Adventures in Neuroscience could never be more exciting. Well, maybe a little.
Sunday, April 30, 2006
The Neurophile is officially ill. Expect posting over the next several days to reflect this, such as our official new "so-tired-we-refer-to-ourselves-in-the-third-person-plural" policy. We have also considered plating our throat culture to see what happens, but then we realized that the idea was not only overly geeky but also flat-out dumb. So instead, we decided to show our loving audience a blurry photo of a plate of bioluminescent bacteria that was lying around the lab last Spring:
Saturday, April 29, 2006
Because I haven't come up with enough ways to waste my time...
|Your Theme Song is Born to Be Wild by Steppenwolf|
"I like smoke and lightning
Heavy metal thunder
Racin' with the wind
And the feelin' that I'm under"
A total independent spirit, you can't be held down or fenced in.
You crave the feeling of wind on your face... and totally freedom.
Actually, the only reason I posted this is that I wanted to be able to point out "You crave the feeling of wind on your face... and totally freedom." I like the sound of that.
Friday, April 28, 2006
Wow, that's dumb.
Continuing the political news, this is quite possibly the stupidest thing I've read in the month of April. Not that it's that horribly surprising, considering the source:
A Spanish language version of the national anthem was released Friday by a British music producer, Adam Kidron, who said he wanted to honor America's immigrants.
When the president was asked at a Rose Garden question-and-answer session whether the anthem should be sung in Spanish, he replied: "I think the national anthem ought to be sung in English, and I think people who want to be a citizen of this country ought to learn English and they ought to learn to sing the national anthem in English."
Friday Random Ten: 28 April 2006
Actually, I started listening to this, and then they put Johnny Cash on at the coffee shop. And you can't deny the man in black: I am sure you all understand the universal truth in this statement. So the moral of the story? This is all a horrible, horrible lie:
1. DJ Spooky and Dave Lombardo - The Art Of War (Back To The Lab) (from Drums of Death)
2. DJ? Acucrack - Scaldron (from Mako vs. Geist)
3. Wyclef Jean - Bay Micro'm Volume (from Welcome to Haiti Creole 101)
4. Goblin - Wampyr (finale) (from The Goblin Collection)
5. Spahn Ranch - Dubnosis (from Beat Noir)
6. Jello Biafra & the Melvins - Caped Crusader (from Never Breathe What You Can't See)
7. RL Burnside - Back Luck City (from Wish I Was in Heaven Sitting Down)
8. Dead Kennedys - Hellnation (from Frankenchrist)
9. Ella Fitzgerald with The Day Dreamers - That Old Feeling (from Ella Fitzgerald Disc 1: With Friends 1936-1950)
10. Midival Punditz - Kesariya (from Midival Times)
Breaking News: a war protest march just went by. At least, I assume it was a war protest. For all of a half a minute, they were chanting "What do we want? Peace! When do we want it? Now!" Or at least, I heard people chanting "Peace! Now!" and sort of filled in the rest. The rest of the time, they were chanting "The people! United! Will never be defeated!" Which I've never thought was a very good march chant, because it sort of lacks useful meaning in that situation. But that's just me...
It was still rather heartening to see it occurring, even if it was a bit anemic-looking. Not that I got up and joined them; which sort of destroys my ability to criticize, I must admit.
Win Some, Lose Some
Plus: May have just gotten myself a post-graduation job which, although not quite up my alley, still sounds rather interesting.
Minus: I can slowly feel myself slowly developing the hideous disease the Girl has had for the past two+ weeks. Expect posting to evolve into a continuous fever dream over the next few days accordingly.
Thursday, April 27, 2006
One Million Hardcore Members
(You know when you're making barely recognizable references to The Warriors, you're pretty much assuming all your readers are techno fans. Which may be true.)
But anyways, I've been meaning to post something about this for a few weeks, and was just reminded about it: The English Language: 900,000 Words, and Counting
An organization called Global Language Monitor estimates there are more than 900,000 words in the English language, and more are being added every day. Alex Chadwick talks with Paul Payack, president of Global Language Monitor, about his organization's method of counting words and the quickly approaching one-million-word milestone.
Really, I only bring this up because I believe each and every one of us is morally obliged to do our part to help the English language reach its seventh digit. Therefore, I expect everyone who reads this to make up at least one new word each week. Get cracking.
On a completely tangential note--which I may have brought up before--I totally get the coolest ads.
I found my favorite part:
Building upon the sucesses of our acute research probes, we are thrilled to offer the chronic probes for research. The front end of the chronic probes (the penetrating shanks) is basically the same as that of the acutes, but the chronic probes have an integrated silicon ribbon cable that is flexible in the direction that is normal to the brain surface. Although our probes are almost plug and play, surgical technique is especially important for the success of the chronic experiments.
My Love Is Immense
I have just a few short minutes, grabbed between my physiology midterm and the beginning of lab, to share a secret with you:
I love Mark Cuban.
It's a secret love, an unrequited love, but it's love nonetheless. I mean, who could read this and not immediately swoon?
Shareholders, there is a good chance that a CEO, who lives in a totally different world than you do is telling the media that he is doing, what he is doing, in your name. Firing those people to increase earnings by 1c per share. Its for you. Outsourcing jobs. Its for you. Making windfall profits because oil prices are skyrocketing, its for you. Paying the last CEO who just quit on you tens of millions of dollars. Its for you. Paying himself tens of millions of dollars, and negotiating a Platinum parachute. Its for you. Is this what you, as a shareholder wants ?
Sharedholders are supposed to be the owners of the company. Shareholders are supposed to select the board, which in turn hires the CEO. Shareholders are supposed to weigh in on corporate issues and direction. Are you exercising your rights as a shareholder ? Or are you a corporate Ho ?
I mean, how much more romantic can you get? Sure, a bit more attention to typing and grammar could be appreciated. But it's the thought that counts. And the thought... is awesome.
It's a pity Valentine's Day only comes once a year, because I don't want to have to wait ten long months to send the card.
Can MN possibly get in on some of this action? Please? Do we need Pawlenty's approval, or can Mike Hatch go ahead on his own?
And what does it say about how focused I am on school that it took me using wikipedia to confirm I got Mike Hatch's name right to discover that there's a gubernatorial election this year?
WASHINGTON - Ten states fired a new legal salvo at the federal government Thursday in a long-running court battle over global warming and pollution from power plants.
The states, joined by environmental groups, sued the
Environmental Protection Agency over its decision not to regulate carbon dioxide pollution as a contributor to global warming.
New York, California, Connecticut, Maine, Massachusetts, New Mexico, Oregon, Rhode Island, Vermont, and Wisconsin filed the lawsuit in the U.S. Court of Appeals for the District of Columbia Circuit.
The states, led by New York Attorney General Eliot Spitzer, want the government to require tighter pollution controls on the newest generation of power plants.
Courtesy of Mike Sterling... we are reminded once again that not even the Elder Gods are safe from the power of marketing:
NECRONOMICON PLUSH BOOK!
It can be yours for only $99.99. Because, you know, everyone needs a fuzzy soft book of the Names of the Dead around the house...
A moment of purest bliss.
Yeah, I realize I just promised I wouldn't be posting anything today because of the tests. But I just had a moment of purest existential* ecstacy.
Putting down the phylum overview for a moment, I wandered outside to catch a few minutes of sunlight and fresh air to run over some stuff in my head. Right before I head back inside, someone pulls up and stops at the stop sign next to the bio building. Listening to "Radioactivity." It was delightful.
I Heart Kraftwerk.
* Yes, I realize this is complete abuse of the word "existential." What are you going to do, kick me off of the Secret Philosophy Council?
So I've been Science Blogged, apparently. I'm not sure which is worse:
A: That my immediate thought is, "Crap! I haven't posted anything in the last twenty-four hours!"
B: That I've spent the time finding this out and worrying about it... when I have a final in two hours.
C: That every website eventually becomes a verb.
Sigh. Feel free to register votes below.
Hello, all. Welcome to the Neurophile.
And, for the record: just because bio-matter doesn't talk, isn't conclusive evidence that it doesn't take directions. I demand the right to a peer review!
And I'm off to studying. Dead air Thursdays will continue after this message...
Wednesday, April 26, 2006
Site maintenance update.
I just turned on word verification for comments. I'm getting sick of trolling through the archives a couple times a week and tracking down the spam comments to delete them. Hopefully this will cut down on that.
Yes, I realize there are bloggers out there who would kill for that to be all they had to do about spam comments.
Last post for the night. Then I go to BED.
I have to admit, it's amusing to note when I can feel free to call attention to a spam commenter... because they post a link to http://neurophile.blogspot.comwww.camerasforall.com/
Sigh. Even the joiks can't get it right.
Does it come across that I'm procrastinating?
Sure I have two tests in two days to study for--and a job hunt to conduct--but honestly I'm spending my time thinking that this is almost enough to convince me to get a satellite radio.
Tuesday, April 25, 2006
Monkeys monkeys monkeys monkeys monkeys
Maybe it's just my first mocha chiller of the summer wearing off, but I would have to say this video essay on the monkeys ruling the world is quite entertaining. I could almost call it touching, but then I would leap on my display of weakness, wrestle myself to the ground, and then stand on top of my submitting prone body and pound on my chest screaming.
Yeah, I've got some issues to work out...
Get your hands off my brother
I somehow manged to forget that April is National Poetry Month. Considering my nearly 5 year tenure at the late Hungry Mind's bookstore arm, I'm feeling more than a bit guilty. Fortunately, I had John Lynch to remind me.
Now, I've had a crap last couple of days, so this was really all I needed to spend the night curled up with Nicole Blackman's Blood Sugar. If you know her at all, it's probably from her work with musicians like KMFDM or Bill Laswell.
Reading Nicole Blackman when you're blue is like--well, a lot like listening to the blues when you're down. It's very cathartic, because misery loves company, and it makes you feel better while reminding you that such is direct evidence that all humans are insane. This book is one of maybe two or three books amongst my five bookcases-worth that has a bookmark in it at all times; marking "Indictment," the poem that the KMFDM track "Dogma" is re-worked from. However, "Indictment" is three pages long without line breaks, so I'm just plain not transcribing it for you. This one's still a bit on the long side, so I'm sort of wishing I'd figured out how to code in cuts on Blogger at some point. Oh, well. I live to make my readers suffer, I guess.
"Get Your Hands Off My Brother"
Get your hands off my brother
I don't care if his name is Stephen or Daniel
or James or Billy or even if I don't know his name at all.
They are all my brothers and you have no right
no right at all, to attack any one of them.
What is it about love that makes you so scared and angry?
You fear what you don't understand
but how could a gay man earn such a beating?
You think you are mighty because
you are 18, ineloquent and full of rage
standing over a man with blood pouring from his nose.
Where in the world did you get the idea
that murdering a man will make your life any better?
These men are all my brothers because
they were the ones who came
to pick me up from a phone booth
after I got thrown out of a car.
They rubbed my shoulders in taxis when I was tired
and bought me a drink when I didn't have the money.
They went with me to Audrey Hepburn films
and taught me the meaning of words like 'fierce' and 'worthy.'
They made me understand that life should be about
things that are wonderful, things that are beautiful.
These are the men with whom I have the most in common
and they taught me more than Cosmo ever did.
They drank cup after cup of tea with me
when I was unraveling and reeling from being dumped for no reason.
They taught me that love is love
and who should be the one to judge?
We used to say that if I was a gay man
or they were straight
that we would be lovers.
But in many ways,
they have been more loving to me
than the men I loved.
When my courage failed
they showed me the power
of a good Billie Holiday tune.
They told me to do what I believed in,
that a glass of wine can fix almost anything,
that the music you listen to
is the soundtrack to your life,
that $1.25 and a sense of style
will take you anywhere in this city.
They said Everyone is a star
and everyone shines
it just may be that yours
is a little different than mine.
They taught me that everyone wants
someone to come home to,
someone to look after,
that everyone adores a tender touch,
that everyone needs someone to hold them
and say shh when they cry,
that everyone likes to talk and laugh
and cook and watch TV and kiss.
They taught me that being a loving person
means sometimes getting your heart broken.
Whether by violence or virus
I've lost some of my guardian angels.
Patrick was killed in Boston
and I never had the chance to say thank you.
Lee died in New York
and I never had the chance to say goodbye.
Peter didn't want me to see him sick
so I didn't know until after he'd gone.
I hated him for that.
I loved him for that.
I made them promise they'd be at my wedding
and they made me promise that there would be
balloons at their funerals.
And I did because they taught me
how important promises are.
But it's not his time now
and I will not let you take him from me,
so get your hands off my brother.
(You have no right, no right in the world,
to drive through the city
breaking the wings off angels.)
He may be face down on the pavement but I'm not
and I will fight you to save his life
because every day
in so many ways
he saved mine.
Okay, so this is stupid.
No, really stupid. I have no idea how I've managed to convince myself this is worth posting about, and tomorrow morning I'll probably wake up in a drunken stupor and look at this, only to crawl into bed and cry myself back to sleep while mourning my own insipidness.
But so anyways, I happened to notice that there was a link in my AdWords banner reading "Minnesota - Local: Looking for Nervous System Info in Minnesota? Find it here!" As a Minnesotan interested in the nervous system, I decided I was curious enough to click on the link. All of the search results are for Walgreens, because their cached version of the Walgreens front page has a link to the "Walgreens Health Library," featuring info from the Mayo Clinic. One of the categories is "Brain & Nervous System."
The link for this category doesn't work.
Doh. Oh, well.
We (as in the Royal We) here at The Neurophile, Inc. consider it an essential part of our daily tasks to track down and bring to your attention examples of exaggeration in popular science articles about drugs and addiction. Today we have for your perusal a classic example of this innate tendency towards hyperbole of this sort. We noticed in our RSS links the other day a ScienceDaily article with the title, Both Alcoholism And Chronic Smoking Can Damage The Brain's Prefrontal Cortex.
As we are always keeping a keen eye out for intriguing articles about drug addiction, we immediately noted it for later viewing. Upon reading it today, the first thing that came to our attention: nowhere in the article is potential damage caused by alcohol consumption or smoking mentioned. In fact, the journal article they are referring to has a much more conservative (not to mention technically accurate) title: "Chronic Smoking and Alcoholism Change Expression of Selective Genes in the Human Prefrontal Cortex." So a change in gene expression = brain damage?
Oh, I don't think so.
However, it is an intriguing article nonetheless. Basically, they seem to be looking at some genes that seem to be implicated in the neural response to chronic alcohol use but have had some contradictory reports of the changes in expression. They theorized that these differences are due to inattention to the comorbidity between heavy alcohol use and heavy smoking. So they did a comparison between both smoking and nonsmoking alcoholics and nonalcoholics, vs. both alcoholic and nonalcoholic smokers and nonsmokers. This allowed them to distinguish between those effects that are due to smoking, those that are due to chronic alcohol use, and those that are due to interactions between the two. In this respect, it's all quite neat.
Although they did find some evidence of potential damage to the prefrontal cortex (PFC), it's all by implication. One of the genes, GLAST1, is a glial glutamate transporter which can be upregulated in response to excitotoxicity caused by excessive glutamate. Two of the other genes, MDK and TIMP3, can also be potential signs of excitotoxicity or drug-induced apoptosis. However, this is far from being a conclusive explanation for the change in expression in this instance, and the authors of the article make no attempt to claim it is anything more than conjecture at this point.
It is of note that alcoholism is well known to induce some long-term damage to the PFC, in the form of a loss of grey and white matter. However, a cursory review of the article refers to a role of smoking in changing grey and white matter levels in temporal and parietal areas (see picture here), but I saw no mention of any direct evidence that smoking actually causes damage to the PFC itself.
So the title of the ScienceDaily piece seems to just be an attempt to grab some attention by making a claim that the article they're talking about doesn't even attempt to support. Sigh.
On the upside? I was mightily impressed by their one paragraph explanation of what gene expression means:
All of our cells have exactly the same deoxyribonucleic acid (DNA), which means they all have the same genes. Different cells can appear and work so differently with the same genes (giving us, for example, unique eyes, skin, hair, etc.) because only some genes are used or 'turned on' in each cell. This is called gene expression. The sequence of events is for DNA, or genes, to make ribonucleic acid (RNA), also called a 'message,' which is then used to make proteins. These proteins determine the appearance and function of each cell and, in turn, the proteins' existence depends on gene expression. Thus, gene expression is a normal function of all cells and is well regulated by the body to avoid mistakes.
I'm not just impressed that they covered it so well with great brevity, I'm incredibly impressed that they covered it at all. It's the sort of things that too often gets glossed over due to lack of space and the desire to get to the meaty bits of someone's results. So for that part, at least, we here at the Neurophile salute ScienceDaily.
But cut down on the fear-mongering a bit, okay? It's not like we don't already know that alcoholism and heavy smoking are bad for us.
This synapse would like a cheeseburger, please
According to Reuters, researchers at Harvard Medical School have found neurons responsible for choice:
The scientists, who reported the findings in the journal Nature, located the neurons in an area of the brain known as the orbitofrontal cortex (OFC) while studying macaque monkeys which had to choose between different flavors and quantities of juices.
They correlated the animals' choices with the activity of neurons in the OFC with the valued assigned to the different types of juices. Some neurons would be highly active when the monkeys selected three drops of grape juice, for example, or 10 drops of apple juice.
Other neurons encoded the value of only the orange juice or grape juice.
"The monkey's choice may be based on the activity of these neurons," said Padoa-Schioppa.
Earlier research involving the OFC showed that lesions in the area seem to have an association with eating disorders, compulsive gambling and unusual social behavior.
This seems to raise as many questions as it answers: what other types of choices are these neurons involved in? For example, is this population of cells just involved in food-related choices, or involved in expression of overall preferences, or simply in making comparisons? Are these neurons actually making the decisions, or are they sending some sort of "preference" value to another location that makes the decisions?
I imagine many of these are probably addressed in the Nature article. I'll try to make some time later in the week to look it over, but Magic Eight-Ball tell me "yeah, right, sucker."
I should also point out that this is made doubly interesting by the fact that I vaguely recall OFC playing an uncertain role in drug addiction. Of course, that may be more uncertain to me than to others. But this makes it clear that I have another structure I need to pay attention to in reference to reward and decision-making pathways... I suspect that as time approaches infinity, the number of structures I'll need to pay attention to similarly approaches infinity.
Wow, that's a lot of brain.
Monday, April 24, 2006
Time for a shift in approach?
A question for the masses
Does anyone else ever spit on something and then bark out explicit orders to their saliva to "start amylasin'"? Or is that just me?
Sunday, April 23, 2006
Um, that's sort of ironic...
A: Come on, I couldn't resist...
B: I'm apparently in totally the wrong field.
| The Chloroplast |
You scored 66 Industriousness, 38 Centrality, and 23 Causticity!
| You're the Chloroplast! |
Most of the Earth's energy comes from the chloroplast's ability to capture the energy of the sun and fix cabon dioxide for conversion to starch. Like the mitochondria, they have their own DNA and live somewhat independantly from the rest of the cell.
In terms of real life, you have it all! You're the person everyone wants or wants to be. Just watch out for being overconfident, as you may end up alone.
|My test tracked 3 variables How you compared to other people your age and gender:|
|Link: The Which Cell Organelle are you? Test written by fading_shadows on OkCupid Free Online Dating, home of the 32-Type Dating Test|
Saturday, April 22, 2006
Part 3: The Ultimate Fate of the Vesicle
If you haven't yet, you'll probably wish to peruse Part 1, Part 1.5, and Part 2.
I have two things to say in advance:
1. I'll know when I've grown up and become a real science blogger, because I'll be able to write all this in a single post, rather than have to break it up into trois.
2. Now's the part where you're going to hate me. Because I am now going to argue that I have explained to you enough about the difference between endocytosis and kiss-and-run that I can show you that the Nature news piece written about the article I've been jonesing over... is wrong.
Why is that? Let's review the difference between endocytosis & kiss-and-run: in endocytosis, the vesicle membrane joins with the plasma membrane, and then stays as part of the plasma membrane until it later gets pulled back out of it. In kiss-and-run, the vesicle transiently bonds with the plasma membrane, before pulling back, potentially before it's even had the chance to release all its transmitter.
Now let's see what the Nature news piece has to say about what this article has demonstrated:
Following fusion, the vesicle membrane is recycled back inside the cell to form a new vesicle that is refilled with neurotransmitter ready for the next round of communication. The initial fate of the vesicle once it has released its contents is a matter of some contention. One theory — termed 'kiss-and-run' — is that the vesicle membrane remains as a separate entity from the main plasma membrane, like a drop of oil on water, to allow efficient recycling of the membrane-bound molecules and proteins used by the vesicles for identification, docking and fusion.
By labelling a vesicle-membrane protein called synaptotagmin with a fluorescent tag and using STED microscopy, Jahn and colleagues could follow the fusion of individual vesicles at the plasma membrane (Fig. 2 on page 937). Their study provides some of the most compelling evidence to date that at least some membrane constituents remain grouped together after vesicles fuse with the plasma membrane (rather than diffusing freely within the membrane like a drop of water on water), which is consistent with the kiss-and-run theory.
Now as far as I can tell, they're not talking about kiss-and-run at all. They're talking about the fate of the vesicle during endocytosis. Now, I realize that it's quite possible that there is not a single person reading this who cares about this. But I will point out in my defense that I spent two hours last nite poring over the actual paper trying to figure out what it had to do with kiss-and-run, convinced I wasn't understanding it correctly, before I realized something: for the first time in my life, I was confident that I was right and Nature was wrong.
It makes a guy paranoid, I tell ya.
Anyways, onto the paper. So this lab had this revolutionary imagine technique, and decided to apply it to vesicle recycling. To track the vesicles, they developed antibody tag for the vesicle protein synaptotagmin. It's function doesn't really matter in this context, what matters is that it's integral to the vesicle--and only found in the plasma membrane due to vesicle fusion--so antibodies bound to it will show the locations of vesicles in the cell, and where vesicles have fused with the plasma membrane. They practiced their technique on the labelled preparation to show the difference in resolution attainable:
d, Comparison of confocal (left) and STED (right) counterpart images of a labelled preparation reveals a marked increase in resolution by STED. Scale bar, 500 nm.
They then performed a series of experiments to prove that their technique for separately visualizing surface and internalized pools of vesicles would viably distinguish between the two. Basically, they first labelled the cells under conditions preventing endocytosis, and visuallized it. Since there was no access to the inside of the cell for the antibodies, only surface antibodies would be visualized. They then added attempted labelling with primary antibodies under conditions allowing endocytosis; this was followed by labelling the primary antibodies on the surface with non-fluorescent antibodies before permeabilizing the cells and adding secondary fluorescent antibodies. Thus, in this preparation the surface populations of synaptotagmin would be blocked from fluorescent labelling, while only the internal populations of vesicles that had undergone endocytosis would be fluorescently labelled.
Once they demonstrated that this was a viable approach, they then visualized this with the STED technique:
g, STED image of surface-stained synapses (conditions as in a[low temperature & no calcium - JME]). Scale bar, 1 microm. h, STED image of internalized vesicles (conditions as in c[permitting active endocytosis; surface staining blocked; permeabilized after fixation - JME]). i, Quantification of the brightness of single dots (in arbitrary units), compared with the dot brightness derived from single primary antibodies adsorbed to glass (see Methods). The graphs represent averages of 3–5 independent experiments (plusminus s.e.m.). Note that the bin size is 100 units for the single antibody graph and 300 units for the other images.
So what does this show us? First off, note that the synaptotagmin is sorted into discrete dots. Combined with the fact that their graph shows us that each dot--in both the surface and internalized images--seems to represent multiple antibodies, this shows us that synaptotagmin seems to maintain aggregated into discrete pools after fusing with the plasma membrane. Also, there are more dots in the internalized image--demonstrating the high rate at which endocytosis occurs--but the surface dots are generally brighter, since the surface is exposed to the antibodies for a longer period of time during its preparation, thus increasing the efficiency of labelling.
Next, they strongly stimulated the cells in order to promote large-scale rounds of exocytosis and endocytosis while their antibodies were present. They then analyzed the comparative brightness of the stimulated and unstimulated surface images, and followed by analyzing the dot diameters from a number of preparations:
a, Typical STED image of a heavily stimulated, surface-stained, non-permeabilized preparation. Compare with Fig. 2g. Scale bar, 1 microm. b, Comparison of dot brightness of the surface pool in stimulated and unstimulated preparations (mean plusminus s.e.m. from 4–5 independent experiments). c, Quantification of dot FWHM for different preparations (see Methods). We analysed the dots from 3–5 different experiments. To ensure that dot FWHM measurements were not affected by dots that were closely together, a stringent chi2 cutoff of less than 0.01 (difference between the fit and the data) was placed on the lorentzian fit to the dots.
So what does this show us? Even after heavy, extended endocytosis, synaptotagmin is still localized in discrete batches on the plasma membrane. These are clusters of approximately the same brightness during both conditions of heavy endocytosis and during conditions in which endocytosis is predicted: thus, synaptotagmin is equally clustered in both circumstances. Finally, the fact that dot size maps very consistently across preparation implies that each dot represents the staining of a single vesicle.
So this shows us that when vesicles fuse with the membrane during endocytosis, not only does the synaptotagmin from each vesicle not diffuse across the membrane, but it seems to remain aggregated in amounts corresponding to the original vesicle. This strongly implies that when the vesicle fuses with the membrane, it somehow manages to maintain a distinct entity separate from its surroundings. How is this accomplished? Well, never let it be said that Neuroscience is not a discipline with plenty of questions remaining for future generations of researchers.
Willig KI, Rizzoli SO, Westphal V, Jahn R, Hell SW (2006) STED microscopy reveals that synaptotagmin remains clustered after synaptic vesicle exocytosis. Nature 440:935-939.
Saturday Random 10
Working on the last STED post, but I'm splitting time with preparing the presentation for my Neurosci paper, catching up on the last two weeks of Physiology that I skipped while working on the paper, and general slacking off because it IS Saturday afternoon, after all. Also? It's Earth Day. Remember to recycle something.
1. Collide - Slither Thing
2. Jah Wobble - The Angel
3. RL Burnside - Black Mattie
4. the Goblin - Suspiria (Main Title)
5. Nina Simone - I Got It Bad And That Ain't Good
6. Banco de Gaia - Harvey and the Old Ones
7. Bebel Gilberto - Winter
8. Moby - Bad Days
9. Brother Ali - Bitchslap!
10. Danger Doom - Mince Meat
Friday, April 21, 2006
Symposium on Drug Addiction at the U of M
I realize this is WAY too last minute... but if anyone's reading this, in the area, and interested in drug addiction, we've got a line-up for you today:
Neurobiology of Drug Abuse symposium today at 1:30-4:30 PM
Location: 2-101 Nils Hasselmo Hall.
Speakers: Toni Shippenberg, Mark Wightman, and our own Mark Thomas (filling in for Antonello Bonci).
It's gonna be awesome.
By the way, I have no idea if those PubMed links will work on another computer.
Kiss-And-Run or Kiss & Sit?
Alright, so your promised Part Two (Electric Boogaloo) was slightly delayed by some mass confusion on my part. But I think I've got it all worked out now.
So, first some assorted backgrounds for the non-neuro-inclined:
The first thing you need to know about is the existence of neurotransmitters. Fortunately, you only really need to know a few things:
1. Neurotransmitters are chemicals neurons use to communicate with each other. This occurs at a junction between two parts of a cell known as a synapse.
2. The basic, watered-down version of transmitter release is as follows: inside the axon terminal a batch of vesicles sit around, full of transmitter. These are sitting, prepared to release their cargo into the synaptic cleft (the space between the presynaptic and postsynaptic parts). When the signal to release comes, the vesicle's membrane is joined with the plasma membrane, opening the vesicle to the synaptic cleft and allowing its contents to diffuse out.
What happens next? That's what we're here to talk about.
Really, what we're looking at here is an important question: what happens to the vesicle once its cargo is released? There are two main pathways we want to compare here. I'll give you a link now to this somewhat disturbing java animation that The Daily Transcript linked to when he posted about the article we're going to talk about.
So, in simplified terms, we're dealing with two pathways that are called "endocytosis" and "kiss and run". If you've taken some bio classes, you're probably at least acquainted with the idea of endocytosis. In this example of the scenario, the vesicle completely fuses with the plasma membrane of the neuron (known as exocytosis), which enables complete release of transmitter. Later, a chunk of membrane is pulled back in from the plasma membrane (via clathrin-mediated endocytosis--don't worry, you don't need to know this part) and fuses with a cell organelle known as the endosome. It's then recycled from the endosome and gets filled back up with all its neurotransmitter goodness, so it can re-dock and re-prepare to release it.
Now, this sounds like a lot of work, doesn't it? And you're right: this is a process that takes around a half a minute or so. And when you're thinking about the time frame on which your nervous system works, you're probably not thinking about taking a half minute to get anything done. Or maybe you are. We could agree to disagree on this. But that's where "kiss-and-run" comes in.
If I understand correctly, the idea of kiss-and-run was developed based on the observation that vesicles could reform in just a few seconds after a weak, transient stimulation. Basically, in kiss-and-run, it's thought that the vesicle "kisses" the membrane, transiently opening a pore which releases some of its transmitter load, before pulling back and "running" away. This way, instead of having to put a vesicle together from scratch at the endosome, you have a half-full vesicle that you can fill the rest of the way while it's sitting in line and waiting for it's turn to come around again. Under this hypothesis, the vesicular release via exocytosis and endocytosis only occurs during prolonged stimulation.
Now, from what I've seen, kiss-and-run has been fairly well demonstrated, although not conclusively so. This is going to be important when we get to Willig et al's paper, which is going to have to be part three of this series, because this post is already way too long.
Thursday, April 20, 2006
B8F6 40X Ruby 3
B8F6 40X Ruby 3
Originally uploaded by Mal Cubed.
I thought I'd dig into the files and give you a bit more of an idea what we're talking about. This is far from a perfect example, especially since I don't have my notes and therefore remember with 100% certainty what we're looking at.
But I think this is a fiber tract that we labeled with fluoral ruby, at 40X (again: I think). Now, this isn't the highest magnification you can go to, nor is this the best equipment/exposure/etc that are available, but nonetheless you can already see objects tend to be somewhat low in detail.
Light Smaller Than Light: Rayleigh's Diffraction Barrier Broken
Regular posting resumes.
People who work with really really small things--in our own humble example, neurons--are generally acquainted with Rayleigh's diffraction barrier. It goes by a number of names: Rayleigh's law of resolution maxima, the Rayleigh criterion, and so forth. But the gist of is that there is a hard limit to the maximum resolving power one can achieve via optical microscopy, partially due to the properties of visible light.
If you haven't encountered this idea before, click on the link above, as wiki can explain it better than I can. But the basic version: for our purposes, I think we can get away with describing the resolving power of a microscope as one's basic ability to distinguish between objects in a field being viewed at a certain magnification. This is dependent on a function whose variables include the wavelength of the light involved, the refractive index of the medium being viewed through, and the sine of the angular aperture. Examining our three variables: the sine function maxes out at 1 (although for practical reasons, the limit is generally 0.94). For reasons I cannot claim any knowledge of, the best refractive index achievable seems to be 1.56, with an oil immersion.
Now, I know what you're thinking: WOW, that's REALLY REALLY REALLY SMALL. And you're right.
But: let's compare it to a few numbers:
Size of an average neuron's soma (the cell body): 10-25 micrometers. That's around 50-125 times the size of our barrier. Not bad.
Size of an average dendrite (the processes that receive information from other cells) or an axon (the processes that send information to other cells): ~1 micrometer. Now, that's still five times the resolution barrier.
But at the same time, realize that this limit is the minimum space objects need to be separated by to be distinguishable from each other. This means that you're pretty much screwed when it comes to trying to visualize things smaller than the level of an individual dendrite or axon--which is where all the interesting stuff is happening. To be sure, there are a number of way to get around this. You can tag specific proteins with fluorescent dyes, so that only they will appear on the scope. But if it's a highly localized protein, then you're still in trouble. You can also visualize via electron microscopy, but the preparation required prevents you from working with living biological systems.
But this morning, thanks to Alex Palazzo, I discovered that a new technique--called stimulated emission depletion (STED) microscopy--has been developed to work around this limitation. Apparently Stefan Hell and his colleagues take his name literally*, as this technique can be used on fluorescently labelled preparations to achieve a resolution of approximately 50 nm. And, in theory there is no fixed limit to the resolution achievable by this technique. Last week, they published their first paper from practical use of this technique, and Nature has published a brief overview of the technique.
So how'd they do it?
I'm glad you asked.
From Nature's overview, by Garth Simpson:
The first beam excites molecules just as in traditional fluorescence microscopy — as the molecule absorbs the energy from the light, it is promoted up to a higher energetic state, and as it relaxes back to the ground state, it releases the energy in the form of light. The second beam, at a different wavelength, suppresses this fluorescence by 'stimulated emission', in which molecules are actively pumped down out of the excited state by light (in essence, absorption driven backwards). In sufficiently intense optical fields, stimulated emission becomes more efficient than fluorescence and is the dominant effect, drastically reducing the fluorescence.
In STED microscopy, the normal fluorescence is suppressed by a depletion beam that is shaped like a doughnut and contains a node of zero intensity — a hole — at the centre of the focus. So, any fluorescent light that is detected arises just from this hole of about 50 nm across where the depletion beam is absent (Fig. 1). Scanning this narrowed viewing point across the sample allows a higher-resolution image to be built up, much as a computer screen made up of smaller pixels will provide a sharper image...
But a picture is worth a thousand words, so here you go:
In the upper left corner, you can see a blue light produced by excitation of a fluorophore. In the upper right corner, you can see the orange STED beam. This is basically blocking the flourescence of the excited molecules in its range by knocking them down a peg (in terms of energy states) before they can release any light. Then in the lower left corner, you see a green light representing what's left after the two lights interact. And the graph in the bottom corner represents the flourescence profile after their interaction.
So what have they used this technique on to get me so enthused? Well, if you really really care you've probably already clicked on the link and found out. If not, you can either click on it now (if you're the impatient sort), or wait until later tonight for the exciting conclusion of our two-part post. Because, um, right now I've gotta get running to class.
*In German, "Hell" means "brightly."
Simpson GJ (2006) The diffraction barrier broken. Nature 440:879-880.
Willig KI, Rizzoli SO, Westphal V, Jahn R, Hell SW (2006) STED microscopy reveals that synaptotagmin remains clustered after synaptic vesicle exocytosis. Nature 440:935-939.
EDITED at 7:30 PM because I accidentally linked to the U-of-M-access Nature pages.
EDITED on Wednesday, 26 April 2006 after a fundamental physics error was called to my attention.
Tuesday, April 18, 2006
Tom Cruise = Favorite Crazy Person
I just used the phrase "reaches fruition" in my paper. Now if I could only fit in the word "eschatonic" or the phrase "inevitable triumph of the forces of darkness over your pitiful forces of light," this would be a Great Day.
Monday, April 17, 2006
Not Dead Yet.
I've been sitting here working on the paper for the last six hours. In that time, I've written seven pages and revised the one table I've prepared thus far back and forth at least a dozen times. Current page count is 13 out of 15, with the conclusion left to go as well as at least a half page each from two previous sections. This could be problematic, and will probably just result in me gutting all of the really introductory stuff out of the background section. Which is depressing and irritating, but it's the quickest and easiest solution to my lack of conciseosity.
I've also drunk 4+ cokes (yeah, I know, I'm an utter caffeine wimp), eaten a boatload of sugar and made it halfway through a totally excellent turkey, dried cherry and red pepper sandwich.
Regular service should hopefully resume tomorrow; perhaps on Wednesday. We'll see how sore my fingers get by then.
Wednesday, April 12, 2006
Still working on paper.
Dead by dawn. Dead by dawn.
And tomorrow, I get to suddenly switch gears and spend the next day and a half cramming for my Cell Bio test when I've been basically ignoring the class (except for my mandated attendance) for the last 2+ weeks.
Maybe more later tonite, since my ability to get further work done on the paper is pretty much kaput for days that start with a 'W'.
In other news, relatively normal blogging should now resume in less than a week. It's sort of odd that I'm still a month off from the end of the semester (and thus gradumatating), and yet I still feel crushed enough by the paper to make me feel like I'm pretty much done after next Tuesday. We'll see how well that goes in the long run...
Note to self:
I need to remember to not mentally berate researchers for having the temerity to not have researched what I want them to. Because, you know, it's not THEIR job to provide more data for my paper.
Tuesday, April 11, 2006
Some articles to look at next week when I have time
New Scientist: All the pleasures of alcohol, with no downsides
New Scientist: Cocaine-triggered brain changes reversed in rodents
A Brief Public Service Announcement (aka break from the paper writing)
That's all for the moment.
I'm now a member of the Society for Neuroscience!
Saturday, April 08, 2006
Just This Once
Okay, so I try to stay out of the whole creationism thing, because arguing with nut jobs is sort of boring and mostly irritating, and I don't really need the hits THAT badly.
But anyway, Pharyngula linked to an article reporting that Dr. Dino's finally got shut down for his rejection for such secularist modern conventions as... building permits.
As the article puts it:
Owners of the park, which shows how dinosaurs may have roamed the Earth just a few thousand years ago, did not obtain a building permit before constructing the building in 2002. They have argued in and out of court that it violates their "deeply held" religious beliefs, and that the church-run facility does not have to obtain permits...
Unfortunately for them, the government disagrees with them. And, it points out, so does the bible:
"Scripture also says 'Render unto Caesar what Caesar demands.' And right now, Caesar demands a building permit," County Commission Chairman Mike Whitehead said.
That's the funniest thing I think I've read this entire week.
Thursday, April 06, 2006
Quick Post That Will Make Sense to Maybe One Person Who Reads This (Or More)
So I've been working on this paper all week, and I was telling everyone the last couple of days that it all made sense so long as psychostimulant sensitization-induced LTD was mediated by a change in AMPAR function rather than endocytosis.
I realized this afternoon that I was wrong, due to something key that I'd forgotten about the Marina Wolf paper I'd been reading on Monday, which I shan't go into right now.
But anyways, I realize that this afternoon and what's the next paper I grab from the pile of stuff I need to read? This:
Nucleus accumbens long-term depression and the expression of behavioral sensitization
Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.
I'm glad I figured that out this afternoon, because otherwise I'd spend this entire paper trying to figure out how they got it wrong. ;-P
Wednesday, April 05, 2006
New Drug vs. Old Drug?
Sometimes my fascination with my research areas gets the best of me. Case in point: my initial reaction on reading a CSM article posted to Yahoo!, titled "A new scourge sweeps through Argentine ghettos: 'paco'," is intense curiosity:
A recent study by the Argentine Secretariat for Prevention of Drug Addiction and Control of Narcotrafficking, known by its Spanish initials SEDRONAR, showed paco has outpaced all other drugs in rates of adolescent users in the last two years. Based on the results of the study, officials say 70,000 Argentines between 16 and 26 years old in the greater Buenos Aires area have tried paco.
I immediately start running through an internal checklist of psychoactive plants and drugs used in South America, trying to figure out which might have become a street drug. I'm completely coming up blank, because none of the ones I can think should be addictive enough--or even particularly appealing enough--to become a street drug.
At this point, I'm fascinated. That means there's something there I don't know about. I burn my way through the article, trying to find out what it is, thirsty to discover this new drug out there. And there's a part of me that's a bit let down to discover... it's just a cocaine byproduct:
The paco sold here is a chemical byproduct, a leftover when Andean coca leaves are turned into a paste, then formulated into cocaine bound for US and European markets. Paco was once discarded as laboratory trash, says Dr. Ricardo Nadra, an Argentine government psychiatrist who works with paco addicts. But Argentina's devastating financial collapse in 2001 left the poorest even poorer, creating an impoverished demand for "cocaine's garbage," he says...
...Because it's smoked rather than sniffed, and because of the physiological impact the confluence of chemical toxins have, experts like Dr. Roberto Baistrocchi, an Argentine pharmacologist who has studied the drug, say paco is exceedingly addictive and can cause lasting physical damage. "More than any other drug, paco is the most dangerous." says Nadra.
Last April, La Nacion, a leading newspaper here, quoted Claudio Mate, a ranking health official from Buenos Aires' provincial government, as saying that intense paco consumption can cause "cerebral death" in as little as six months.
It's part of being a scientist, I guess. An interest in topics that others would find boring or even repulsive; and sometimes it even ranges into a fascination best described as "morbid."
But I've gotta say, paco sounds like nasty stuff. But if there's anything that we should have learned by now, it's that intense poverty generally goes hand in hand with drug abuse. And as the meth explosion in America over the last decade has shown us, people desperate for a fix will turn to whatever's made available:
Like crack in 1980s America, paco has become a metaphor for societal problems.
Parroting a common refrain from experts interviewed for this story, Nadra says paco is fundamentally a social and economic issue. He says the roots of the growing scourge of paco are "social and spiritual dislocation" caused by an increase in poverty.
Ceftriaxone--a widely available antibiotic--may be usable to treat HIV dementia, a Johns Hopkins study suggests:
The study looked at two proteins, called Tat and gp120, that are part of the virus that causes HIV infection and that are implicated in the development of HIV dementia, according to Dr. Rumbaugh, the study's lead author. HIV is the only virus that makes Tat and gp120, which are produced during its normal life cycle, though other viruses make similar proteins. Dementia is a common side effect of long-term HIV infection, but there are no known specific treatments for this complication. According to Rumbaugh, Tat and gp120 are believed to cause dementia by reducing the expression of a brain chemical called EAAT-2 (excitatory amino acid transporter-2). EAAT-2 absorbs the neurotransmitter glutamate from the space between neurons (the synapse), thereby preventing excess neuronal excitation, which in turn can cause cell death and brain damage.
Ceftriaxone, used to treat pneumonias, sexually transmitted diseases, bacterial meningitis and other infections, is a known stimulator of EAAT-2 expression and protects against neuronal injury in mice with nervous system disorders. To test ceftriaxone's potential in HIV, Rumbaugh and colleagues grew human neuronal cell cultures in a lab from existing human neuron cell lines, treated them with a range of doses of ceftriaxone, and exposed them to Tat or gp120. They found that the antibiotic protected the neurons against both HIV proteins. The dose of ceftriaxone needed for protection was well within the range currently used for treatment of bacterial infections.
Tuesday, April 04, 2006
Busy Times Ahead
It occurred to the Neurophile that he should warn you about something.
Also, it apparently occurred to the Neurophile that he wasn't referring to himself in the third person anywhere near as much as he ought.
But anyways, the Neurophile has a big term paper due two weeks from today. He has thus far written zero pages, and read approximately (he hopes, wishes, preys on the weak) 1/2 of the articles he will probably end up needing to to verify or disconfirm his hypothesis.
So busy times are a-comin', and posting may thin out in the meanwhile. Although, the Neurophile is forced to admit that this could easily cause his posting rate to triple. All possibilities must be considered.
Perhaps someday, I will have trained you all--the loyal legions of the Neurophile--in enough of the basics of neuroscience that I can meaningfully explain the paper to you. Because there's a certain level in which I'm having quite the rollicking time researching it, despite the giant monstrosity it is slowly evolving--via the transmission of heritable traits, natch!--into.
Science Museum: Geek Prom: Any Questions?
One of these days, I'm going to give in to my urge to just start randomly selecting post titles from the list Firefox provides me when I click on the text field. But that's neither here nor there.
Yes, too much of my blogging is stolen from Dr. Myers these last few days, but if you bring it up at a party, I've got a knife.
Anyways, due to his non-magical powers, I discovered the existence of the imminent Geek Prom at the Science Museum of Minnesota on Saturday, 22 April 2006.
On the one hand, I am generally loathe to participate in ritualistic events involving odd costuming, bland social interactions, and other forms of oneupsmanship. Yes, I just managed to encapsulate my irritation at everything from comic conventions to churchgoing in one sentence. But anyways, that's because I'm an overly cynical jerk, which you should not let get in the way of yourself having a good time. I myself would like to attend, as it occurs right at the end of my Hell Week.
At the very least, I figure it should be ~237% as interesting as Goth Prom. To their credit, however, I must point out that they've finally figured out that Monday at the beginning of finals might be a bad time for some of their clientele. If I recall correctly, I think last year was the time I went and just read about visual systems networks for my Neuroscience final the next day while swilling red wine.
But I could just be making that up. These things do happen.
Pianka Strikes Back
KXAN from Austin has gotten in touch with Dr. Eric Pianka, and evidence continues to suggest he is a sane human being who says reasonable things. For those of you just turning in:
Some are accusing a UT scientist of advocating genocide to control the world's population.
Does it sound crazy?
The professor whose ideas are under scrutiny says it's not just crazy, it's not true.
UT Ecology Professor Dr. Eric Pianka does not want everyone on Earth dead.
"I don't bear any ill will towards anybody," Pianka said...
..."If we don't control our population, microbes will. Why do we have these lethal microbes that kill us in the first place? The answer is, there's too many of us," Pianka said.
Pianka says he would never advocate genocide or extermination like some suggest he does.
"I've got two granddaughters, man. I'm putting money in a college fund for my granddaughters. I'm worried about them," Pianka said.
KXAN, it's worth noting, has their full interview with Pianka at the sidebar at present. It's ~20 minutes or so, worth checking out if population control is a big topic with you, or if you still need persuasion that the entire Texas Academy of Sciences aren't intent on destroying the species.
So the question at hand: is this an isolated event, or part of a trend? Now that we have a Republican War on Science, with science being distorted by the administration and prominent Republicans in Congress; do we have to worry about concerned citizens taking the distortion into their own hand?
We can hope that people might learn to chill out and tune back in with the real world now that Pianka's stepped forward... signs aren't promising. Oh well, keep looking to the sky and never forget:
Monday, April 03, 2006
Apparently, people still haven't figured it out. So I'm going to keep this up until they do. So remember, remember this third of April:
Can you dig it?
A Vacuous Apology; A Not-So-Subtle Distinction
First off, I just got back from class, loaded up the blog, looked at this morning's Dr. Dick comment, chuckled, and felt bad about it.
That was a low blow. For this, I apologize to Mr. Dembski. In the future, I will restrain myself from responding to the opposition's juvenile ad hominem assaults with my own. Unless they're--at the very least--much funnier than that one was. Also, this is theoretically a family blog so I should keep the dick jokes to a minimum. Theoretically.
Second: Apparently the conservative blogosphere is quite irate about Golden Gate Planned Parenthood's new initiative, a rather standard viral marketing scheme in which one can win movie tickets by telling a friend about them, or register in an iPod drawing by making an appointment. As LifeNews puts it:
"These are some of the schemes Planned Parenthood is using to lure teenagers into its deadly facilities,” said Douglas Scott, president of Life Decisions International, a group that organizes boycotts of companies that contribute to the abortion business.
“Now which age group is most likely to be swayed by this kind of gimmick?” Scott asked. “This incentive is clearly aimed at young people.”
“Planned Parenthood has resorted to common corporate tactics in an effort to get young people to encourage their peers to voluntarily become the pro-abortion group's new victims," he said.
I'm not trying to talk down to people here, or assume they're stupid or anything, but come on: do these people realize the diversity of services Planned Parenthood offers for both genders? Or do they just not care? Is it evil to get an affordable physical from a non-profit, just because they also offer abortions, contraception, and STD testing? Or is it just intrinsiclaly sinful to encourage teenage girls to get cheap, regular gynecological exams? I'm very confused on this: I'm sort of forced to believe by the content of comments that this large group of people that has nothing better to do with their time than rail about the evils of Planned Parenthood doesn't actually have the slightest clue what they actually DO other than perform abortions for women in need. It comes across as a bit ridiculous.
Sunday, April 02, 2006
Sunday Random Ten
This is my blog, and I can do what I want.
1. Ladytron - High Rise
2. Jello Biafra & the Melvins - Dawn of the locusts
3. Jedi Mind Tricks - The Worst
4. Death Ride 69 - Digital Submission
5. DJ? Acucrack - Balthazar's Revenge
6. Wyclef Jean Feat. Admiral T. - Fanm Kreyol
7. Spahn Ranch - The Warmth of Silence
8. Junkie XL Feat. Solomon Burke - Catch Up to My Step
9. Brother Ali - Prince Charming
10. Marvin Gaye - Sexual Healing (live)
I think, it sometimes becomes a bit too apparent around here how much I don't want to muck with graphs or data in Excel to make sure cells are all pointing at each other properly at certain points...
With that said, I was inspired by this to finally join in on this and bring you this:
So always remember,
I think it all speaks for itself, don't you?
MONDAY MORNING EDIT: I woke up this morning and discovered thanks to PZ Myers and Welsley Elsberry that Bill Dembski--in a desperate attempt to distract visitors to his blog from his own insanity--has started taking after Mims in referring to Dr. Pianka as "Dr. Doom," making this campaign even more appropriate.
I blogged yesterday about UTAustin professor Eric Pianka (aka “Dr. Doom”) and his advocacy of killing 90% of the world’s human population with airborne Ebola. Could Pianka be charged with terrorism/conspiracy to commit a terrorist act? What happens if a student actually takes his suggestion to heart and kills a bunch of people? Why shouldn’t we think that Dr. Doom himself would commit the act of human destruction he is advocating? How is what he is saying any different from somebody at an airport saying that he plans to plant a bomb there.
I can assure you, Mr. Dembski, that "Dr. Doom" probably has no such plans. I can offer you several lines of reasoning:
1. Just because you've quoted someone else who is making something up about someone, that doesn't make what they've made up true.
2. Dr. Doom is not in fact a professor at any branch of the University of Texas. That's because Dr. Doom is not a real doctor. It's true: he rests on false laurels. Also? Doesn't exist.
3. Dr. Pianka, on the other hand, who DOES exist, is a professor of Zoology. A quick perusal of his research projects turns up a dearth of grants titled, "aerosolization of Ebola Zaire." Or do you think the sneaky bastard's been putting all his money for researching the evolution of the varanus lizard to this purpose for the last three years? Must be, because since evolution doesn't happen, you have no idea what he could possibly have been studying, right?
Christ. I'm sorry, Mr. Dembski, but my 11.5 month old nephew could call you out on this one. If Dr. Pianka is Dr. Doom, then you are Dr. Dick. And pretending you could ever be a doctor is a strong enough compliment to more than balance out the insult.