A fall break experience I do not care to repeat

So while most of my fellow undergraduates were leaving town to go somewhere, anywhere, other than Morris for fall break, I had to stay behind. Sure, staying in Morris is not really all that bad, I mean, some people actually live here (sorry Professor). But I will be honest-it really is not on my list of top places to live. It is just, well, boring. I had to stay behind because I had some animals I had to take care of, and I will admit, I was looking forward to spending time lying in bed, working with my horses, and catching up on my senior seminar. Little did I know exactly how much time I would spend doing the first, and hardly any of doing the latter two.

Yep, this break I got floored with a virus. AND I literally mean floored. We shall call it the flu, because I had all the flu-like symptoms. Headache. Swollen lymph nodes. Achy neck and back. Fever. Achy stomach. Dizziness. So I spent a wonderful Saturday doing all the things a person my age would love to do, and then spent Sunday, Monday, Tuesday, Wednesday and some of today confined to my bed. Sure, you can say,

well you slept through most of it, so it couldn’t have been all that bad

But believe me, what little I was awake for was horrible. Mostly because it was absolutely gorgeous outside, I didn’t have any classes to attend, and yet my body was waging a war inside of me.

So, I understand the basic principle of how viruses work, but how can one virus have a multitude of diverse symptoms? What’s with the headache, and the achy joints? Do viruses affect neurons the same way they can affect other cells? Do they even invade neural cells?

Fall Break

The beginning of this week was fall break at our college campus. We had the weekend off as well as Monday and Tuesday. Since I had been planning to return home to northern Minnesota for the first time since moving down to west central Minnesota in August, I decided to take Thursday and Friday off also. The few days I spent away from this desolate prairie wasteland and back among the conifers and lakes were phenomenally enjoyable.

This is my first year of college away from home and a long way from home it is. I remember the first few weeks I was down here, only vaguely though, a lot of adapting has taken place since then. The three-day dragged out orientation process for freshmen and transfer students at the end of August was intensely boring. I had been informed by mail that my presence was required but it would have been great had I known what it entailed and that I very well could have gotten away with not attending (this sounds negative, I know, but I’m sure some of you can relate). I remember the immense amount of time and effort it took to meet new people and figure out who to make friends with. Luckily the homework load had not picked up yet and there was plenty of free time to devote to this. Did I mention I had never bought my own groceries before coming to college? The first night I went to buy food I had no idea what I needed to sustain myself in a semi-healthy manner. The first five items I put in my basket had something to do with hotdogs. I’ve since learned a few things about grocery shopping and cooking. Although the first weeks were uncomfortable and sometimes frustrating, it was well worth the effort to take them on.

The drive home was long and rainy. There were a few deer that crossed as I approached them but staying attentive kept my vehicle intact. My lily plant sat quietly on the front passenger floor and when I inadvertently opened the glove box on its head I caught myself apologizing. Talking to a plant seemed odd to me so I ignored it and its personal temperature preference for the rest of the trip.

When I finally got home just before midnight, I sat in my living room with a bowl of soup, quietly but excitedly looking at everything I hadn’t seen for a while. The pictures hanging on the wall, the bookshelf filled with various things, the scent of my dad’s cooking brought forgotten memories rushing back to me. The plant atop the bookshelf with vines that had hung down half way in August had now reached the floor. My dad, who was sitting in his recliner on the opposite side of the room with his own bowl of soup, talked about things that had happened while I was gone, the new addition on the back of the garage, why our silverware was different, and how my aunts and uncles are doing.

The weekend flew by quickly and before I knew it I was sitting in neurobio again yesterday morning (we have wednesday discussions in the cafe now so PZ can get coffee). The time I spent among the seemingly infinite number of trees and lakes in northern Minnesota was enough to keep me going until I can go back again. For now it’s just good to know that everything I call home and everyone who means the most to me are still up there, safe and sound.

Student Post: What I learned in skool today…

… well not today. I learned very little today , but generally, here are some interesting things I’ve picked up in class:

-If you sever a cat’s cerbral cortex from its hindbrain it can still walk on a treadmill (in a harness that compensates for the poor feline’s lack of balance). This was the topic of one of PZ’s many tangents.

-One way to inhibit the HIV virus is to make a drug that targets a protein our cells make. The key is to identify a protein the virus needs but that we do not. CYC202, a cyclin-dependant kinase inhibitor, may be one such drug.

-“HIV virus” is redundant, but hey, so is the genetic code.

-If you race flatworms in a maze, grind up the fastest ones, and feed the product to flatworms having yet to try the maze, you might find that they run the maze faster than their non-cannibal counterparts. Of course, you would consider that flatworm may simply be highly nutritious, because you’re a scientist, and that’s what they pay you the big erlenmeyers for.

-Badger culling. That’s right. Badger. Culling. It’s used to decrease badger/cow contact in Great Britain as badgers function as a bovine tuberculosis infection reservoir for cattle.

-EtOH and H20 are miscible. Whew… and to think I almost made myself an acetone martini…

i-0527fbd3810080473469f4ca7b721485-Badger.jpg

It’s always much more complicated than you think

I mentioned before Cosma Shalizi’s excellent discussion of heritability; add to that now his summary of g. We’ve got a few pompous no-nothings lurking in the comments who are fond of declaiming that they know that they have proof that the brain works in such-and-such a way, and that we can blithely assert an average stupidity exists in broad swathes of humanity (said broad swathes typically sweep across very diverse groups, united only by the obvious ephemera of skin color), but they need to read and comprehend those articles in order to learn that their certainty of a heritable simplicity is a phantasm.

Reality says that race is a category error, and that IQ foolishly tries to pin complexity into a cramped and tiny corner, and that human minds are both diverse and similar … and the great gross simplifications of racists, scientific and otherwise, are lies to comfort fearful bigots.

Cosma has another post that summarizes the exasperation we should all feel.

CSHL acts against Watson

I am distressed at this news: the Cold Spring Harbor Laboratory has suspended Chancellor Jim Watson over his comments about race.

I disagree with Watson passionately, and he is completely wrong in his opinions about Africa and women and who knows what else…but he has the right to say it, just as we have the right to disagree vehemently and volubly with him. This does the CSHL no good: it’s a declaration that their director must be an inoffensive, mealy-mouthed mumbler who never challenges (even stupidly).

Maybe that’s what they want — someone diplomatic, who’ll woo donors and visitors with soft words — and I can understand that desire. It’s a sign, though, that CSHL will not be administered by anyone willing to assert controversy, and that’s too bad.

I know, his personal opinions were repellent. But what concerns me is that future leaders of the institution will also not be able to be forceful and loud and aggressive, as Watson has always been, in favor of causes I care about. You have to be able to tolerate the tenure of assholes in order to have the possibility of heroes.

TRPV1 Ion Channels

I noticed that PZ posted one of our take-home exam questions on Pharyngula and so I decided to make an entry with my answer (I okayed this with PZ first although he did warn me of the certainty of harsh reader criticism). The question referred us to a recent article in Nature about TRPV1 ion channels and asked us to describe TRPV1 ion channels and the testing that was done on them.

The transient receptor potential cation channel (TRPV1), also referred to as vanilloid receptor subtype 1, is a ligand-gated cation channel (2). This means that the channel contains organic molecules that can form covalent bonds with positive ions and is thus operated chemically. TRPV1 ion channels are non-specific and can be found on TRPV1 nociceptor (pain sensing) neurons in the central nervous system and peripheral nervous system. It may be related to thermal hyperalgesia (abnormally increased sense of pain) in both regions (2). The TRVP1 ion channel The opening in the TRPV1 ion channel was determined experimentally to be large enough to pass a 452 Da (1 Dalton = 1.657×10-24 g) dye molecule through (1). The TRPV1 ion channel, when opened by the proper agnostic, can allow anesthetic molecules to be introduced into nociceptic neurons, making it an important channel some regional anesthesics.

Most anesthetics are hydrophobic, cell membrane permeable, and function by blocking sodium ion channels on the inside of the cell. This blocks sensory nerves as well as motor and autonomic nerves (1). The main idea behind Binshtok, Bean, and Woolf’s experiment was to formulate an anesthetic that blocks the pain of sensory nerves but not motor and autonomic functions. They sited multiple sources stating that when QX-314, a charged derivative of lidocane, is introduced to the inside of a nerve cell it can inhibit sodium channels and produce analgesia. QX-314 was experimentally found to have no significant effect on nociceptor neurons externally. QX-314 is impermeable to nerve cell membranes but with a mass of 263Da is small enough to fit through TRPV1 ion channels. Capsaicin is a TRPV1 agonist, meaning it has an affinity for TRPV1 channel receptors and can affect them physiologically, in this case causing them to open.

Binshtok, Bean, and Woolf observed the membrane potential changes of rat dorsal root ganglia of various diameters exposed to QX-314 (an anesthetic), capsaicin (a TRPV1 agonist), and a mixture of the two. The voltage clamp method was used to determine whether or not the neuronic sodium nerve channels were inhibited and also which nerves channels were inhibited on. The voltage clamp method involves two wires placed in the axoplasm of a nerve cell. The first wire measures potential across the membrane and the second wire propagates electrical current (3). The voltage across the membrane is controlled while the ionic current is measured. Using this method, they found that QX-314 and capsaicin applied together could block the generation of action potentials (1). This effect can be attributed to neuronic sodium channel inhibition. If sodium channels are blocked then the depolarization phase of the action potential cannot take place and a wave of depolarization, a nervous signal, cannot be propagated along the neuron (3). The voltage clamp method used in this experiment involved blocking potassium and calcium ion currents so that the sodium ion current could be recorded by itself.

Binshtok, Bean, and Woolf concluded that neither QX-314 nor capsaicin produced significant effects on nociceptor neurons when applied individually but almost entirely block nociceptor sodium channel function when applied together. The brilliant idea behind all of this is that, if QX-314, an anesthetic, is introduced along with capsaicin, a TRPV1 agnostic, it will only travel through the TRPV1 ion channels of nociceptor neurons. Sodium channels in nociceptor neurons will be blocked while other neurons that lack TRPV1 will remain unaffected. The end result is an anesthetic that blocks painful sensation but does not compromise autonomic and motor nerve function.

References:
1. Alexander M. Binshtok, Bruce P. Bean, & Clifford J. Woolf. Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers. Nature. 4 October 2007. Vol449 pp607-610.

2. M.Cui, P.Honore, C.Zhong, D.Gauvin, J.Mikusa, G.Hernandez, P.Chandran, A.Gomtsyan, B.Brown, E.K.Bayburt, K.Marsh, B.Bianchi, H.McDonald, W.Niforatos, T.R.Neelands, R.B.Moreland, M.W.Decker, C.H.Lee, J.P.Sullivan, C.R.Faltynek. TRPV1 receptors in the CNS play a key role in broad-spectrum analgesia of TRPV1 antagonists. 13 September 2006. Neuroscience Research. Global Pharmaceutical Research and Development. Abbott Laboratories.

3. Elaine N. Marieb. Human Anatomy and Physiology. Sixth Edition. Pearson, Benjamin, Cummings. 2004.