finally getting excited about all of this. Just for giggles -and because I'm a giant dork!- I've posted my abstract - so you can see how silly this profession of mine is:
ABSTRACT
In HIV-associated dementia (HAD) or HIV-associated neurocognitive disorder (HAND), neurologic disease that occurs during central nervous system (CNS) infection with Human Immunodeficiency Type-1 (HIV-1), neuronal death does not correspond with the degree of neurologic dysfunction, rather loss of neurologic function correlates with simplification of dendritic arbors and defective synaptic transmission. This is an important distinction to make since dendrites are able to undergo profound injury yet still be able to regenerate to form functional synapses. Discovering the mechanisms of injury is important since blocking the injury to the neuron, or removing the causative agent, will prove therapeutic. Using a recently developed technique that utilizes quantum dot (QD) coated coverslips to produce an electrical current; I will be able to generate action potentials in hippocampal neurons. Morphologic and functional integrity of the neuronal processes can be observed after inducing an action potential in the presence of virologic neurotoxins such as gp120 and tat. Using real time imaging, I can observe whether HIV-1 neurotoxins make normal synaptic activity excitotoxic; resulting in irreversible injury to synapses. Using the QD system, I will observe the microglial response to the dendritic injury from electrical stimulation with tat and gp120. It is unclear whether a microglial response to this injury will lead to further synaptic injury or limit synaptic damage. By assessing the response to the injury in the presence and absence of a recombinant Adenoviral vector under an F4/80 promoter containing a siRNA against purinergic receptors responsible for microglial motility, I will determine if microglia are acting in a neuroprotective fashion. Evidence has also suggested that damaged neurons will provide an “eat me” signal which will attract microglia to engulf the synapses. Using neuronal-RFP and glial-GFP mixed cultures, I will observe the RFP presense in microglia, which will imply a role for microglia in synaptic degradation. It is possible that fractalkine (FKN), an enzymatically cleavable chemokine expressed on neurons, and its receptor CX3CR1 expressed on microglia, are mediators in this adhesion process between microglia and neurons and may either enhance or mitigate damage to synapses. Using the QD system I can further elucidate the role of FKN in these interactions. Taken together these experiments will provide insight into the mechanism of neuronal injury in the context of HAD.
In HIV-associated dementia (HAD) or HIV-associated neurocognitive disorder (HAND), neurologic disease that occurs during central nervous system (CNS) infection with Human Immunodeficiency Type-1 (HIV-1), neuronal death does not correspond with the degree of neurologic dysfunction, rather loss of neurologic function correlates with simplification of dendritic arbors and defective synaptic transmission. This is an important distinction to make since dendrites are able to undergo profound injury yet still be able to regenerate to form functional synapses. Discovering the mechanisms of injury is important since blocking the injury to the neuron, or removing the causative agent, will prove therapeutic. Using a recently developed technique that utilizes quantum dot (QD) coated coverslips to produce an electrical current; I will be able to generate action potentials in hippocampal neurons. Morphologic and functional integrity of the neuronal processes can be observed after inducing an action potential in the presence of virologic neurotoxins such as gp120 and tat. Using real time imaging, I can observe whether HIV-1 neurotoxins make normal synaptic activity excitotoxic; resulting in irreversible injury to synapses. Using the QD system, I will observe the microglial response to the dendritic injury from electrical stimulation with tat and gp120. It is unclear whether a microglial response to this injury will lead to further synaptic injury or limit synaptic damage. By assessing the response to the injury in the presence and absence of a recombinant Adenoviral vector under an F4/80 promoter containing a siRNA against purinergic receptors responsible for microglial motility, I will determine if microglia are acting in a neuroprotective fashion. Evidence has also suggested that damaged neurons will provide an “eat me” signal which will attract microglia to engulf the synapses. Using neuronal-RFP and glial-GFP mixed cultures, I will observe the RFP presense in microglia, which will imply a role for microglia in synaptic degradation. It is possible that fractalkine (FKN), an enzymatically cleavable chemokine expressed on neurons, and its receptor CX3CR1 expressed on microglia, are mediators in this adhesion process between microglia and neurons and may either enhance or mitigate damage to synapses. Using the QD system I can further elucidate the role of FKN in these interactions. Taken together these experiments will provide insight into the mechanism of neuronal injury in the context of HAD.
:)
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