Here's an excellent example of what's wrong with the way the ENCODE Consortium is interpreting their data. Congratulations to Michael Eisen! I wish I had said this: A neutral theory of molecular function.1
Read the whole thing very carefully and heed the lesson. Here's a excerpt,
I think a lot about Kimura, the neutral theory, and the salutary effects of clear null models every time I get involved in discussions about the function, or lack thereof, of biochemical events observed in genomics experiments, such as those triggered this week by publications from the ENCODE project.
It is easy to see the parallels between the way people talk about transcribed RNAs, protein-DNA interactions, DNase hypersensitive regions and what not, and the way people talked about sequence changes PK (pre Kimura). While many of the people carrying out RNA-seq, ChIP-seq, CLIP-seq, etc… have been indoctrinated with Kimura at some point in their careers, most seem unable to apply his lesson to their own work. The result is a field suffused with implicit or explicit thinking along the following lines:
I observed A bind to B. A would only have evolved to bind to B if it were doing something useful. Therefore the binding of A to B is “functional”.
One can understand the temptation to think this way. In the textbook view of molecular biology, everything is highly regulated. Genes are transcribed with a purpose. Transcription factors bind to DNA when they are regulating something. Kinases phosphorylate targets to alter their activity or sub-cellular location. And so on. Although there have always been lots of reasons to dismiss this way of thinking, until about a decade ago, this is what the scientific literature looked like. In the day where papers described single genes and single interactions, who would bother to publish a paper about a non-functional interaction they observed?
But experimental genomics blew this world of Mayberry molecular biology wide open. For example, when Mark Biggin and I started to do ChIP-chip experiments in Drosophila embryos, we found that factors were binding not just to their dozen or so non-targets, but the thousands, and in some cases tens of thousands of places across the genome. Having studied my Kimura, I just assumed that the vast majority of these interactions had evolved by chance – a natural, essential, consequence of the neutral fixation of nucleotide changes that happened to create transcription factor binding sites. And so I was shocked that almost everyone I talked to about this data assumed that every one of these binding events was doing something – we just hadn’t figured out what yet.
.....
Rather than assuming – as so many of the ENCODE researchers apparently do – that the millions (or is it billions?) of molecular events they observe are a treasure trove of functional elements waiting to be understood, they should approach each and every one of them with Kimurian skepticism. We should never accept the existence or a molecule or the observation that it interacts with something as prima facia evidence that it is important. Rather we should assume that all such interactions are non-functional until proven otherwise, and develop better, compelling, ways to reject this null hypothesis.
Read the comments, especially the one from former colleague Chris Hogue on how to interpret phosphorylation of proteins and signal transduction. That's not going to be popular in my department!
I just have one small quibble with Michael's post. Not all textbooks describe the cell as if it were a finely tuned Swiss watch and not all textbooks take an adaptationist approach to evolution. Mine doesn't.
1. As a result of this post I've now relegated Jonathan Eisen to "brother of Michael Eisen" rather than the other way around. Sorry, Jonathan.
The Nature issue containing the latest ENCODE Consortium papers also has a New & Views article called "Genomics: ENCODE explained" (Ecker et al., 2012). Some of these scientist comment on junk DNA.
For exampleshere's what Joseph Ecker says,
One of the more remarkable findings described in the consortium's 'entrée' paper is that 80% of the genome contains elements linked to biochemical functions, dispatching the widely held view that the human genome is mostly 'junk DNA'. The authors report that the space between genes is filled with enhancers (regulatory DNA elements), promoters (the sites at which DNA's transcription into RNA is initiated) and numerous previously overlooked regions that encode RNA transcripts that are not translated into proteins but might have regulatory roles.
And here's what Inês Barroso, says,
The vast majority of the human genome does not code for proteins and, until now, did not seem to contain defined gene-regulatory elements. Why evolution would maintain large amounts of 'useless' DNA had remained a mystery, and seemed wasteful. It turns out, however, that there are good reasons to keep this DNA. Results from the ENCODE project show that most of these stretches of DNA harbour regions that bind proteins and RNA molecules, bringing these into positions from which they cooperate with each other to regulate the function and level of expression of protein-coding genes. In addition, it seems that widespread transcription from non-coding DNA potentially acts as a reservoir for the creation of new functional molecules, such as regulatory RNAs.
If this were an undergraduate course I would ask for a show of hands in response to the question, "How many of you thought that there did not seem to be "defined gene-regulatory elements" in noncoding DNA?"
I would also ask, "How many of you have no idea how evolution could retain "useless" DNA in our genome?" Undergraduates who don't understand evolution should not graduate in a biological science program. It's too bad we don't have similar restrictions on senor scientists who write News & Views articles for Nature.
Jonathan Pritchard and Yoav Gilad write,
One of the great challenges in evolutionary biology is to understand how differences in DNA sequence between species determine differences in their phenotypes. Evolutionary change may occur both through changes in protein-coding sequences and through sequence changes that alter gene regulation.
There is growing recognition of the importance of this regulatory evolution, on the basis of numerous specific examples as well as on theoretical grounds. It has been argued that potentially adaptive changes to protein-coding sequences may often be prevented by natural selection because, even if they are beneficial in one cell type or tissue, they may be detrimental elsewhere in the organism. By contrast, because gene-regulatory sequences are frequently associated with temporally and spatially specific gene-expression patterns, changes in these regions may modify the function of only certain cell types at specific times, making it more likely that they will confer an evolutionary advantage.
However, until now there has been little information about which genomic regions have regulatory activity. The ENCODE project has provided a first draft of a 'parts list' of these regulatory elements, in a wide range of cell types, and moves us considerably closer to one of the key goals of genomics: understanding the functional roles (if any) of every position in the human genome.
The problem here is the hype. While it's true that the ENCODE project has produced massive amounts of data on transcription binding sites etc., it's a bit of an exaggeration to say that "until now there has been little information about which genomic regions have regulatory activity." Twenty-five years ago, my lab published some pretty precise information about the parts of the genome regulating activity of a mouse hsp70 gene. There have been thousands of other papers on the the subject of gene regulatory sequences since then. I think we actually have a pretty good understanding of gene regulation in eukaryotes. It's a model that seems to work well for most genes.
The real challenge from the ENCODE Consortium is that they question that understanding. They are proposing that huge amounts of the genome are devoted to fine-tuning the expression of most genes in a vast network of binding sites and small RNAs. That's not the picture we have developed over the past four decades. If true, it would not only mean that a lot less DNA is junk but it would also mean that the regulation of gene expression is fundamentally different than it is in E. coli.
[Image Credit: ScienceDaily: In Massive Genome Analysis ENCODE Data Suggests 'Gene' Redefinition.
Ecker, J.R., Bickmore, W.A., Barroso, I., Pritchard, J.K. (2012) Genomics: ENCODE explained. Nature 489:52-55. [doi:10.1038/489052a]
Yoav Gilad
& Eran Segal
The latest version of the Carnival of Evolution pointed to an article by Steven Quistad on Small Things Considered. The article reviewed a recent paper on endogenous retroviruses [The Rise of Genomic Superspreaders].
Retroviruses are RNA viruses that go though a stage where their RNA genomes are copied into DNA by reverse transcriptase. The virus may integrate into the host genome and be carried along for many generations producing low levels of virus particles [Retrotransposons/Endogenous Retroviruses ]. Most of these events will occur in somatic cells so the integrated virus is not passed along to progeny but from time to time the virus integrates into germ line DNA and this is heritable.
There are 31 such events in our lineage, meaning that we have copies of 31 different retroviruses in our genome. The retroviruses may have produced copies in germ line DNA such that each of the 31 retroviruses is now represented by a family of sequences scattered throughout the genome. Today, these retrovirus sequences represent a total of 8% of our genome! That's over 200,000,000 base pairs of DNA. There are about 100 thousand different sites.1
There's no selective pressure to maintaining the functionality of these retrovirus sequences so, as you might have guessed, most of them have accumulated mutations over millions of years. (The original insertion events took place at various times ranging from 100 million years ago to only a few million years ago.) Almost all of the 8% consists of defective retrovirus sequences. It's junk.2
But it's a special kind of junk because retrovirus DNA has strong promoters that bind various transcription factors and the flanking enhancers ensure that the region around these promoters will be in open chromatin regions that have all the characteristics of real promoter sites. A substantial proportion of the defective retroviruses will still produce transcripts because the promoter region may not be mutated even though there may be lethal mutations elsewhere in the sequence.
What does this mean? It means that there will be thousands of junk DNA sites that bind transcription factors and RNA polymerase and may even be transcribed. When you're doing whole genome analyses, like those in the ENCODE study, you need to be careful to distinguish between functional promoters and non-functional promoters.
1. The typical retrovirus genome is about 3,000 bp in length but many of the defective retrotransposon sequences have been are truncated by deletions.
2. Except for an extremely small number that might have acquired a secondary function such as enhancing expression of a nearby gene.
This month's Carnival of Evolution is hosted by The Stochastic Scientist, Kathy Orlinsky. Read it at: Carnival of Evolution 51: Darwin's Restaurant
Welcome to the 51st Carnival of Evolution, henceforth known as Darwin’s Restaurant. You may have noticed that the motto of my blog is ‘Science—there’s something for everyone.’ Well, that’s also true of evolution. Whether your passion is transitional fossils or reducible complexity, you’ll find something tasty on this menu.
There's some cool stuff this month.
The next Carnival of Evolution (September) will be hosted by The Genealogical World of Phyogenetic Networks. If you want to volunteer to host others, contact Bjørn Østman. Bjørn is always looking for someone to host the Carnival of Evolution. He would prefer someone who has not hosted before. Contact him at the Carnival of Evolution blog. You can send articles directly to him or you can submit your articles at Carnival of Evolution.
CFI is sponsoring a conference in Ottawa (Ontario, Canada) on "Celebrating Reason at the End of the World." The title of the conference is Eschaton 2012. Go to the website to find out what "eschaton" means and how to pronounce it.
The meetings will take place from Friday Nov. 30 to Sunday Dec. 2 at a hotel in downtown Ottawa. The list of prominent speakers includes ...
- PZ Myers (Biologist and author of the Pharyngula Blog)
- Eugenie Scott (Executive Director of National Center for Science Education)
- Ophelia Benson (Columnist for Free Inquiry magazine and author of Butterflies and Wheels Blog)
- Christopher DiCarlo (Philosopher of Science and author of How to Become a Really Good Pain in the Ass
There's a whole bunch of less prominent speakers as well. My talk will be on Saturday morning. It's titled "Scientists vs IDiots."
Later on I'll be on a panel about science education with PZ Myers and Eugenie Scott. This should be lots of fun.
See you there! We'll eat poutine and beaver tails.
Jonathan McLatchie must have hardly been able to contain himself when he wrote: Latest ENCODE Research Validates ID Predictions On Non-Coding Repertoire.
Readers will likely recall the ENCODE project, published in a series of papers in 2007, in which (among other interesting findings) it was discovered that, even though the vast majority of our DNA does not code for proteins, the human genome is nonetheless pervasively transcribed into mRNA. The science media and blogosphere is now abuzz with the latest published research from the ENCODE project, the most recent blow to the “junk DNA” paradigm. Since the majority of the genome being non-functional (as has been claimed by many, including notably Larry Moran, P.Z. Myers, Nick Matzke, Jerry Coyne, Kenneth Miller and Richard Dawkins) would be surprising given the hypothesis of design, ID proponents have long predicted that function will be identified for much of our DNA that was once considered to be useless. In a spectacular vindication of this hypothesis, six papers have been released in Nature, in addition to a further 24 papers in Genome Research and Genome Biology, plus six review articles in The Journal of Biological Chemistry.
...
This new research places a dagger through the heart of the junk DNA paradigm, and should give adherents to this out-dated assumption yet further cause for caution before they write off DNA, for which function has yet to be identified, as “junk".
Not much I can say right now. I'm up to my ears trying to convince sane people that the ENCODE papers are wrong. The IDiots are just going to have to wait.
The Smithsonian Museums are highly respected but that doesn't mean their website is scientifically accurate [Junk DNA Isn’t Junk, and That Isn’t Really News].
Remember in high school or college, when you learned about all that DNA inside of you that was junk? The strings and strings of nonsense code that had no function? A recent blitz of papers from the ENCODE project have the world abuzz with news that would rip that idea apart.
But, like many things that stick around in text books long after science has moved on, the “junk DNA” idea that ENCODE disproved, didn’t really need disproving in the first place. Even in 1972, scientists recognized that just because we didn’t know what certain DNA regions did, didn’t make them junk.
This is getting very depressing.
A few hours ago I criticized science journalists for getting suckered by the hype surrounding the publication of 30 papers from the ENCODE Consortium on the function of the human genome [The ENCODE Data Dump and the Responsibility of Science Journalists].
They got their information from supposedly reputable scientists but that's not an excuse. It is the duty and responsibility of science journalists to be skeptical of what scientists say about their own work. In this particular case, the scientists are saying the same things that were thoroughly criticized in 2007 when the preliminary results were published.
I'm not letting the science journalists off the hook but I reserve my harshest criticism for the scientists, especially Ewan Birney who is the lead analysis coordinator for the project and who has taken on the role as spokesperson for the consortium. Unless other members of the consortium speak out, I'll assume they agree with Ewan Birney. They bear the same responsibility for what has happened.
I've been trying to keep up with the ENCODE PR fiasco so I immediately click on a link to Michael Eisen's blog with the provocative title it is NOT junk. The article is: This 100,000 word post on the ENCODE media bonanza will cure cancer.
Michael Eisen is an evolutionary biologist at the University of California at Berkeley. He's best known, to me, as the brother of Jonathan Eisen. 
Michael, like me and hundreds of other scientists, is upset by the ENCODE press releases. One of them is: Fast forward for biomedical research: ENCODE scraps the junk.
The hundreds of researchers working on the ENCODE project have revealed that much of what has been called 'junk DNA' in the human genome is actually a massive control panel with millions of switches regulating the activity of our genes. Without these switches, genes would not work – and mutations in these regions might lead to human disease. The new information delivered by ENCODE is so comprehensive and complex that it has given rise to a new publishing model in which electronic documents and datasets are interconnected.
Here's the interesting thing. Many of us are upset about the press releases and the PR because we don't think the ENCODE data disproves junk DNA. Michael Eisen's perspective is entirely different. He's upset because, according to him, junk DNA was discredited years ago.
The problems start before the first line ends. As the authors undoubtedly know, nobody actually thinks that non-coding DNA is ‘junk’ any more. It’s an idea that pretty much only appears in the popular press, and then only when someone announces that they have debunked it. Which is fairly often. And has been for at least the past decade. So it is more than just intellectually lazy to start the story of ENCODE this way. It is dishonest – nobody can credibly claim this to be a finding of ENCODE. Indeed it was a clear sense of the importance of non-coding DNA that led to the ENCODE project in the first place. And yet, each of the dozens of news stories I read on this topic parroted this absurd talking point – falsely crediting ENCODE with overturning an idea that didn’t need to be overturned.
Eisen is wrong, junk DNA is alive and well. In fact almost 90% of our genome is junk.
This is what makes science so much fun.
ENCODE (ENcyclopedia Of DNA Elements) is a massive consortium of scientists dedicated to finding out what's in the human genome.
They published the results of a pilot study back in July 2007 (ENCODE, 2007) in which they analyzed a specific 1% of the human genome. That result suggested that much of our genome is transcribed at some time or another or in some cell type (pervasive transcription). The consortium also showed that the genome was littered with DNA binding sites that were frequently occupied by DNA binding proteins.
THEME
Genomes & Junk DNAAll of this suggested strongly that most of our genome has a function. However, in the actual paper the group was careful not to draw any firm conclusions.
... we also uncovered some surprises that challenge the current dogma on biological mechanisms. The generation of numerous intercalated transcripts spanning the majority of the genome has been repeatedly suggested, but this phenomenon has been met with mixed opinions about the biological importance of these transcripts. Our analyses of numerous orthogonal data sets firmly establish the presence of these transcripts, and thus the simple view of the genome as having a defined set of isolated loci transcribed independently does not seem to be accurate. Perhaps the genome encodes a network of transcripts, many of which are linked to protein-coding transcripts and to the majority of which we cannot (yet) assign a biological role. Our perspective of transcription and genes may have to evolve and also poses some interesting mechanistic questions. For example, how are splicing signals coordinated and used when there are so many overlapping primary transcripts? Similarly, to what extent does this reflect neutral turnover of reproducible transcripts with no biological role?
This didn't stop the hype. The results were widely interpreted as proof that most of our genome has a function and the result featured prominently in the creationist literature.
Ed Yong is a science journalist and usually he's a very good one. This time, however, he should have gotten the other side of the story.
Ed interviewed Ewan Birney for a story on the function of sequences in the human genome [ENCODE: the rough guide to the human genome].
According to ENCODE’s analysis, 80 percent of the genome has a “biochemical function”. More on exactly what this means later, but the key point is: It’s not “junk”. Scientists have long recognised that some non-coding DNA probably has a function, and many solid examples have recently come to light. But, many maintained that much of these sequences were, indeed, junk. ENCODE says otherwise. “Almost every nucleotide is associated with a function of some sort or another, and we now know where they are, what binds to them, what their associations are, and more,” says Tom Gingeras, one of the study’s many senior scientists.
And what’s in the remaining 20 percent? Possibly not junk either, according to Ewan Birney, the project’s Lead Analysis Coordinator and self-described “cat-herder-in-chief”. He explains that ENCODE only (!) looked at 147 types of cells, and the human body has a few thousand. A given part of the genome might control a gene in one cell type, but not others. If every cell is included, functions may emerge for the phantom proportion. “It’s likely that 80 percent will go to 100 percent,” says Birney. “We don’t really have any large chunks of redundant DNA. This metaphor of junk isn’t that useful.”
The creationists are going to love this.
You blew it Ed Yong. Why didn't you ask him about the 50% of our genome containing DEFECTIVE transposons and the 2% that's pseudogenes, just for starters? Then you could ask him why he believes that all intron sequences (about 20% of our genome) are functional [What's in Your Genome?].
"Almost every nucleotide ..."? Gimme a break. Don't these guys read the scientific literature?
This is going to make my life very complicated.
I thought that people like Chuck Norris were big fans of the idea that America is the greatest country in the world. Apparently I was wrong.
This is an appeal to evangelicals to prevent the triumph of evil and 1,000 years of darkness.
[Hat Tip: Friendly Atheist]
Methodological Naturalism is an a priori argument in favor limiting science to investigations of the natural world. It serves to protect religion from science since most religious questions are concerned with the supernatural and science, by fiat, isn’t allowed to ask those questions. Coincidentally, it also protects philosophy from science since metaphysical questions now become the exclusive domain of philosophy.
There are some philosophers who see through this house of cards but they are few and far between. It’s mostly scientists—and those who think like scientists—who say "What the heck are they talking about?"
Maarten Boudry, Stefaan Blancke, and Johan Braeckman from the Department of Philosphy at the University of Gent (Belgium) represent the heretics and dissenters among philosophers. If you want a summary of posts on this topic go to: Is Science Restricted to Methodologial Naturalism?. Here’s an excerpt from Grist to the Mill of Anti-evolutionism: The Failed Strategy of Ruling the Supernatural Out of Science by Philosophical Fiat (Boudry et al. 2012).
I began this discussion a few days ago by questioning the purpose of some common philosophical arguments. The example I selected concerned the claim that evolution is unguided. A prominent philosopher, Elliott Sober, tells us that even though there’s no evidence that evolution is guided it is still possible to imagine a supernatural being who could control evolution by tweaking molecules at the level of quantum mechanics. If this being was clever enough, and wanted to leave no trace of his activity, then one could imagine a situation where evolution was guided without anyone realizing it. Thus, theistic evolutionists need not despair because the scientific way of knowing can’t legitimately say that evolution is unguided.
I used the analogy of The Flying Spaghetti Monster Steals Meatballs to poke fun at this spurious way of reasoning.
Last week's molecule was raltitrexid, an anti-cancer drug [Monday's Molecule #183]. The winner was Raul A. Félix de Sousa. Raul has won ten times since I restarted Monday's Molecule last November.
This week's molecule is another strange-looking molecule with a very specific purpose. Identify the molecule and its role in mammals.
Post your answers as a comment. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)
Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)
In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.
Winners will have to contact me by email to arrange a lunch date. Please try and beat the regular winners. Most of them live far away and I'll never get to take them to lunch. This makes me sad.
Comments are invisible for 24 hours. Comments are now open.
UPDATE: The molecule is warfarin or Coumadin®, a rat poison and an anticoagulant. It's a competitive inhibitor of vitamin K reductase and this blocks blood clotting. The winner is Matt McFarlane, one of the few people who can actually collect a free lunch. Please contact me by email.
Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 9: no winner
April 16: Raul A. Félix de Sousa
April 23: Dima Klenchin, Deena Allan
April 30: Sean Ridout
May 7: Matt McFarlane
May 14: no winner
May 21: no winner
May 29: Mike Hamilton, Dmitri Tchigvintsev
June 4: Bill Chaney, Matt McFarlane
June 18: Raul A. Félix de Sousa
June 25: Raul A. Félix de Sousa
July 2: Raul A. Félix de Sousa
July 16: Sean Ridout, William Grecia
July 23: Raul A. Félix de Sousa
July 30: Bill Chaney and Raul A. Félix de Sousa
Aug. 7: Raul A. Félix de Sousa
Aug. 13: Matt McFarlane
Aug. 20: Stephen Spiro
Aug. 27: Raul A. Félix de Sousa
Sept. 3: Matt McFarlane
I try really hard not to ban anyone from commenting on Sandwalk but there are some things I will not tolerate.
Someone named David Roemer recently tested the limits of my patience, and failed. He is now banned.
Here's what happened. I received an email message from David Roemer about a comment of his that did not appear on Sandwalk. I don't know why it didn't appear. I don't remember seeing it.
Shortly after receiving the email message I received a copy of a message David Roemer sent to the chair of my department. Here's the beginning ...
Dear Dr. XXX,
Prof. Moran, I believe, didn't approve of the following comment I made on his Sandwalk blog. He has every right to do so, but he has a moral duty not to coverup the misinformation contained in the AJP article I mention in my censored comment:
Natural selection only explains the adaptation of species to the environment. Not enough is known about the innovations natural selection acts upon to understand how mammals evolved from bacteria in only 3.5 billion years (common descent). The only theory that attempts to explain common descent is ID, but there is no evidence for ID.
IDiots try to make their theory look better by comparing it with natural selection. Atheists go along with this scam because they don’t want to admit that ID is a better theory than natural selection in some sense.
A corollary of the limitations of natural selection is that the second law of thermodynamics doesn’t apply to evolution, just as it doesn’t apply to the evolution of stars. Nevertheless, there is scientific literature about whether evolution violates the second law. Authors on the “does not” side argue that heat energy from the sun accounts for the increase in order (decrease in entropy). Heat, of course, tends to increase disorder.
This nonsense reached an extreme level in an article published by the American Journal of Physics (Entropy and evolution, Nov. 2008). This article actually calculates the entropy of the biosphere using the Boltzmann constant and an estimate of the thermodynamic probability of life. I’m trying to get the AJP to retract this absurd article.
I'm copying David Novak because he is on the Institute Board of First Things, which is refusing to publish my attached essay explaining why the AJP article is absurd. Both Novak and Moran are helping the AJP lie about evolution and thermodynamics.
My chair will be amused by this sort of thing. There's nothing he could do about it even if he wanted to.
This is one of the criteria for banning. Anyone who tries to get someone fired or reprimanded by going over their head to their employer will be banned. Anyone who harasses the family and friends of someone they disagree with will be banned. There are no exceptions.
I've also banned John Kwok for doing the same thing in an attempt to silence Jim Shapiro.
John starts his defense by explaining the correct use of "begging the question." I agree with him 100%. I hate it when people misuse this phrase by thinking it means "prompts me to ask the question."
He then goes on to give an example ... [Begging questions about philosophy, science and everything else]
But we expect better of the educated and cosmopolitan. It comes, therefore, as a continuing pain to me that scientists will often offer this piece of question beggary:
- Science finds out things
- Philosophy does not find out things the scientific way
- Therefore philosophy is a waste of time and effort
The begged premise here is that only knowing things the scientific way is knowledge, or if the philosopher in question doesn’t say that knowledge is what philosophy offers, that only knowing things the scientific way is worthwhile. Some may even hint that only science delivers beauty, too.
It pains me to read this because I expect so much better of an educated and cosmopolitan Australian.
I'm not aware of any scientist who argues like this.
There was a time, not so long ago, when science and philosophy coexisted in (relative) peace and harmony. This began to change when science came under increasing attack from religion and from others who simply denied the knowledge that had been produced by the scientific way of thinking. (The latter group included advocates of parapsychology. The modern versions include those who deny climate change and those who think vaccinations cause autism. These groups are not necessarily religious.)
The rise of anti-scientism provoked a response from scientists, just as you might expect. Scientists began to speak out against the irrational claims of these science deniers. The counter-attack necessarily covered many people with strong religious beliefs. Gradually, many scientists came to the realization that the main problem was not the specifics of evolution or whether ESP could be tested. The real battleground was a war between rationalism and superstition. This led to a number of scientists coming out in support of atheism and focusing their attention on the flaws in religious thinking (i.e. superstition).
Now, you would think that philosophy would be a natural ally in this fight since the most important feature of philosophy is its ability to distinguish logical arguments from ones that are illogical. In other words, philosophy should be on the side of rationalism and not on the side of superstition.
I been watching proceedings at the Republican National Convention in Florida. If you think it's annoying for most liberal Americans, imagine what it's like for us furriners!
Coincidentally, we watched the last episode of The Newsroom a few days ago then decided to re-watch all ten episodes. It's one of the best shows on television. Makes me sad that The West Wing was cancelled. It's not a show that Republicans will enjoy.
Here's the clip from the first episode that sets the tone for a new kind of TV news show. The hero, Will McAvoy, is a cable news anchor who wants to tell it like it is instead of chasing ratings. The excerpt is from a town hall meeting at Northwestern University. A student has just asked why America is the greatest country in the world. (The student shows up again in Episode #10 when she wants to become a "greater fool.")
The short video by Bill Nye ("The Science Guy") attracted a lot of attention [Bill Nye: Creationism Is Not Appropriate For Children ].
Not to be outdone, Ken Ham and the Creation Museum have taped a response ...
We are [responding to Nye] today with a video rebuttal featuring our “science guys” — Dr. David Menton and Dr. Georgia Purdom of our AiG and Creation Museum staff. These two PhD scientists were asked to reply to Mr. Nye, whose academic credentials do not come close to Drs. Menton and Purdom.
I present this for your amusement. I feel a bit sorry for Georgia Purdom since there's a high probability that some of her grandchildren are going to reject creationism. I wonder how she'll deal with that?
Tim Radford reviews The Selfish Gene by Richard Dawkins [The Selfish Gene by Richard Dawkins – book review]. The review is a bit late—the book was published in 1976—but I suppose the old adage of "better late than never" applies.
Actually it's not as bizarre as you might think. Lot's of people don't understand the ideas that Dawkins was pushing. He was mostly pointing out that evolution is a phenomenon that takes places at the level of genes and populations. Dawkins tweets that Rafford "gets it" in his review.
Lovely retrospective review of The Selfish Gene by Tim Radford, the Guardian's distinguished science writer. He gets it.
Jerry Coyne and I have been thinking along the same lines. We've been reading a lot of books by philosophers and reading their articles and blogs. We're exploring the idea that philosophy and science are different ways of knowing, as the philosophers want us to believe. We've taken to heart the criticism from our philosopher friends that scientists have to understand more about philosophy.
Jerry and I (and many others) have reached the tentative conclusion that much of what passes for modern philosophy is a house of cards. It doesn't tell us anything. It doesn't produce knowledge, or truth.
A few years ago my university (University of Toronto) decided to take a look at student evaluations. A committee was formed and this was its terms of reference.
In recognition of the need to periodically revisit practices related to the evaluation of teaching, the Course Evaluation Working Group was formed in the Fall 2009 (Appendix B) and was asked to:
- Review current course evaluation practices across the University of Toronto and at peer institutions;
- Review current research on course evaluation policies and practices;
- If necessary, make recommendations to improve existing policies and practices.
This sounds like a good idea. As you know, I am very skeptical about student evaluations [On the Significance of Student Evaluations]. It's abut time that universities took a long hard look at the process with a view to abolishing student evaluations or drastically revising them and reviewing their importance in promotion and tenure decisions. It's even more important to revise the policy on using student evaluations to judge the effectiveness of part-time lecturers and teaching assistants. At the very least, their role in determining teaching awards should be critically examined.
If I were in charge of this project I would pick a committee composed almost entirely of the following groups:
- front-line lecturers in introductory classes, including tenured faculty, untenured faculty, full-time lecturers, and part-time lecturers
- teaching assistants (graduate students)
- undergraduates
There would have to be substantial representation from undergraduates since they feel strongly about the issue and any drastic changes would require their consent and cooperation.
I would avoid having any administrators on the committee since the purpose of the committee was to evaluate existing university policy. In general, administrators are reluctant to make radical changes and they have trouble thinking outside the box. Furthermore, most of them don't have time to think seriously about the issue.
Administrators think differently than I do. Here's how they constructed the committee (see Course Evaluation Working Group.
- Edith Hillan (Vice-Provost, Faculty and Academic Life; Co-Chair)
- Jill Matus (Vice-Provost, Students; Co-Chair)
- Grant Allen (Vice-Dean, Undergraduate, Faculty of Applied Science and Engineering)
- Gage Averill (Dean and Vice-Principal, Academic, UTM)
- Cleo Boyd (Director, Robert Gilliespie Academic Skills Centre, UTM)
- Corey Goldman (Associate Chair [Undergraduate], Department of Ecology & Evolutionary Biology, Faculty of Arts & Science)
- Pam Gravestock (Associate Director, Centre for Teaching Support & Innovation)
- Emily Greenleaf (Faculty Liaison & Research Associate, Centre for Teaching Support & Innovation)
- Jodi Herold-McIlroy (Wilson Centre, Faculty of Medicine)
- Glen Jones (Associate Dean, Academic, OISE) Helen Lasthiotakis (Director of Academic Programs and Policy)
- Marden Paul (Director, Planning, Governance & Assessment)
- Cheryl Regehr (Vice-Provost, Academic Programs)
- Carol Rolheiser (Director, Centre for Teaching Support & Innovation)
- Jay Rosenfield (Vice-Dean, Undergraduate Medical Education, Faculty of Medicine)
- John Scherk (Vice-Dean, UTSC)
- Elizabeth Smyth (Vice-Dean, Programs, School of Graduate Studies)
- Suzanne Stevenson (Vice-Dean, Teaching & Learning, Faculty of Arts & Science)
No students. No teaching assistants. No part-time lecturers. Very few people who are currently teaching large undergraduate courses. Almost every person has an administrative positions of some sort—most of the positions take up a considerable portion of their time and some of them are full-time jobs.
That's what thinking like an administrator looks like.
I don't think my university is unusual. We have thousands of very smart students and teachers but all the important committees seem to be composed of people with heavy administrative responsibilities. Does anyone understand the logic here?
Maybe it's just my imagination, but I think I detect a change on Evolution News & View and on Uncommon Descent. For years these blogs have been attacking evolution without paying the least attention to what their opponents are saying. Lately, however, there seem to be some authors who are actually listening to their opponents and trying to address the main criticisms of the IDiot position.
Sometimes you even see articles that are close to being scientifically correct and I've even seen articles that recognize the existence of modern evolutionary theory (i.e. not Darwinism).
The good articles are still quite rare but I'm encouraged by the fact that they are listening.
The latest contribution is by Stephen A. Batzer, a contributor to Evolution News & Views since May 10, 2012. Batzer has a Ph.D. in Mechanical Engineering (see The Salem Conjecture). He's responding to an earlier post of mine where I attempted to explain to Casey Luskin why he was wrong about evolutionary theory [Is "Unguided" Part of Modern Evolutionary Theory?]. Recall that Luskin was saying that the "unguided" nature of evolution was a core part of the theory of Darwinian evolution.
The Flying Spaghetti Monster is all-powerful and all-knowing and she loves meatballs. She is also very sneaky and doesn't want to leave any evidence of her existence. That's why she's very careful to only steal meatballs that won't be missed. (How often do you count the meatballs in your spaghetti?).
As far as I know this is a perfectly valid philosophical argument. If you accept the premises then it's quite possible that meatballs are disappearing from kitchens and restaurants without us ever being aware of the problem.
I'm not a philosopher but I strongly suspect that there aren't any papers on the possible existence of the Flying Spaghetti Monster in the philosophical literature. I doubt that there are any Ph.D. theses on the topic.
Last week's molecule was a small protein machine that pumps protons across a membrane (ubiquinol:cytochrome c oxidoreductase) [Monday's Molecule #182]. The winner was Stephen Spiro. I think he's a student at the University of Toronto (UT) but it's a campus I haven't heard of in a place called "Dallas."
This week's molecule is a lot less complicated although it's rather strange looking. This molecule has a very specific use. Name the molecule—the common name will do—and describe its use.
Post your answers as a comment. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)
Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)
In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.
Winners will have to contact me by email to arrange a lunch date. Please try and beat the regular winners. Most of them live far away and I'll never get to take them to lunch. This makes me sad.
Comments are invisible for 24 hours. Comments are now open.
UPDATE: The molecule is raltitrexed, also known as Tomudex. It's an inhibitor of the enzyme thymidylate synthase, the enzyme responsible for converting dUMP to dTMP. The drug is effective as an anti-cancer agent since it prevents cell division by blocking DNA synthesis. The winner is Raul A. Félix de Sousa (again).
Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 9: no winner
April 16: Raul A. Félix de Sousa
April 23: Dima Klenchin, Deena Allan
April 30: Sean Ridout
May 7: Matt McFarlane
May 14: no winner
May 21: no winner
May 29: Mike Hamilton, Dmitri Tchigvintsev
June 4: Bill Chaney, Matt McFarlane
June 18: Raul A. Félix de Sousa
June 25: Raul A. Félix de Sousa
July 2: Raul A. Félix de Sousa
July 16: Sean Ridout, William Grecia
July 23: Raul A. Félix de Sousa
July 30: Bill Chaney and Raul A. Félix de Sousa
Aug. 7: Raul A. Félix de Sousa
Aug. 13: Matt McFarlane
Aug. 20: Stephen Spiro
Aug. 27: Raul A. Félix de Sousa
Lots of people are having their genomes sequenced or otherwise analyzed for specific alleles. Those people should get all the information that comes out of the analyses although, hopefully, it will be scientifically correct information and any medical relevance will be explained by experts.1
There's another group of people who submit their genomes for research purposes only and they usually sign consent forms indicating that their name will not be associated with the results. Under those circumstances, the researchers should never have access to the individual's name or any circumstances that are not relevant to the study.
Apparently that simple ethical rule is not always standard practice. Gina Kolatea writes about some ethical issues in the New York Times: Genes Now Tell Doctors Secrets They Can’t Utter.
Here's an example from her article ...
One of the first cases came a decade ago, just as the new age of genetics was beginning. A young woman with a strong family history of breast and ovarian cancer enrolled in a study trying to find cancer genes that, when mutated, greatly increase the risk of breast cancer. But the woman, terrified by her family history, also intended to have her breasts removed prophylactically.
Her consent form said she would not be contacted by the researchers. Consent forms are typically written this way because the purpose of such studies is not to provide medical care but to gain new insights. The researchers are not the patients’ doctors.
But in this case, the researchers happened to know about the woman’s plan, and they also knew that their study indicated that she did not have her family’s breast cancer gene. They were horrified.
This is a rather simple case of the researchers violating a standard protocol. They should not have known the identity of the patient and they should not have known what she intended to do.
Most of the "ethical problems" in the article are of this type. They involve researchers who are supposed to be concentrating on research and not on the treatment of individual patients. Those researchers have no idea whether the patients already know which alleles they carry or whether they are already undergoing medical treatment. That's just as it should be. If a DNA donor doesn't want to be contacted then it's ethically wrong for the researchers to violate that contract no matter how justified they think they are being. Furthermore, it should be impossible for them to find out the name and address of the donor so the issue should never come up.
John Hawks thinks this is an interesting ethical problem and he wants his students to discuss it in his classes [Grasping the genomic palantir].
That case is ethically straightforward compared to others, because the researchers could make a difference to an immediate medical decision. On the other hand, how many risk-free research participants went ahead with prophylactic mastectomies because researchers didn't know about their plans?
I think the article will be a good one for prompting student discussions in my courses, and I'll likely assign it widely. But I think the central ethical problem discussed in the article is temporary.
What will students learn from discussing issues like these? What controls are in place to make sure that students are informed about all the ethical issues? Will they be told that standard scientific protocols were violated once the researchers knew what the patient intended to do?
1. "Experts" do NOT include employees of any for-profit company that took money for sequencing the genome.
Jeff Mahr is trying to teach his students how to think critically so he asked them a question about a graph. Check it out to see if you would pass his course: Clearly Critical Thinking?.
There's an interview with Tomoko Ohta in the August 21, 2012 issue of Current Biology: Tomoko Ohta.
You should know who she is but in case you don't, here's part of the brief bio ...
In 1973, she presented her first major paper entitled ‘Slightly deleterious mutant substitutions in evolution’. This theory was an expansion of Kimura's ‘neutral theory’, which Ohta called the ‘nearly neutral theory’ of molecular evolution. Her theory emphasizes the importance of interaction of drift and weak selection, and hence the role of slightly deleterious mutations in molecular evolution. With the accumulation of genome data, some of the predictions of the nearly neutral theory have been verified. The theory also provides a mechanism for the evolution of complex systems. Her other subject is to clarify the mechanisms of evolution and variation of multigene families. She has received several honors, including the foreign membership of the National Academy of Sciences, USA and Person of Cultural Merit, Japan.
It's very important to understand the essence of Nearly Neutral Theory since it explains the relationship between fitness and population size. Everyone needs to understand that Ohta demonstrated how slightly deleterious alleles can be fixed in a population. Her work showed that an allele can become effectively neutral in small populations even though it may actually lower the fitness of an individual. It's a way of explaining the limits of natural selection and of extending the Neutral Theory of Kimura.
She describes what happened when she joined Kimura's group at Tokyo.
At that time, Kimura was thinking of combining the theory of stochastic population genetics, the field he had been working on, with biochemical data on the nature of the genetic material. He proposed his now famous ‘neutral theory of molecular evolution’ in 1968. The ‘neutral theory’ proposed that most evolutionary changes at the molecular level were caused by random genetic drift rather than by natural selection. Note that the neutral theory classifies new mutations as deleterious, neutral, and advantageous. Under this classification, the rate of mutant substitutions in evolution can be formulated by the stochastic theory of population genetics. Kimura's theory was simple and elegant, yet I was not quite satisfied with it, because I thought that natural selection was not as simple as the mutant classification the neutral theory indicated, and that there would be border-line mutations with very small effects between the classes. I thus went ahead and proposed the nearly neutral theory of molecular evolution in 1973. The theory was not simple, and much more complicated, but to me, more realistic, and I have been working on this problem ever since.
This has nothing to do with Darwinism even though it's a fundamental part of modern evolutionary theory. You can't have an intelligent discussion about genome evolution, adaptationism, molecular evolution, or junk DNA without a firm grasp of Nearly Neutral Theory.
It's a shame there's no Nobel Prize for evolution.
I want to draw your attention to an article in the July/August 2012 issue of Biochemistry and Molecular Biology Education (BAMBED). The authors are Michael Klymkowski and Melanie Cooper and the title is "Now for the Hard Part: The Path to Curricular Design."
There is a growing acknowledgement that STEM education, at all levels, is not producing learners with a deep understanding of core disciplinary concepts [1]. A number of efforts in STEM education reform have focused on the development of ‘‘student-centered’’ active learning environments, which, while believed to be more effective, have yet to be widely adopted [2]. What has not been nearly as carefully considered, however, is the role of the curriculum itself as perhaps the most persistent obstacle to effective science education. It is now time to examine not only how we teach, but also what we teach and how it affects student learning.
This is an important point. Most of the science education reforms that are being proposed these days focus on style rather than substance.
In the long run, it really doesn't matter whether you are employing the very latest pedagogical techniques if what you are teaching is crap.
But we also need to recognize that there's a relationship between what we teach and how we teach it. If you want to teach scientific thinking—as opposed to memorizing pathways—then there may be superior ways to do it.
Recognizing how challenging it is to build scientific understanding requires that we recognize that scientific thinking, in and of itself, is by no means easy and is certainly not ‘‘natural.’’ We are programmed by survival based and eminently practical evolutionary processes to ‘‘think fast’’ [8]. In contrast, scientific thinking is slow, hard, and difficult to maintain. If students are not exposed to environments where they must practice and use the skills (both metacognitive and procedural) that they need to learn, they may fall back on fast, surface level answers, and fail to recognize what it is that they do not understand.
Scientific thinking (and critical thinking) have to be experienced and practiced. That means you have to make time for that in your course.
Klymkowsky, M.W. and Cooper, M.M. (2012) Now for the hard part: The path to coherent curricular design. Biochemistry and Molecular Biology Education 40:271–272. [doi: 10.1002/bmb.20614]
Here's a podcast on the origin of life. Check out the website to see who's talking [Origin Stories].
For some strange reason the show begins with Greek mythology. Then it moves on to real science. There are three origin of life scenarios ...
- Darwin's warm little pond ... equivalent to primordial soup.
- Panspermia ... which doesn't solve anything.
- Hydrothermal vents ... which aren't explained
The moderator seems to think that primordial soup has problems and panspermia is a nonstarter but he doesn't explain the hydrothermal vent story and doesn't even mention Metabolism First.
The second half of the show features soundbites suggesting that the origin of complex organic molecules on Earth is a problem but they could form in interstellar space. But this is exactly the "problem" that Metabolism First tries to explain so it's puzzling that there was no advocate of this view on the show.
This is a complicated topic that is not compatible with the format of this show. How do you, dear readers, think it rates as science journalism? Is this a good way to get the general public interested in science?
The blurb on the website suggests that the series is highly rated by fellow journalists.
A show that explores the bigger questions. Winner of "Top New Artists" and "Most Licensed by Public Radio Remix" awards at PRX's 2011 Zeitfunk Awards.
The IDiots have found a paper by Wen et al. (2012) with a very provocative title, "Pseudogenes are not pseudo any more."
Naturally, lawyer Casey Luskin is all over this: Paper Rebuffs Assumption that Pseudogenes Are Genetic "Junk," Claims Function Is "Widespread". And just as naturally, the folks at Uncommon Descent (probably lawyer Barry Arrington) jump on the bandwagon: Junk DNA: Yes, paper admits, it WAS thought to be junk.
The authors of the paper, including Templeton Prize winner Francisco J Ayala, claim that pseduogenes exhibit two puzzling properties: (a) similar processed pseudogenes occur in mouse and humans suggesting that they are conserved, and (b) many pseudogenes are transcribed.
Processed pseudogenes arise when mRNA transcripts are reverse transcribed and inserted back into the genome. They usually come from genes that are highly expressed in germ line cells. Such genes tend to be highly conserved in related species. Mammals are closely related on the scale that were talking about. It's not surprising that a few new pseudogenes in such lineages are very similar in sequence. They're still pseudogenes. The vast majority of known pseudogenes are evolving at a rate that approximates the rate of mutation indicating that they are not constrained by negative selection.
Many pseudogenes are derived from gene duplications followed by mutations in one of the copies that make them incapable of producing a functional product. There's no reason to suspect that the first of these debilitating mutations will prevent transcription; therefore, one expects that many pseudogenes will be transcribed.
Some pseudogenes have been co-opted to provide a different function. There aren't very many examples but that doesn't stop the IDiots from making the fantastic leap from 0.0001% to 100%. (Pseudogenes represent about 1% of the genome [What's in Your Genome? ] so even if we assume that every single pseudogene is not a pseudogene, it hardly makes a dint in the amount of junk DNA.)
I discussed all this when I reviewed Jonathan Well's book The Myth of Junk DNA. The relevant chapter is Chapter 5 [Junk & Jonathan: Part 8—Chapter 5]. That review was posted in May 2011. It seems clear that the lawyers on the IDiot websites haven't read it.
Here's what one of them says on Uncommon Descent.
Darwin’s followers considered junk DNA powerful evidence for their theory, which is really a philosophy (often a cult), and that they often expressed that view, often triumphantly. Others insist it is true anyway.
The problem they hope to suppress is that if lots of junk in our DNA is such powerful evidence for their theory, then little junk throws it into doubt. That is, if it is such a good theory, why was it wrong on a point that was announced so triumphantly?
So it is a good thing that the science-minded public is reminded of the historical fact that Darwinism was supported by junk DNA. And it will be fun when the squirming editorials come out in science mags, warning people not to read too much into this, Darwin is still right.
I'm not even going to bother pointing out how stupid that is. If you're reading Sandwalk, chances are high that you could detect the lies1 with your eyes closed.
1. Yes, "lies." At this point there's no other explanation.
Wen, Y-Z., Zheng, L-L., Qu, L-H., Ayala, F.J., and Lun, Z-R. (2012) Pseudogenes are not pseudo any more. RNA Biology 9: 27 - 32. [doi: 10.4161/rna.9.1.18277]
Last week's molecule was a ganglioside (GM2) that's associated with Tay-Sachs disease [Monday's Molecule #181].
This week's molecule is one of the most important enzymes in the known universe. What is it?
Post your answers as a comment. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)
Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)
In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.
Winners will have to contact me by email to arrange a lunch date. Please try and beat the regular winners. Most of them live far away and I'll never get to take them to lunch. This makes me sad.
Comments are invisible for 24 hours. Comments are now open.
UPDATE: The molecule is complex III or ubiquinol:cytochrome c oxidoreductase, the enzyme responsible for the Q-cycle and the transport of proton across the plasma membrane of bacteria and the inner mitochondrial membrane in eukaryotes. This week's winner is Stephen Spiro.
Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 9: no winner
April 16: Raul A. Félix de Sousa
April 23: Dima Klenchin, Deena Allan
April 30: Sean Ridout
May 7: Matt McFarlane
May 14: no winner
May 21: no winner
May 29: Mike Hamilton, Dmitri Tchigvintsev
June 4: Bill Chaney, Matt McFarlane
June 18: Raul A. Félix de Sousa
June 25: Raul A. Félix de Sousa
July 2: Raul A. Félix de Sousa
July 16: Sean Ridout, William Grecia
July 23: Raul A. Félix de Sousa
July 30: Bill Chaney and Raul A. Félix de Sousa
Aug. 7: Raul A. Félix de Sousa
Aug. 13: Matt McFarlane
Aug. 20: Stephen Spiro
Ms. Sandwalk's birthday is coming up in a few weeks and I'm getting nervous. I always seem to choose the wrong present. Turns out that a telephoto lens for her camera isn't very romantic. Who knew?
This year it's a sure thing. I worked on bacteriophage T4 as a graduate student and she helped me type my thesis. It's the perfect gift. [NEW - Green T4 Bacteriophage Earrings]
Right?
This year's special issue of Scientific American is "Beyond the Limits of Science." One of the articles is about human evolution. The title is Super Humanity in the print issue but the online title is Aspiration Makes Us Human.
The author is Robert M. Sapolsky, a professor of biology and neurology at Stanford University in California (USA). Stanford is a pretty good school so he probably knows his stuff.
Here's how Sapolsky starts off ...
Sit down with an anthropologist to talk about the nature of humans, and you are likely to hear this chestnut: “Well, you have to remember that 99 percent of human history was spent on the open savanna in small hunter-gatherer bands.” It's a classic cliché of science, and it's true. Indeed, those millions of ancestral years produced many of our hallmark traits—upright walking and big brains, for instance.
This doesn't make sense.
Let's assume that our ancestors left Africa only 50,000 years ago. If that represents 1% of our evolutionary history then it means that our species and it's immediate direct ancestors lived on the African open savannah for 4,950,000 years.
Could that possibly be true even if you only count the main line of descent? What is the evidence that supports these claims? How much of the early history of Homo sapiens was influenced by adaptation to open savannah? Does anyone have a scientific answer to this question?
Setting aside the "main line," we now have good evidence that modern Homo sapiens acquired alleles from Neanderthals, Denisovans, and, perhaps more ancient Homo erectus. All three spent substantial time evolving in places that looked nothing like the open savannah in Africa. The proportion of the "invading" alleles may be only 10% or less but that's still significant.
Do we know for sure that all of the important features of modern humans came from alleles that were fixed by adaptation on the savannah? What if some of the more important behavioral alleles came from Neanderthals and became fixed because they were so much fitter than the savannah alleles?
Take the alleles that make women like to shop, for example. Maybe they arose in the Denisovans because they have access to better trade routes in central China? Maybe the women on the savannah preferred to store their cash in elephant tusks?
The evolutionary psychologists have developed awesome explanations for human behavior based on their detailed understanding of the social structure of hunter-gatherer groups living on the savannah for millions of years. What if our genetic ancestors lived elsewhere? The bad news is that all those just-so stories will be wrong. The good news is that they can publish a completely different set of stories and get twice as many publications.
I stole this title from the Friendly Atheist, Hemant Mehta [Atheists Have to Address the Social and Emotional Needs of People (or the Church Wins)].
Watch the video. Hemant makes the point that large churches in the USA provide a number of social services that, apparently, aren't available anywhere else. He points out that asking someone to give up their religion is asking them to give up all kinds of other things like volunteer groups, daycare, and support groups. Hemant thinks that atheists need to create "churches" that will fill these needs.
This is the same argument made by another prominent American atheist, Dan Dennett [What Should Replace Religion?].
I don't get it. Why should atheists have to form their own "churches"? In Canada these services are provided by local community centres—there are four within a short drive of were I live. The one within walking distance is called South Common Community Centre. It has a swimming pool (see photo above), a public library, many gyms and exercise rooms, and meeting rooms. There's daycare and classes of various sorts, dozens of volunteer organizations and support groups, swimming lessons for adults and children and lots more. The community centres are funded by civic government and paid for by taxes. They are open to everybody.
Some of them rent out space for church services on Sundays but they are definitely secular. They are not atheist centres.
The best way to provide the services that people need has already been invented. It's called socialism. It's wrong to assume that the only solution is competing services supplied by various religious churches plus one non-religious church.
Is it impossible to work in America toward the goal of secular social services for all? Is that why the only solution seems to be for atheists/humanists to form their own competing religion to provide those services for nonbelievers?
