Bad Luck for Men

 
Today is Friday the 13th and the bad news for men is a report that women may have discovered how to have babies without us [The prospect of all-female conception]. All the babies will be girls.

Fortunately, Steve Palter is on to it over at docinthemachine [Babies Without Men: Creating Sperm From A Woman’s Bone Marrow]. He's a fertility specialist and he reviews the science behind the story. As it turns out, pathenogenesis may not work. Imprinting may save us (temporarily) from a fate worse than death.

It all started when we let them vote. Our great-grandfathers knew it would come to this eventually.

Inhibiting Blood Clots: Anticoagulants

 
There are several naturally occurring blood clot inhibitors. The most important is antithrombin. As the name implies, antithrombin blocks the activity of thrombin and this prevents the formation of fibrin and clotting networks. It makes sense that blood clotting has to be terminated because otherwise it would grow and block the vein cutting off blood supply.

Antithrombin III, the main antithrombin activity, is a protein that binds to thrombin in the presence of an oligosaccharide called heparin. Heparin is a glycosaminoglycan (GAG) which means that it’s formed by stringing together amino sugars (glycosamines). There are seven different kins of GAG’s in humans and heparin is one of them. The repeat unit in heparin is a sulfated glucosamine plus a sulfated iduronic acid residue [Monday’s Molecule 320].

The heparin oligosaccharide is bound to a very specific protein to form heparin proteoglycan. The physiologically important oligosaccharide is called heparan sulfate. It is found on the surface of normal endothelial cells and it is this molecule that binds antithrombin III.

The combination of antithrobin III-heparin+thrombin blocks processing of fibrinogen and prevents clotting. This is why patients are treated with heparin to prevent blood clotting or to dissolve blood clots that have formed during pulmonary embolisms, strokes, or clotting in leg veins. Heparin can also be used to coat medical equipment to prevent clotting on exposed surfaces. Heparin is an anticoagulant.

A different inhibitory mechanism is initiated when thrombin binds to a membrane protein called thrombomodulin. Thrombomodulin is a glycoprotein [Glycoproteins] found on the surface of normal endothelial cells.

The thrombin:thrombomodulin complex activates Protein C, which combines with Protein S to form a protease. Activated Protein C (APC) degrades Factors Va and VIIIa. These are the two factors required for activation of Factor X in extrinsic and intrinsic activation respectively [Blood Clotting: Intrinsic Activity, Blood Clotting: Extrinsic Activity and Platelet Activation]. Thus, degradation of these factors prevents further activation of prothrombin and clotting activity ceases.

Nobel Laureate: Fritz Lipmann

 

The Nobel Prize in Physiology or Medicine 1953.



Fritz Albert Lipmann (1899-1986): "for his discovery of co-enzyme A and its importance for intermediary metabolism"

Fritz Lipmann won the Nobel Prize in 1953 for his discovery of the cofactor Coenzyme A (CoA). Initially Coenzyme A was found to be the cofactor that bound acetyl groups for oxidation by the citric acid cycle. (Also known as the Krebs cycle. Hans Krebs shared the Nobel Prize with Lipmann in 1953 [Hans Krebs].) Here's how Lipmann's discovery is described in the presentation speech.

It is necessary to introduce compounds from the outside into the Krebs cycle in order to keep it in operation, because theoretically speaking the integral components are not used up in the process. The principal incorporation takes place through Lipmann's 2-carbon compound. It had been generally assumed that this compound was closely related to acetic acid. It was known that large amounts of acetic acid are formed in the metabolism of the cell. This acid possesses two carbon atoms and could fit well into the mechanism of the Krebs cycle. It seemed quite certain that the 2-carbon compound was acetic acid, but that it was active in some unknown form. Lipmann maintained for several years that acetyl phosphate, a compound formed from acetic acid and phosphoric acid was the active principle and he defended this idea against a growing scepticism of his colleagues. Just when most biochemists became convinced that this compound would not fit into the mechanism of the Krebs cycle, and were ready to abandon the whole idea, Lipmann announced his discovery of coenzyme A. Now suddenly everything fitted perfectly - the last notch of a combination lock fell into its place.

Coenzyme A is a compound with a rather small molecule, which, when united with the enzyme-protein, acquires the property of binding acetic acid. Acetic acid is normally quite unreactive but when bound in this way it becomes labile and reactive and represents the previously mystical 2-carbon compound which combines with a 4-carbon compound to form citric acid. A new way for the transmission of energy in the cell was demonstrated by this discovery.

We now know that Coenzyme A plays a role in several other biochemical reactions, including one of the reactions of the citric acid cycle where succinyl-CoA is a key intermediate. It also plays a role in fatty acid synthesis (via malonyl-CoA) and in fatty acid degradation (via acetoacetyl-CoA).


Lipmann's name is associated with one of the most spectacular cases of scientific fraud. In the early 1960's a postdoctoral fellow in Lipmann's lab managed to fake a lot of data and he published several scientific papers with Lipmann. All of the data, including the notebooks, were elaborately constructed to look real. One of my colleagues, Byron Lane, (now retired) was given the unenviable task of uncovering the fraud when he was working in Lipmann's lab.

[Lipmann photo from the National Library of Medicine]

The Tangled Bank #77

 
The 77th edition of The Tangled Bank is up at Aetiology. Thanks to Tara Smith.

T. Ryan Gregory on the Sandwalk

 
Gregory is the man behind the genome size database at the University of Guelph, Ontario (Canada). I stole this picture from [A nod to (and from) the Sandwalk] at Genomicron.



I'm happy to post any other pictures of people on the Sandwalk. Just send them to me as an email attachment.

We'd be better off without Religion

 
Here's an interesting guestion. On Tuesday, March 27th 2,000 people showed up at Westminster Central Hall in London to hear Richard Dawkins, Christopher Hitchens, and AC Grayling debate Baroness Julia Neuberger, Roger Scruton, and Nigel Spivey on the subject "We'd be better of without religion." [Articles of Faith, We'd be better off without Religion]. I'm practically certain that you could never get 2,000 people out to such an event in Toronto. How about other cities; New York, Morris, San Francisco, Houston?

Assuming that the answer is no, what's different about London and how can we copy it?

Isn't it strange that the "aggressive atheists" are getting so much positive attention? From what you hear on some of the blogs you'd think that the crowd would be throwing rocks rather than listening attentively.

Evidence for Evolution

 
Here's another one of those videos that are supposed to prove evolution. Before you watch it, let me give you the counter-argument. The amino acid glutamate is encoded by two different codons GAA and GAG. There is no bias in favor of one or the other so evolution would predict that the codons for glutamate can freely mutate from GAA to GAG or from GAG to GAA. If we examine several different species then we expect to see differences in the glutamate codons according to the neutral theory of evolution.

However, when we look at all the glutamate codons from α- and β-globin genes in humans, chimps, and monkeys we see that all the codons are identical. There has not been one single change as predicted by evolution. The chance of this happening if evolution is correct is 16 million to one. Thus, these genes must have been designed by an intelligent being who choose to use the same DNA sequence for all primates.

I don't like Intelligent Design Creationism. It's bad science. However, we aren't going to win any arguments by using silly examples that can easily be refuted by anyone with a brain. Is this is an example of the sort of framing that we're supposed to be practicing?

Relax ....

 
Shelley Batts ask why is [this] so relaxing [This Blue Whale Wants You To Relaaaaaaax]. Good question Shelly, but after watching the whale for ten minutes I'm just too mellow to care about an answer.

Violent Video Games and Crime Victims

 
I love this graph. Thanks to Koen Crolla for posting it on Rosio Pavoris.

Science Policy Forum: Framing Science

 
Many people have accused me of misrepresenting the Nisbet & Mooney article in Science magazine (Science 6 April 2007: Vol. 316: p.56). So, let's step through it and see what we can learn.

Issues at the intersection of science and politics, such as climate change, evolution, and embryonic stem cell research, receive considerable public attention, which is likely to grow, especially in the United States as the 2008 presidential election heats up. Without misrepresenting scientific information on highly contested issues, scientists must learn to actively "frame" information to make it relevant to different audiences. Some in the scientific community have been receptive to this message (1). However, many scientists retain the well-intentioned belief that, if laypeople better understood technical complexities from news coverage, their viewpoints would be more like scientists', and controversy would subside.

I believe that average citizens would be better off if they understood the science behind these controversial issues. As a scientist, I feel competent to explain the science. I also have opinions about things like evolution and embryonic stem cell research and I don't hesitate to proclaim those opinions. Since I'm a scientist, I tend to reason like a scientist. I don't have any great desire to learn how to reason any other way.

I do not believe that the controversy over evolution, for example, will subside when people learn the scientific truth about evolution. I don't recognize the strawman that Nisbet and Mooney have constructed. They say that "scientists must learn to actively "frame" information to make it relevant to different audiences." Let's see what they mean by that. I'm looking forward to seeing the evidence that they've done a better job than scientists of explaining scientific issues. Presumably that evidence is just coming up in the next paragraph.

In reality, citizens do not use the news media as scientists assume. Research shows that people are rarely well enough informed or motivated to weigh competing ideas and arguments. Faced with a daily torrent of news, citizens use their value predispositions (such as political or religious beliefs) as perceptual screens, selecting news outlets and Web sites whose outlooks match their own (2). Such screening reduces the choices of what to pay attention to and accept as valid (3).

I'm well aware of the fact that many citizens do not think like a scientist. I did not "assume" otherwise. I don't know very many scientists who do. In most countries scientists are well-respected and when they say that something is a scientific fact they tend to get the benefit of the doubt. In other words, in those countries the primary source of information about science is scientists, not politicians and pastors. This doesn't seem to be true in America. I wonder what Nisbet & Mooney are proposing to do about it?

Still waiting for the evidence that Nisbet & Money have done a better job by paying attention to "framing."

Frames organize central ideas, defining a controversy to resonate with core values and assumptions. Frames pare down complex issues by giving some aspects greater emphasis. They allow citizens to rapidly identify why an issue matters, who might be responsible, and what should be done (4, 5).

This sounds like psychobabble to me. It's a paragraph without content. It doesn't tell me a thing about what a "frame" is and how it might differ from what I've been doing all my life. It doesn't tell me what a "core value" is. It doesn't tell me why I should have to construct an argument that "resonates" with someone else's—possibly incorrect—assumptions. It also doesn't tell me why I should listen to Nisbet & Mooney.

Consider global climate change. With its successive assessment reports summarizing the scientific literature, the United Nations' Intergovernmental Panel on Climate Change has steadily increased its confidence that human-induced greenhouse gas emissions are causing global warming. So if science alone drove public responses, we would expect increasing public confidence in the validity of the science, and decreasing political gridlock.

Science alone does not drive public responses. Nobody believes that. However, it is the duty of scientists to faithfully report on the science, making sure they get it right. That's what scientists do.

It is the duty of scientists to report on the scientific consensus in a field. If there is no unanimity on an issue it is absolutely essential that a true scientist reveal the controversy as long as it's a legitimate scientific controversy. Hiding a scientific controversy for the sake of political gain is unethical. I hope that's not where they're going with this.

Despite recent media attention, however, many surveys show major partisan differences on the issue. A Pew survey conducted in January found that 23% of college-educated Republicans think global warming is attributable to human activity, compared with 75% of Democrats (6). Regardless of party affiliation, most Americans rank global warming as less important than over a dozen other issues (6). Much of this reflects the efforts of political operatives and some Republican leaders who have emphasized the frames of either "scientific uncertainty" or "unfair economic burden" (7). In a counter-strategy, environmentalists and some Democratic leaders have framed global warming as a "Pandora's box" of catastrophe; this and news images of polar bears on shrinking ice floes and hurricane devastation have evoked charges of "alarmism" and further battles.

That's an interesting bit of information on American politics. I'm not terribly interested but let's see where it's headed.

Recently, a coalition of Evangelical leaders have adopted a different strategy, framing the problem of climate change as a matter of religious morality. The business pages tout the economic opportunities from developing innovative technologies for climate change. Complaints about the Bush Administration's interference with communication of climate science have led to a "public accountability" frame that has helped move the issue away from uncertainty to political wrongdoing.

Scientists have established that global warming has occurred and much of it is probably due to human activity. The question before us is what should we do about it? The action will depend to some extent on what are the predicted consequences of global warming. Scientists can play a role here by reporting on the various climate models and how reliable they are.

Many scientists have already decided that we should do something about global warming by cutting back on carbon dioxide emissions. Most of them reject the argument based on religious morality and most of them probably reject the argument based on "economic opportunities." If there's a point here, I'm not seeing it.

I assume there are some scientists who know about global warming and know that humans are contributing but who don't know whether we should do something about it. Nisbet & Mooney seem to be making an assumption about the opinion of all scientists.

BTW, I still haven't seen any evidence that these two authors have been more persuasive than the average scientist. I'm sure it's going to be mentioned very soon. It's pretty important, don't you think?

As another example, the scientific theory of evolution has been accepted within the research community for decades. Yet as a debate over "intelligent design" was launched, antievolutionists promoted "scientific uncertainty" and "teach-the-controversy" frames, which scientists countered with science-intensive responses. However, much of the public likely tunes out these technical messages. Instead, frames of "public accountability" that focus on the misuse of tax dollars, "economic development" that highlight the negative repercussions for communities embroiled in evolution battles, and "social progress" that define evolution as a building block for medical advances, are likely to engage broader support.

American scientists did not counter with "science-intensive" responses. Instead, for the most part they countered with legal arguments for keeping Intelligent Design Creationism out of the public schools. They let the Creationists set the agenda by fighting the battle in the courts where the Creationists could win even when they lose. Scientists turned the fight over to the lawyers.

I totally reject the argument that we should focus on the economic advantages of evolution over creationism on the grounds that it's something that the public will understand. I reject it because it is probably untrue and it's a cop-out. No respectable scientist will argue that evolution should be accepted over Intelligent Design Creationism because America will be more prosperous if citizens accept evolution.

The evolution issue also highlights another point: Messages must be positive and respect diversity. As the film Flock of Dodos painfully demonstrates, many scientists not only fail to think strategically about how to communicate on evolution, but belittle and insult others' religious beliefs (8).

Some religious beliefs deserve to be belittled and insulted. Is this just another argument for appeasement and so-called "tolerance" dressed up to look more intellectual?

Let's think strategically for a minute. The fight is between religion and science. Let's not forget that key point as we try to understand what Nisbet & Mooney are wanting us to do about it. The fight is not about whether belief in evolution offers better economic advantages. Even if that were true, the average Christian fundamentalist would not accept evolution. And if it turned out not to be true there would be very few scientists switching to Intelligent Design Creationism.

It sounds like we're getting close to learning how Nisbet & Mooney would handle this issue. I can't wait to see what they've done to advance the cause of evolution and defeat Intelligent Design Creationism. I'm sure they wouldn't be lecturing scientists on how to behave if they didn't have proof that their way is better.

On the embryonic stem cell issue, by comparison, patient advocates have delivered a focused message to the public, using "social progress" and "economic competitiveness" frames to argue that the research offers hope for millions of Americans. These messages have helped to drive up public support for funding between 2001 and 2005 (9, 10). However, opponents of increased government funding continue to frame the debate around the moral implications of research, arguing that scientists are "playing God" and destroying human life. Ideology and religion can screen out even dominant positive narratives about science, and reaching some segments of the public will remain a challenge (11).

I can't figure this out. There are people who oppose embryonic stem cell research because God tells them it's wrong. What are we supposed to do about that? Do we understand and appreciate what they're saying and debate the issue of religion vs. science? Or do we try and convince them that they should go against God's word because some other people might be cured by stem cell research? That'll really work, right? I don't get the point here.

Some readers may consider our proposals too Orwellian, preferring to safely stick to the facts. Yet scientists must realize that facts will be repeatedly misapplied and twisted in direct proportion to their relevance to the political debate and decision-making. In short, as unnatural as it might feel, in many cases, scientists should strategically avoid emphasizing the technical details of science when trying to defend it.

This article is so confusing that I really don't know how to respond. I don't know any scientist who thinks that emphasizing technical details is all there is to good science education. Sometimes the authors seem to be arguing that we should use non-scientific arguments to advance our case. Other times they seem to be saying that we should avoid talking about religion—this would be like ignoring a hippo in the room. And still other times they seem to be saying that we need to improve the teaching of science.

And they do all this without ever showing me why I should even bother listening to them. I don't see one single example of an article by either Mooney or Nisbet that illustrates the superiority of their method. Come on, guys, if you're going to criticize scientists for the way they write about science then at least have the courtesy to establish your credentials.

I can tell you one thing. This article sure would have benefited from peer review.

Marcus Ross, Michael Behe, and Paul Nelson at Temple University

 
Today, Marcus Ross is speaking at Temple University on the topic of geology and the Cambrian Explosion [Marcus Ross and Peter Dodson at Temple University]. Recall that Ross is a Young Earth Creationist: he believes that the Earth is less than ten thousand years old. Appearing on the same stage as Ross is the paleontologist Peter Dodson from nearby University of Pennsylvania. Dodson will present the case for rationality.

The talks are being organized by a group of student societies under the title DECIDE FOR YOURSELF: Evolution and Intelligent Design. Tomorrow night it's the turn of Michael Behe, speaking on biology, plus someone who they've recruited to represent the side of rationality in the field of evolution. I know for a fact that several people have turned them down (including me). This is a Discovery Institute dog-and-pony show. Paul Nelson will be the final speaker, on philosophy, a week from today. Nelson is also a Young Earth Creationist. (No one has yet been selected to present the rational case for philosophy, as far as I know.)

Students have every right to sponsor such events even if it's under the false impression that there's a legitimate scientific debate over the age of the Earth. However, I seriously doubt that it will be attended by people with an open mind. If anyone goes to the lecture, please send a report.

The fact that students have a right to invite IDiots on to their campus does not mean we have to defend their decision. I think they are being very naive and uneducated. As far as I'm concerned, it speaks badly of Temple University that groups of students such as Temple University Chemistry Society, Geology Society, and the Philosophy Society would even consider listening to Young Earth Creationists. What in the world are they thinking?

Gene Genie #5

 
The next edition of Gene Genie will be hosted by Neurophilosophy. That's the neurophilosopher on the right (right) outside the Natural History Museum in Kensington, London (UK). Please send your articles to him ASAP. We have lots of genes to cover and only six decades to do it.

(The guy in the blue shirt also has a blog.)

Monday's Molecule #21

 

Name this molecule. You must be specific but we don't need the full correct scientific name. (If you know it then please post it.)

As usual, there's a connection between Monday's molecule and this Wednesday's Nobel Laureate. This one's easy once you know the molecule and make the connection. The prize (free lunch) goes to the person who correctly identifies both the molecule and the Nobel Prize.

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Gene Genie #4

 
Welcome to the 4th edition of Gene Genie: "A blog carnival on genes and gene-related diseases. We plan to cover the whole genome before 2082."

The first three editions are: Gene Genie #1 at Scienceroll, Gene Genie #2 at Sciencesque, and Gene Genie #3 at Genetics & Health.

Our first gene is called the hemochromatosis gene (HFE) [OMIM 235200]. Defects in this gene, located on chromosome 6 at p21.3, interfere with iron uptake and storage. Hsien Hsien Lei discusses a mutation that increases the risk of stroke [HFE Gene Associated with Three Times the Risk of Stroke]. She also discusses a new book by Sharon Moalem called Survival of the Sickest. It turns out that the first chapter covers hemochromatosis.

Steven F. Palter posts on a very sensitive topic—whether a patient wants to know if they carry a possibly lethal genetic mutation. For example, what if you are at risk for Huntington's disease and you simply do not want to know whether you will die in your 40's or not? That's fine as long as you don't have children but do you want to pass the defective gene to your children if you carry it? How can you have children without risk if you don't want to know whether you are a carrier or not? It turns out there's a way and Steven Palter explains how in Beyond Genetic & Prenatal Testing- Pre-embryo Testing - Hiding the Results From the Patient.

Tim Erickson presents Random OMIM Search Term of the Day: ?Amber? posted at Sciencesque. In case you don't know about OMIM, it stands for Online Mendelian Inheritance in Man and it's quite possibly the best scientific database site on the internet. Anything you want to know about genetic disease in humans is there.

Tim's random search takes him to the DSPP gene on chromosome 4q21.3 and a fascinating, and slightly gory, discussion about tooth decay.

My own contributions are a summary of the number of genes on each human chromosome [Summary of Genes on Human Chromosomes, RNA Polymerase Genes in the Human Genome (POLR1A, POLR2A, POLR3A, POLR1B, POLR2B, POLR3B) and Genes for Hemophilia A & B and von Willebrand disease (F8, F9, VWF).

Altogether, we've discussed 11 more genes in this edition of Gene Genie. By my reckoning, that only leaves about 23,900 to go.

Genes for Hemophilia A & B and von Willebrand disease

 
The roles of Factor VIII and Factor IX in blood clotting are described in a recent posting [Blood Clotting: Intrinsic Activity]. Defects in the gene for Factor VIII cause a bleeding disorder called hemophilia A [OMIM 306700]. The gene is called F8 and it's located on the X chromosome at q28. The fact that it's X-linked means that males are more likely to be affected than females since females would have to be homozygous for the recessive allele. Heterozygous females are unaffected.

Deficiencies in Factor IX are caused by mutations in the F9 gene, which is also located on the X chromosome (q27.1-q27.2). The disease is called hemophilia B or Christmas disease. Factor IX used to be called Christmas factor after Stephen Christmas (1947-1993), the first patient with a known defect in this clotting factor [OMIM 306900]. It took some time, and a considerable amount of effort, to determine that there were two different genes on the X chromosome and hemophilia A was a different disease than hemophilia B.

The disease nomenclature is complicated by the fact that defects in the gene for von Willebrand Factor (vWF) are sometimes called hemophilia B. The correct name is von Willebrand disease. Recall that von Willebrand Factor associates with and stabilizes Factor VIII. Deficiencies of vWF are phenotypically equivalent to deficiencies in Factor VIII [OMIM 193400]. The gene for von Willibrand Factor is VWF and it's located at 12p13.3. The fact that it's autosomal means that the disease is not sex-linked.

Several of the VWF alleles confer a dominant phenotype. This is sometimes due to an insufficiently in the amount of von Willebrand Factor in blood plasma. The genetic term is haplo-insufficiency. It means that two functional alleles, one on each chromosome, are necessary in order to supply a sufficient amount of protein.