Research Blogging is finally working

I joined research blogging in the hopes of attracting more attention to my blog. But for nearly a month, none of the posts I tagged were appearing in research blogging. I finally resolved my issue, and for the sake of others who may encounter this issue, here is my solution.

The problem lies with the way blogger handles custom-entered HTML. Basically, a critical part of the HTML needed by RB gets stripped. To fix this, AFTER posting your post, re-edit it in HTML mode. Within the RB citation find every "< span" and add "class="Z3988"" after it.

Oh, and there is no space between '<' and "span", but blogger won't even let me type that...


 Simple fix, but it would be nice if blogger would not edit HTML I enter myself

Alt Med fails again

Some of you may have heard of this "alternative medicine" fad going around (OK, its been going around for centuries, although we used to call it things like witchcraft, and snake-oil).  And despite its name, it is not medicine.  Out of the thousands of alt med products out there, there is a tiny handful (3, as of my last count) that actually have clinically measurable benfitits.

Today we're NOT adding another to that list.  For decades (perhaps centuries) people have been claiming that Ginko biloba helps your brain work.  Its been touted as a cure for everything from insanity, to ADD, to senile dementia.

So some real scientists put this claim to the test, and treated just over 3000 elderly people with a high dose of GB.  The end result - nothing, nadda, not one damned thing.  Those who received the GB under went age-related cognitive decline at the exact same rate as those who didn't get any GB.

And for those of you who want to know what the proven 3 are...

1. Ginger, for motion sickness
2. Ginseng polysaccharides (AKA ColdFX) to reduce cold symptoms/infections
3. Melatonin, for jet lag

And while those work, compared to conventional drug-based interventions, they aren't all that great.  ColdFX, for example, reduced cold-virus infections by ~25% and shortens colds by a few days.  I actually know a few people who were involved in the developed of this product, and it was developed through hard-core science...and you cannot just use ginseng; you need to eat 5-6lbs/day to get an effective dose of Poly-Furanosyl-Pyranosyl-Saccharide.

Who's dumber?

So by now everyone's most likely heard of the Christmas-day terrorist attempt.  If you haven't the short version is a Nigerian kid became a fundamentalist, built a bomb, smuggled it onto a plane by stitching it into his pants, and then was too stupid to figure out how to make it go boom.

To make matters worse, the security types had been warned about this guy - by his own family.  That's right - they (they, as in the TSA and their respective counter-parts in Europe, the UK and Canada) knew he was talking about doing something like this, and didn't do a single thing to prevent it from happening.  Even though he was on watch lists, they let him ON THE PLANE.

And the only reason something bad did not go down was our terrorist-wannabe lacked the brain power to figure out how to set off his little fire cracker.

In response to this there has been a new "security" crackdown.  The new rulez:

1. only 1 carry-on bag
   
2. no using anything, or getting up to pee, 1 hour before landing
3. you must be patted down by security before boarding.

The end effect of these new rules - long lines at the airport, cancelled flights, irritated passengers, and the harassment of a guy who had the misfortune of being both of the same nationality as our wanna-be terrorist, and also really having to pee.

Now I fail to see how any of the above, except perhaps #3, could enhance our security while flying.  If anything, it seems to be a knee-jerk reaction intended to distract people from the utter failure by those supposedly entrusted with our security.  To make matters worse, the news industry seems to have swallowed this hook, line and sinker.

So tell me, who is dumber?

1. The terrorist, who couldn't blow up his own bomb
2. The security forces who failed to stop a guy they were warned about well in advance, and who had this guy on their security lists
   
3. The news papers, for failing to pick up on #2, and instead are reporting near-solely on the crap done by the morons responsible for point #2 to assure the rest of us that they aren't truly incompetent.
   

Evolution of the immune system - and making myself a liar

But a few hours ago I put out a christmas/solstice/new years greeting and said it would be the last post for a while.  5 seconds after posting that my e-mail received a table of contents from Nature Reviews in Immunology which touched upon one of my favourite topics - the evolution of our immune system.  I've been out of the immunology loop for a few years, and was pleasantly surprised to see how far that field has advanced.

I've also had a few beers.  The combination of ethanol intoxication and my inherent geekyness is going to turn me into a liar - here's another pre-xmas post...

The article requires a subscription.  Its so good I'd like to screw copyright and post the whole thing here, but the consiquences of that could be dire, so I wont.

As per usual, a bit of background first.

Since the beginning of life, species have been finding ways to fend off other species that want to prey on them.  The classical example is antibiotics - chemicals made by fungi, molds and bacteria, to kill other bacteria, fungi and molds which would compete or prey on them.  Not too surprisingly, when life figured out stringing more than one cell together was a good idea, life continued to evolve ways of defending itself against forign invaders.

The first animal systems - innate immunology - was rather simple.  Animals simply evolved receptors which identified conserved molecules found on pathogens, but not in the host.  Over time this lead to a pretty complex immune system - able to detect viral markers (negative-stranded and double stranded RNA, for example), bacteria (endotoxins, peptidyglycans, CpG DNA) and fungi (cell wall components).  But the nature of this system left a  - a huge hole - in this kind of immunity.

Simply put, a pathogen simply needed to change these molecules, or find a way to interfere with the detection of these molecules, to avoid the immune system.  This was the situation until the rise of vertebrate animals - and is the topic of this fascinating article.

Upon the rise of vertebrate animals - animals with a backbone & centralised nervous system - a huge (r)evolution in immunity occurred: the formation of the adaptive immune system.  Without going into a lot of detail, this system generates a series of "randomised" receptors but first combining together 2-3 chunks of DNA (through a process called VDJ recombination).  This is further "randomised" through a series of mutagen events.  The end effect of this is our bodies make billions of cells, each with a unique receptor.  Some of these receptors are non-functional - as in they identify nothing.  Others may identify pathogens or other forign antigens.  And yet others might recognise out own bodies.  Through a process of selection, those which recognise our own bodies are eliminated (errors in this process lead to autoimmune diseases, like multiple sclerosis), leaving behind a set of cells who identify unknown targets.

When a pathogen is encountered any of these cells that identify that pathogen become active, and act to kill the pathogen.  But its not just one kinds of cell that does this, but two.  B-cells make these random receptors, and when activated secrete these receptors into our blood.  You know of these - their called antibodies - and they act to bind up pathogens.  A second cell also makes random receptors, called 'T cells", but they don't secrete their receptor.  Instead, these cells regulate our immune responses - ramping them up when we need them, and shutting them down (and remembering the pathogen) once sterility has been achieved.

How this system evolved is fairly well established - a virus invaded our genome, incorporated into another receptor, and when things settled down it had created a recombining receptor.  Its a fascinating topic, but would be a blog post or five of its own.

What doesn't get mentioned is that this event occurred at a central point in vertebrate evolution - the evolution of jaws.  And since this occurred at this point those vertebrates that didn't get the jaws - hagfish and lampreys (see pic on right) also incorporated the virus, developed an adaptive immune system, but did it in a completely different way.  In fact, there are some scientists who think it was this differential incorporation of the virus that lead to the formation that lead to jawless verses jawed fishes.  And while a fascinating argument, that has little to do with this post.  Instead I want to talk about the "alternate" immune system that hagfish and lampreys evolved.

Our immune system is based on the identification mainly of proteins, and often small chunks of those proteins.  The "alternate" system is more generic - it tends to recognise larger complexes; often protein-sugar composites.  At the receptor level the differences are huge - its blatantly obvious that different genes were invaded by the virus, to make these two systems.   But even so, they way these systems work is remarkably similar - the lampreys have two types of adaptive cells, and one of those makes a secreted receptor.  The arrangement of the re-combinable genes is simular, as is the mechanism of recombination.  And yet the receptors they make are not simular in the least.

This has long been a headache for evolutionary biology - in both cases you have two systems working with each other - a diverse set of elements that gets recombined, and a system to recombine them.  But here's when the evolution gets confusing - on one hand we have a conserved method of recombining the genes; suggesting that the recombination mechanism was shared by both jawed and jawless vertebrates.  But the target of that recombination mechanism is different - leucine-rich repeats in the case of jawless fish, immunuglobulin domains in the case of antibodies and the t-cell receptor.

The confusion comes from having a case where you've got a conserved mechanism that seems to have evolved inside of two (or three, since antibodies may have done it differently than the t cell receptor) separate processes.  While I've talked about the recombination being separate from the target, in reality the two are inseparably mixed - the target of the recombination machinery is an unremovable part of the target pieces.

The end effect of this is that we don't know exactly how the two system separated - at least we didn't back in my day.  But today it looks like we now know (see pic at the beginning) - the virus entered the jawless vertebrates, and before any immune system formed the jawed and jawless separated.  Then the two diversified - the jawless forming their LRR-mediated immune system, and us jawed vertibrates with our Ig-mediated adaptive immune system producing their immune system.

Last post for a few days

I suspect that this'll be my last post for a few days, although you never do know...

This atheist is going to spend xmas with his Christian wife and her Christian parents.  Sounds awkward - surprisingly, its not.  In fact, I'm looking very forward to the time we're going to spend together.

Regardless of your beliefs, I wish you the best in the new year, and a happy solstice-esqe holliday of your choice.

But can I still use the word "pontificate"?

So the pope has "copyrighted" his name, image and symbols - including terms such as the word Pontiff; his official-ish title.  This is only sortof a copyright - its legally unenforceable pretty much anywhere in the world.

None-the-less, it makes one wonder if the terms clearly derived from "pontiff" are still usable, or do they fall under the pontifical "copyright".  They're especially concerned about the use of papal terms when people use those terms to imply papal "credibility and authority".

Which brings me around to the term "pontificate" - clearly derived from the term "pontiff", and used in a way as to imply someone is talking in a manner similar to the pope - you know, rambling on aimlessly about topics of which you have no knowledge...

So, can I say "the pope illustrated his usual ignorance when he pontificated about the dangers <sic> of condom use", or does that go against the papal copyright?

T-Cells: Beyond the Resolution Line

I have a diverse set of research interests - high-end microscopy, immunology, infectious disease, cancer, etc.  Its rare that a paper hits the "awesome" end of the scale in most of those categories, but this week Nature Immunology published a paper that got the nerd senses tingling.  In this tour-de-force, Mark Davis's group uses a new form of microscopy to analyse how T-cells work.

As usual, a bit of background first.

T-cells are the major regulatory cell of our immune system.  The express special receptors, called T cell receptors, which they can use to identify cells which have been infected by bacteria or viruses.  After detecting an infection, some T-cells (called CD4 t-cells, or helper t-cells) initiate and regulate the immune response.  Another type of T-cell (CD8 T-cells, or cytotoxic T-cells) go out and destroy infected cell.

The t-cell receptors (TCRs) themselves are complex things, with multiple parts (see pic on right).  There is the alpha/beta chains that detect the infected cell, and then the CD3 chains and the zeta chains which transmit the signal from the receptor into the cell, and the CD4 (or CD8) co-receptor which helps stabilise the interaction between the TCR and the target cell.  Upon engagement these receptors signal by recruiting proteins from within the cell, including one called Linker of Activated T-Cells (LAT), which acts as a scaffold for the rest of the proteins to bind to.

This paper studies the interactions between LAT and the zeta chain portion of the TCR.

The second cool part of the paper is HOW they looked at the TCR.  Microscopy is plagued with one major issue - there is a distinct resolution (diffraction) limit, below which we cannot resolve.  We've all experienced this ourselves, with our own eyes.  Think of driving at night.  When you see a car far off you see only one headlight (a, image to the left) - its not until the car comes closer that you can see two (c, image to left).  Where the one light becomes two is the resolution limit of your eye; microscopes experience a similar limitation.  Under optimal conditions this limit is 200-300nm, while proteins interact in spaces of 30nm or less, meaning we're lacking about 10X the resolution we need to study protein-interactions.

We scientists have a few tricks to get around this limitation.  This paper uses one of the newer of these tricks, called PALM.  The way this works is you use a photoactivatable dye - basically a florescent marker which needs to be activated by a specific wavelength of light before it becomes fluorescent.  The way PALM works is you use a weak activating beam to activate a small portion of the dye.  You then image the dye using a high-powered laser, and you image until all of the active dye is photobleached (the microscopy version of burning out  light bulb).  The resulting image will be a pattern of dots.  You repeat this process time-and-time again, and then mix the dot "images" together to get a single, complete image.

Normally this wouldn't produce anything other than what you would get if you just activated all the dye and then imaged it - you'd end up with nothing more than a resolution-limited image.  But there's a trick here - known as "math" - which lets us break that resolution limit.  Diffraction-limited dots have a specific shape, as you can see in the image above.  This shape is always the same, and the "tip" of the peak lies exactly over the fluorescent molecule.  So by mapping the peak of each dot, we can "break" the resolution limit and see much finer detail - in the case of this paper, down to 25nm!
So what did they find?

We've known for a while that many of the proteins in our cells membranes are not evenly spread out, but instead float around in little "islands".  The clustering of these little "islands" is often what activates these receptors.  But in many cases - like the T-cell receptor - we didn't know what was in these little islands, or what happened to them when they clustered.  There really were three options:

1. The TCR and signalling components like LAT are in the same islands, and clustering activates them through mass-action.
2. The TCR and signalling components like LAT are in separate islands which come together and mix; activating the receptor by mixing normally separate proteins.
3. The TCR and signalling components like LAT are in separate islands which come together but don't mix; activating the receptor by simply bringing things close together, but without actually mixing.

Davis's group has answered this question.  The first image shows the TCR before (left) and after (middle) activation.  You can see several small islands on the left, that come together into "super islands" on the right.  The right-most image is a control of randomly distributed particles, to show they are looking at islands, not spread-out single molecules.

LAT looks almost the same (image on right), with lots of small islands before activation, and fewer big islands after activation.  And while its not obvious when you compare the TCR image with the LAT image, the pre-activation TCR "islands" do not overlap with the pre-activation LAT "islands".

So that answers the first half of our question, LAT and the TCR are in separate islands before activation.  But do they mix, or are they wall flowers?
How this was demonstrated is hard to explain; but they used two mathematical measures to figure it out; Ripleys K-function, and cross-correlation, both of which measure how well two distributions overlap.  Without going into a lot of boring detail, the TCR and LAT cluster togeather upon activation, but the individual clusters of TCR and LAT remain separate; think of a cookie - both chocolate chips and peanuts are in the cookie, but the chips and nuts remains separate.
So that answers the second half of the question - we've got a couple of wall flowers on our hands.

I'm sure to many this doesn't seem that exciting, but from a biologists point of view this is quite the breakthrough.  PALM fast enough to image living cells, while also being able to resolve down small enough to see these little islands.  And they resolved something that's been a mystery since those "islands" were discovered nearly 30 years ago - how do they interact, do they mix, and what do they contain.  While this is just the tip of the iceberg - hundreds of proteins are known to be in these islands - we finally have to tools to start answering these questions.

Lillemeier, B., Mörtelmaier, M., Forstner, M., Huppa, J., Groves, J., & Davis, M. (2009). TCR and Lat are expressed on separate protein islands on T cell membranes and concatenate during activation Nature Immunology, 11 (1), 90-96 DOI: 10.1038/ni.1832

Atheism - cause or consequence?

Fellow Torontonian, and far more successful blogger, Larry Moran (of Sandwalk fame) dug up an interesting study just published in Evolutionary Psychology.
To the atheists out there this paper is pretty much old news - nations which are more secular/atheistic are less violent, less crime ridden, and more socially equitable than are more religious nations.

Many take this as proof that religion is evil.  While that is a correct position, I wonder if that's really what this paper shows.

Luckily the PDF of this paper is free.  Unfortunately, the paper is only available in PDF so I cannot readily post the graphs.  So instead I'll provide one example (see image to the right) - in this case we're looking at murder (on the 'Y')  verses Religion-Secularism  Scale (low = religious, high = secular) on the 'X'.  The letters correspond to various nations U = USA, I = Italy, C = Canada, D = Denmark, etc.

 Long story made short - this paper quantified the religiousness of a handful of western democracies, and then compared that to a variety of other measures like murder rate, suicide rate, social inequity, poverty rates, STI rates, divorce rates, and so forth.  In total religiousness is compared to ~30 different societal measures.
In nearly every case, the more secular societies were better off - lower crime rates, lower degrees of social inequity, longer lasting marriages, and longer & happier lives.  Seems cut-and-dried, but a close look at the graphs (including the one above) revealed something interesting - the USA is an outlier in virtually every field.  Statistically speaking, this is a bit of a pickle - does this mean the USA is an abnormality that is incomparable to the rest of the countries analysed, or does it mean that the "outlierness" in the religious axis is representative of the "outlierness" of the USA in the other measures?

This is a double-edged sword.  If you remove the USA from all the graphs most of the advantages of secularism go away (although some remain - childhood mortality, life expectancy, abortion rate, poverty rate and a few more).  But at the same time, removing the USA from the graph also removes most of the "diversity" in terms of religiousness; meaning that we'd be looking for differences over a very small scale.

And, as a final caveat, we have to keep in mind that these are simply correlations - and as every stats teacher out there will tell you, correlation does not equal causation.  As such this study doesn't tell us religion = violent, less equitable societies.  Its equally possible that violent, less equitable societies = religion.
But my moneys riding on the former, not the latter.

Paul, G.S. (2009) The Chronic Dependence of Popular Religiosity upon Dysfunctional Psychosociological Conditions. Evolutionary Psychology 7: 398-441. [PDF]

Walking the line, using a microscope

While I oft discuss evolution and autism on my blog, I research neither.  My primary interest is actually cell biology, along with a large dose of microscopy.  Once in a while a paper will come along which really hits on both of these topics, and its damned well time I blogged about one.  So, for once, a posting about a really cool cell-biology/microscopy paper.

It was published just a few months ago (OK, I'm a little behind on this posting) in PLOS Biology:  Single molecule imaging reveals differences in microtubule track selection between Kinesin motors.

This paper combines some interesting cell biology along with some cutting-edge microscopy.  But before we hit the paper, a bit of background.

Things need to get transported around inside of our cells.  For example, proteins meant to detect extracellular signals like hormones must move to the cell surface; otherwise they won't work.  Much of this cargo gets moved through small balloon-like structures called vesicles.  Rather than drifting randomly, these "balloons" move along tracks in the cell called microtubules; long, filamentous proteins that form a skeleton within the cell.  The image to the right shows this cytoskeleton; microtubules are in green (blue is the cells DNA, red is another part of the skeleton called actin).

Like a train, these "balloons" require a motor to pull them along the microtubule tracks.  In a cell this job is mediated by motor proteins.  While there are a few kinds of motor proteins, this paper deals with one kind called kinesins.  Kinesins are proteins which tend to be involved in the movement of proteins from where they are made (ER and golgi) to the plasma membrane.  Kinesins are odd proteins, that "walk" along the length of the microtubule in a way that looks kinda like a drunk cowboy stumbling out of a saloon (see the video below).

One outstanding question in the biology of kinesins is how do they know where to go - as you can see in the picture of the cytoskeleton at the beginning of this post, microtubules go everywhere, which makes it hard to understand how things can be selectively moved to specific points in the cell.  As it turns out, microtubules are not quite as simple as I outlined here - they're dynamic, as in they continually grow and shrink.  But among those ever-changing tracks there are a small number of microtubules that are modified in a way which makes them stable.  Furthermore, these stable microtubules do tend to go to specific places - for example, in neurons they lead to the junctions between one neuron and the next.  Perhaps these modified microtubules act as highways that allow cells to specifically move proteins to important places.

That is the question asked by this paper.

The real image geekery comes into play with their methods.  They used one of my favourite imaging tricks - single particle tracking (SPT) - to follow kinesins while the pull their cargo around the inside of the cell.  How SPT works is a blog post or two in itself, but the coles notes version is SPT is a method we can use to monitor the movement of single proteins inside of a cell.  Combined with basic microscopy, this method allowed this group to look at the movement of kinesins along microtubules, and to determine which kinds of microtubules these kinesins prefer.

The long and short of how every experiment in this paper was preformed is this group first preformed single particle tracking of the kinesins, overlayed the map of those track with staining of the microtubules, and then used that overlay to determine which microtubules those kinesins are using (click the pic to the right for an example from their paper).

This study looked at three of the kinesins (out of a total of 14), and found that one of them - kinesin 1 - only moves along the modified (stable) microtubules, while two others (kinesins 2&3) moved along all types of microtubules - including those actively growing.  Even better, they also tracked the movement of proteins moved by these kinesins, to show that not only the motor, but the cargo the motor carries, follows along the respective type of microtubule.

This paper has confirmed what we long suspected - that some motor proteins follow specific "tracks" in the cell.  And while we're a long ways away form understanding exactly how a cell directs this traffic, this paper has provided us our first view of one way that cells direct some products to specific regions of the cell - in this case by using kinesin 1 to move proteins down specific tracks in the cell.

Cai D, McEwen DP, Martens JR, Meyhofer E, & Verhey KJ (2009). Single molecule imaging reveals differences in microtubule track selection between Kinesin motors. PLoS biology, 7 (10) PMID: 19823565

My advice for conferecees

So it conference season again, and I feel that I should share what little wisdom I have with those who happen to stop by my blog.  I originally wrote this to a  grad student, so its student-orientated.  None-the-less, here's my rules for surviving a scientific meeting.

1) Expect to drink a lot, and plan ahead. Make sure the nights before important days you don't over-indulge. If a day looks particularly boring, chances are it'll be a good day to nurse a hang-over.

2) Look closely at the schedule. Quite often there are sessions which are boring, have nothing to do with you, and represent nothing more then a waste of your time. Those are good sessions to skip, and go do some sight-seeing, shopping, touristy stuff, kayaking, rock climbing, etc. 

3) Expect to be constantly tired after the second or third day. Between them, the booze, excessive eating, lack of sleep, and long sessions will kick your ass. Coffee (or other stimulant) is your friend. So is napping through the boring talks. 

4) Don't feel obliged to hang out with your supervisor or lab mates. If they're not being fun, attach yourself to another group. Aside from networking (i.e. making friends) this'll also give you the advantage of hearing what people are really doing, rather than the brief (and sometimes misleading) versions you'll get in talks and posters. Of course, if your prof is a party animal, it is your sworn duty to rescue students who have stick-in-the-mud supervisors. Generally speaking, the larger and rowdier the group, the better. 

5) You can stay longer if you like, depending on if there is anything you want to do outside of the conference. This is an esecially good idea of you're off-contenent. In the case of New Hampshire, show up late and leave early.  There may be other "New Hampshires" out there - be aware. 

6) Some conferences have tours.  Some times they really suck, sometimes they're really 
fun. Best bet - get the details when you arrive and decide from there. You can also often ask the organizers how many students/postdocs are signed up: more = better. If its just profs/spouses, it'll probably blow chunks. 

7) Don't be afraid to ask questions. No matter how dumb you may think the question is, chances are that at least half the audience is as confused as you are.  

8) Don't be shy about tracking down speakers after their talk, if you want more details. Most are quite open to talking (some are hard to shut up). Plus, you have the advantage of getting them to know your face/name; something that may help when you're looking for your next position. 

9) This is the hard part, but let your inner nerd free. Conferences are one of the few places where you can do this, get away with it, and actually end up looking good. 

10) Some people use confernces as a place to hook up. If that's your thing, clean up. If not, beware of the romeos sure to emerge from behind the coke-bottle glasses facade.

The Synopsis

As promised, here is the chapter-by-chapter breakdown of Hovinds "thesis".  Hovind claims to have something like 11 chapters in his thesis, but in reality it has only 4 clearly demarked sections.  Five if you count the dedication page, and six if you assume his last paragraph is a chapter.

Chapter 1: Introduction

• Hovind tells us who he is - he starts by saying 'Hello, my name is Kent Hovind'
• Hovind wants to bring us back to the "true faith"
• Satan is attacking the world

Chapter 2: History of Evolution

• Evolution is a crazy idea
• The laws of physics say it can't happen
• Evolution is a religion
• Small changes are possible, big ones aren't
• Evolutions history starts with the fall of satan
• In ancient Greece evolution was formed (evolution is all science, btw)
• In ancient Greece atheists were formed, and they carried the flame of evolution forward
• Most non-Christian religions are atheistic beliefs
• During the middle ages there were men who were atheists.  They wrote books - evil books.  Many were French.
  
• 20-some pages in we get to Darwin- or at least his father.  His father was an evil, FAT, atheist
• Lamarck, Lyell and Darwin were all evil, immoral atheists.  They made up evolution because they hate god.
• Darwin only gets a 1 paragraph description in this 30-page chapter on the history of evolution!
• Marx invented communism.  He was evil, atheistic evolutionist

 I'd carry on, but you see where this goes.  Every individual who may have been an atheist was also immoral, evil and a promoter of evolution.

Chapter 3: The religion of evolution

• There is no empirical evidence for evolution
• Schools are bad
• Religion has not evolved
• Taking prayer out of school is bad
• Scopes trial was evil
• We should either teach evolution and creationism, or neither
• Websters dictionary says that religions have divine creators, ergo evolution is a religion
• Evolution is the same as humanism, and humanism is a religion therefore evolution is a religion
• Humanist manifesto (a book I've never heard of) outlines evolutions desire to take over the world
• No missing links have ever been found
• Evolution is a religion

Chapter 4: How Old is the Earth

• This is an important question
• God is not limited by time
• What time is it in heaven?
• Scientists have hundreds of ways of measuring the age of the earth
• The methods scientists use are wrong
• The earth is young because of:
• comets
• helium
• the earths spin is slowing down
• the moon is receding
  
• science is silly
  
• I think the earth is about 6,000 years old, therefore it is

"Chapter 5" Conclusions
OK, this is one paragraph.  It reads:

These honest questions deserve honest answers.  I believe we have been lied to about the age of the earth.  Satan, the father of all lies, has come up with this to make a fool of Jesus Christ.  Jesus said in Matthew 19:4 that the creation of Adam and Eve was the beginning.  I believe Jesus was right.

So there you have it, to summarise:

1. Evolution was created by Satan after the fall
2. Evolution is a religion
   
3. Atheists have carried the flame of evolution throughout the ages
4. Atheists are fat, immoral, evil, and most likely French.  If they're not French, they're fucking someone who is.
   
5. The earth isn't old
6. Jesus said...something
7. Creationism wins! YAYYYYYYYYYY!
   

I've read it, so you don't have to

Todays experiment is filled with long periods where I sit on my ass and waste time - AKA incubation periods.  As such I managed to choke down Hovinds thesis in its entirety.  To save ya'll hours of painful reading I've prepared a coles-notes version, and if you want to read further, I've added a few comments of my own.

Later this afternoon I should be able to post a chapter-by-chapter synopsis, for those who care.  But for now...

Hovinds Argument in a Nut Shell:

1. Evolution is a new, evil religion (note: religion, not science)
2. Christianity is an old, not-evil religion and is the sole path to enlightenment

Since evolution is new and evil, while Christianity is old and not-evil, evolution is wrong and creationism is right.

Yep - that's it.  I kid you not.  102 pages, and that's what it boils down to.

My comments
This is not a thesis:
I've written a thesis, and I've read several more.  And while Hovinds document is many things, it is not a thesis.

Thesis are a pretty standardised document intended to inform readers of new knowledge uncovered by the writer.  Almost always they are structured as follows:

1. Introduction that outlines the area of research, what is known, and what unknown areas the thesis is going to delve into
2. Several chapters describing the methods used to find the new information, and what the results of those investigations were.
3. A conclusion which puts the new findings into perspective, and wraps everything up into a nice little package.

Honvids "thesis" does none of the above - his "introduction" tells us that evolution is a religion and evil, he then repeats this same argument over about a dozen chapters, and then he concludes by repeating his introduction.  No new info is introduced - and providing new knowledge is the key purpose of a thesis.  In fact, most of his arguments can be found in the transcripts of the scopes trial, 83 years ago.

This "thesis" is simply traditional creationist arguments condensed into one article.
I don't think this will be a surprise to many, but the entirety of Hovinds "thesis" is simple repetition of creationist arguments going back decades.  Nothing new is added, although Hovind does break up the usual claptrap with piss-poor descriptions of history and character assassinations of various famous (and dead) scientists.

If you've read anything by the "discovery" institute, or any other creationist propaganda machine, you'll have seen everything in Hovinds "thesis" before.


Hovind is frightenly ignorent of basic scientific principals.

In my first post on his thesis I mentioned a few errors Hovind had made in terms of basic scientific principals.  Little did I know that was the tip of the iceberg - in one chapter alone Hovind completely fucked up six separate basic scientific principals or definitions.  I'm not talking slight errors here - I'm talking 100% wrong; completely polar opposite, of what science truly says.

This is particularity terrifying, as in the beginning of his thesis Hovind proudly announces to us that he has been a high school science teacher since 1976.  If that's actually true then he has done irrefutable harm to the education of numerous students over that 30-ish year period.  Seriously - the guy doesn't even have a basic grasp of the laws of thermodynamics.  How the hell can you teach science when you don't even understand one of the most basic principals science has uncovered?

Just goes to prove how stupid they are

Kent Hovinds "PhD" thesis has finally been leaked. For many a year he's touted his PhD (you know, that ol' logical fallacy of argument from authority). But while he's touted his PhD, he's steadfastly refused to allow anyone to read it.

Probably because reading it would:
a) cause your head to explode, and
b) make people realize just how stupid he really is

I'm about half-way through - in less than 30min.  Pretty sad for a thesis; normally these things are much longer, and not written in the language used by a 5-year old child.  The thesis is scanned, so whole-scale quoting is going to be hard.  None-the-less, here's a few gems (any spelling errors are mine):

Hello, my name is kent honvid.  I am a creation/science evangelist.  I live in Pensacola Florida.  I have been a high school science teacher since 1976.

As I said, the guy writes like a child.

Where in the world did the idea come from that things left to themselves can improve with time?  Who would start a crazy idea like that?

Academics try to be impartial, as to ensure their findings are as rational and objective as possible.  Apparently Kent didn't get that memo.

The first law [of thermodynamics] says that matter cannot be created nor destroyed.

Err, no.  The first law of thermodynamics states that the energy of a closed system stays constant.  You can create/destroy all the matter you want; so long as you obey the E=mc² rule.  Oh, and this is his logic behind "there must be a god" - all because the first law says matter cannot be created; ergo, there must be a creator.

Now since the first law allows for matter to be created and destroyed, where does that leave god?

Or, for that matter, if matter cannot be created, what was the creator created from?

 The technical definition of evolution is "change".

Wrong - again.  The accepted scientific definition of evolution is the change in a populations genetic composition over generations.  Lots of evolution (probably most) involves genetic changes that do not result in changes to the organism itself.  Its called genetic drift; maybe you've heard of it?

Much of the rest is a confused, obviously wrong in many places "history" of evolution, obviously wrong "history" of modern religion, and various biblical quotations taken out of context to "prove" his case.

A few more gems:

Evolution is purely a religion
Religion has not evolved (and yet he gives a history of its change!)
We go now the the Humanist Manifesto Two written by Paul Kurtz...

BTW, that last one's not a typo on my part; he actually wrote that - double "the", "two" in the wrong place AND the wrong "to".

His thesis is available from wikileaks.

Hat tip to PZ Myers, over at Pharyngula

We may be godless heatherns, but at least our music doesn't suck

One of my favourite bloggers, the friendly atheist, has come across a real gem of a video.  Its a Christian rap group rapping about "side hugs"; cause hugging normally might give you a boner, and that's a sin.  Its narrated by another atheist - which is by far the best part of the video.

I feel really sorry for the kids subjugated to this kind of crap.  Not only are they having the fairly basic joy of a hug being taken away from them, but they're being brainwashed into thinking that signs of affection are somehow an evil thing.

Not to mention, this music really, really, really sucks!


Compare this to what we atheists have to offer:


and

This seems like a flaw...

So I am now a follower of my own blog - brining my followers upto 3.

Somehow that seems a flaw; I shouldn't need blogger to update me on my own blog...

Detecting Autism at Birth

An occasionally-made claim by the anti-vax movement is that autism cannot possibly be genetic because we don't see it at birth.  Anyone who has a background in developmental biology is rolling their eyes after reading that, but to many it seems a logical argument.

It isn't, because humans are born with an incompletely developed brain, and as such developmental abnormalities can occur after birth.

But that has little to do with this particular claim, as autism can be diagnosed under laboratory conditions at/near birth.  Hence, this claim of the anti-vaxers is yet another of their lies (and boy, do they have a lot of them).

Now one may ask, if autism is detectable at birth, why is it in the real world it isn't detected until 18 months or older?  The reason is pretty simple, and I'm going to use two older papers as examples of why this is the case.  Both are available for FREE at the links below:


Autism detected AT BIRTH, upto 6mo:
PNAS November 10, 1998 vol. 95 no. 23 13982-13987
Aspergers detected in infancy:
PNAS August 10, 2004 vol. 101 no. 32 11909-11914

In both of these papers autism is detected young - from birth to 6mo in the first paper, and aspergers  from 3mo onwards in the second.  The later is particularity interesting, as aspergers is a "mild" form of autism often not detected until the age of 5 or older.

If you look at either of those papers you'll see why autism is not often detected in the very young; to detect autism at these early ages requires hours of analysing the movement of these children.  On the right I have one such example, of a plotting system used to analyse the movement of arms and legs.

In addition to using rigid analysis of movement, both papers also used pre-set criteria to ensure unbiased measurements.  On such example is shown below (on the left) of such a criteria; in particular, the movement pattern of an infant moving from its back to front.

Finally, they looked at facial movements, in particular looking for movements typical of older autistic children.

The conclusion in both papers was clear - the symptoms of autism could be identified in children before six months of age with great reliability.

So why don't clinicians diagnose autism at a younger age?

The answer is simple - the diagnosis of autism at these young ages requires in-depth analysis of hours of video recordings.  Even with modern technology, our ability to automate this kind of analysis is very limited.  Furthermore, even utilising modern motion-capture methods would require specialised (and very expensive) studios and software.  Finally, we'd have to screen each and every child to detect autism, for the simple reason that its unlikely that most parents would recognise the subtle symptoms which occur in infants and seek medical advice.

So contrary to anti-vax claims, autism IS detectable at birth.  Unfortunately, a usable and affordable clinical test is a long ways off - in fact, we'll probably have a genetic test long before we have a motion-based one.

Peer review, why do I bother?

For those of you who know about peer review, you know that the system is broken. But for those of you who aren't in the know, peer review is one of the ways that science journals try to ensure that the studies they publish are properly performed, that the conclusions match the data, and to reduce issues such as fraud.

In theory the process works as follows: You submit your study to a journal, and if it passes the reviewers initial look-over, your study gets sent out to two or three experts in your field who then review your work. They are anonymous (although the authors of the study are not) to protect them from "retribution" if you don't like their review. In theory, the reviewers are supposed to look at the paper, identify any holes, and recommend ways to fix those holes.

Unfortunately, this isn't always what happens. Some reviewers don't put much of an effort into reviewing, so you get half-baked reviews that don't do much to improve the paper but waste a lot of time. Other's will foist off reviews onto untrained grad students or postdocs, and don't vet the review before sending it in. While not always bad, the lack of expertise these individuals have often leads to them concentrating on minutia that is often irrelevant. Other reviewers use the review process as a way to hamper their competitors (whose papers they often receive for review) by recommending unreasonable experiments or even recommending rejection of the paper. And the absolute worst is when you get a real ass hole who thinks you did everything wrong, and demands you rodo every experiment, and rewrite the paper to fit the way they think it should have worked.

To fight this I do my absolute best when reviewing papers, in the vague hope that I may set a good example. I take time to read the paper through - usually several hours, and try to provide reasonable and helpful feedback. In most cases the authors seem to appreciate this and try to address my concerns.

And then there was the last paper I reviewed.

I cannot speak of specifics, due to confidentiality, but the long story short is a group developed a method that is a pretty big advance to one of my fields. Basically, they developed a mass-screening assay for a field that has traditionally used low-throughput methods. As I said, its a big deal - it would have cut my PhD in half, for example. There was one critical problem with their paper though - they didn't actually do the test to confirm that their new readout actually "readsout" what was being measured. To fix that was simple - they had stills from a video already in the paper. All they needed was to do 5min of work and actually analyse that video. I pointed that out, provided a few references in case they didn't know how to do the analysis, and then sent in my review.

In reply, they added the video - without any analysis - to the paper. Or, in other words, they ignored the one recommendation I had, and there is still a gaping hole in their paper.

ARRRRRRRRRRRRRRRRRRRGGGGGGGGGGGGGGGGGGG

So I did the analysis myself - and it turns out their assay works perfectly. It took me a whopping 3min; 2 of which was booting my computer and loading matlab. But this puts me in a real pickle - without that data their paper has a serious flaw, but their method is correct. Normally I'd re-write the editor saying "they need to do this analysis, or reject you need to reject this paper", but since this is a big advance - that works extremely well - I also want to see the paper published ASAP.

Makes me wonder why I bothered putting any effort into the paper. I don't know what I'm going to do yet - but flipping a coin tops the "options list".

Vaccines prevent autism

I'm sure by now most have heard of the latest anti-science trend, the anti-vaccine movement. For those of you who haven't, an MD by the name of Andrew Wakefield was paid off by a legal firm to manufacture data showing that the MMR vaccine causes autism. His "study" (now known to be 100% fraudulent) led to a war on science, pitting snakeoil salesmen and the parents of autistics they scammed against MDs, scientists, and sane people in general.

The end effect of this has been a resurgence of vaccine-preventable diseases, deaths from diseases which just a decade ago were on the verge of extinction, and all kinds of general mayhem. For fairly obvious reasons, scientists and MDs have been working hard to ensure that vaccines are truly safe, and to tell the public the truth.

Today, another nail in Wakefields coffin has been driven in. A scientific study repeated Wakefields original study, using a larger number of people (192 in stead of 12). In addition, they look not just at the MMR vaccine, but also the measles-only vaccine (as Wakefield claimed it was the measles component that caused autism). Their analysis showed something quite interesting. Instead of seeing what Wakefield saw - an assocaition of autism with MMR vaccination, they saw the opposite - MMR and Measles Vaccines are PROTECTIVE against autism.

In brief, the MMR vax reduced the chance of getting autism dramatically (odds ratio of 0.17, 95% CI: 0.06-0.52) and the measles vax reduced the chance of getting autism but not quite as much (odds ratio of 0.44, 95% CI: 0.22-0.91).

I'm sure the anti-vax loons will promptly be telling us this is all part of some conspiracy, but non-the-less, the fact the got such a striking finding using Wakefields own methods pretty much confirms what we all know - Wakefield lied about his results.

One less reason...

I've long been a critic of the whole "organic food" thing. As someone who grew up on farms the whole thing seemed like BS - its well established that the green revolution lead to greater amount of healthy food - how going back to the pre-revolution days could improve that was never clear to me. Over time science has shown my suspicions to be correct - organic food is neither healthier or more environmentally friendly.

Basically, "organic food" is a way of scamming money out of stupid people.

But I have long been a fan of buying locally-produced food. The benefits of this were supposed to be two fold - you help local farms (thus reducing the expansion of so-called "industrial farming") and you were helping the environment by not buying food that had been shipped from half way across the globe.

The first half of that equation is still true - buying local supports local farmers, and helps to keep family farms in business. I have to admit a strong bias here - most of my family remain farmers, and I'd like for them to keep their livelihood.

Unfortunately, the second half of that equation is no longer true (at least not in all cases). In hindsight this was an obvious thing, but rose coloured glasses do tint one's view of the world.

It turns out that it is often more efficient to ship foods from afar than locally, for a few reasons:

1. The assumption that closer food production = lower transportation emissions ignores everything leading upto that local production - shipping of fertilisers, seed, etc. Thus, the footprint of a locally produced food may be the same, or greater, that distantly produced food simply because there isn't a fertiliser company, or seed production firm, near buy.
2. The assumption that closer food production = lower transportation emissions also ignores the efficiency of transport - as much as we like to ignore it, the fact remains that cargo ships and trains have much lower emissions per tonne transported than does a truck or car. In other words, shipping food across a continent to a central distribution centre; and from there to stores, may be more efficient than having hundreds of small trucks transporting local produce to those same markets.
3. Bulk production is often more efficient than small-scale. In plain English, that simply means that a large mega-farm can often produce the same amount of food for less emissions than a smaller farm.

Obviously the equation is a lot more complex than many assume, and whether or not local food is more environmentally friendly is going to vary crop-to-crop and region-to-region. According to the news last night the analysis has now been done for one food - farmed salmon - and the news ins't good for local producers. Turns out, shipping salmon from mega-farms in Asia produces less CO2 than importing equivalent amounts from the smaller farms which are common here in North America. I'm still trying to find the actual paper, but if the news report was correct things do not look good for using local farming as a way to reduce transportation-sourced CO2 .

The genetics of autism and schitzophrenia

Wow, 1.142857143 week & two posts - something must be wrong with me.

Anyone who knows anything, knows that autism is largely - if not entierly - a genetic "disorder". Disorder is in quotes since I think its arguable that some forms of autism represent normal neurovariation, rather than a disease/disorder.

Anyhoo, its also been long known that schizophrenia is also a genetic disorder, and as we've delved into the genetics of both diseases we've found some startling things - notably that many of the genes linked to one disease are also linked to another.

In the early edition of PNAS today (or at least I noticed it today) is a paper that looks at these linkages closely, and finds something very interesting. But before we go into that, lets set the stage:

One of the more common, but least understood, forms of human genetic variation is copy number variations. This simply means that some people will have more copies of a particular gene that others, and some will have less. This can result in biological abnormalities, as some genes need to be present in the right "dose" - too little or too much equals trouble. Many of the genetic variations found in autistics and schizophrenics are these kinds of variations - extra copies, or missing copies of genes.

In this particular paper, Crespi, Stead & Elliot show that autism is schizophrenia's genetic opposite - in cases where schizophrenics have gene duplications, autistics have gene deletions. And the opposite is also true - where autistics have duplications, schizophrenics have deletions.

This is a very interesting finding, as it tells us a lot about what is going in these disoriders. Notably, autism seems to occur when genetic mutations remove the breaks of developmental pathways - autistics seem to have unregulated brain development. Schitzophrenics seem to be the opposite - rather than having out-of-control brain development pathways, they instead have broken brain development pathways.

Of course, the anti-vax loons will ignore this study, and all that in means, inorder to preserve their faith in the non-truth that vaccines cause autism.