It seems like retribution is in order: Richard Roberts wants a leave of absence, as his wife claims to live in “a morally upright manner” even while rumors of associations with a 16-year-old boy swirl about.
James Watson’s sold-out lecture in London has been cancelled. I guess making bogus accusations about the congenital stupidity of a whole continent has consequence.
Greg knows a bit about the anthropology of race, and he also knows how to make fools suffer. Now he has weighed in on Watson.
I’m pretty sure he left boot marks on the old man.
Greg has followed through now with more criticisms of ‘scientific’ racism.
James Watson has really put his foot in it this time. He has a tendency to say some shockingly offensive and bizarre things.
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.
I just had an odd idea for another of those blog memes, and this is very much an experiment. It may be too complex to last long, but I just want to toss it out and see if anything interesting happens; it’s one where the answers may be interesting in one way, but the structure of the questions might be interesting in another way. Here are the instructions:
A two hour presentation was given at a local church last night by creation scientist whom I won’t name. This presentation overall lacked direction and seemed to jump from one topic to another without really stopping to make a point. About a third of the presentation was about dinosaur diversity, talking briefly about neat features that a variety of dinosaurs have. Various weather phenomena that could have caused the flood described in Genesis were vaguely presented without any solid background or logic. Fossils were also discussed, again without really any rhyme or reason.
There were two highlights thorughout the evening. The first was when the presenter enthusiastically exclaimed, “I do believe that there were fire-breathing dragons!” From behind me a women shouted an equally enthusiastic, “Amen!” The second highlight of the presentation was the time allotted for questions at the end when PZ Myers, who had been sitting quietly in the front row throughout the entire hour and a half presentation, raised his hand and fired one off. For some reason, this reminded me of the nationally televised Bush vs. Kerry campaign debates of 2004. Whenever Bush was asked a question, he seemed to stutter ignorantly all over his podium for a few moments and then say some elaborate nonsense that didn’t really provide an answer.
To me, trying to scientifically explain an interpretation of the Bible, an interpretation that may not even be accurate, completely misses the meaning of having faith. Some of my fellow neurobio students agreed with me that science and the Bible should not have to be in opposition. It’s a shame that some creation scientists deliberately ignore valid research in areas such as glacial geology and evolutionary ecology to formulate what they consider to be a scriptural explanation of how the Earth came about. The Bible does not define the chemical and genetic specifics of the origin of this planet and the life existing on it. So is creation science attempting to make the Bible say something it doesn’t? Perhaps people have been set in their interpretations for so long, that it’s too difficult to accept that current research in science (that may not jibe with these long held interpretations) does not have to disagree with the Bible.
In discussing Soul Made Flesh this past Wednesday morning in PZ’s neurobiology class, I brought up what I thought to be an interesting, though somewhat tangential, point. Zimmer mentioned Anne Conway and how ambitious she was in her studies despite not being allowed to attend a university. The fact that females were not given the same opportunities throughout history is something I remember learning about in grade school. But where did the ideology that females are inferior to males begin?
One of my fellow students argued that because females give birth they were probably not expected to hunt and gather food while they were pregnant. I thought about this and although I don’t know for sure, in early civilizations females probably tended fields and gathered crop until while pregnant until they were no longer physically able to, returning to the fields as soon as they recovered from the stress of giving birth. Males, meanwhile, tended to be stronger and did not have to give birth to maintain their population.
Another thought that I had on this topic was that male aggression and anger tendencies probably have something to with the ambition to control their domain. Considering male influence in government, it would be interesting to see the effects of a female United States president. There have been several queens as well as kings in European countries over the last thousand years. Is there a difference in how a country operates that is dependent on the gender of its leader?
Things seem to be much different today than they were a hundred years ago. Females driving, voting, becoming doctors, and all these things that would have been unheard of. Are males falling behind and if they do will females dominate males? Is society moving toward a codominance of gender? There is plenty of debate on this topic and I’m sure it won’t be resolved anytime soon.
References:
Zimmer, Carl. 2004. Soul Made Flesh. Free Press, New York, NY.
Sorry about that last post. I am still trying to figure out how to format this blog correctly. Here are links to the abstracts of the articles I used to design my experiment. Admittedly I played up the sophomoric college student part a bit. Apparently a bit too much. To answer a few concerns about this experiment, the fish are not likely to die. I would never preform an experiment that was cruel or served no purpose other than my own personal enjoyment. While, it is not likely that I will have any groundbreaking results, I hope to further my own personal research experience and possibly recreate some fairly important biomedical research. Drinks like a fish and the second article Ethanol effects on three strains of zebrafish
There are those who have questioned the reason for getting fish drunk. I could stumble through the explanation and make the issue much more confusing than it has to be, or I could just post a few of research articles I used to design my experiment.
Gerlai, R., Lahav, M., Guo, S., Rosenthal, A. 2001. Drinks Like a fish: zebra fish (Danio rerio) as a behavior genetic model to study alcohol effects. Pharmacology, Biochemistry and Behavior. 67:773-782
Dlugos, C.A., Rabin, R.A., 2003. Ethanol effects on three strains of zebrafish: model system for genetic investigations. Pharmacology, Biochemistry, and Behavior. 74:471-780
I hear from Andy that you’ll be able to listen to a debate between Richard Dawkins and John Lennox, both of Oxford, on … oh, I bet you can guess what it’s about. It’s going to be streamed live on a number of Christian talk radio stations, so look it up if you’re interested, it should be on in about an hour and a half.
