Job Prospects for Graduate Students

 

This week's issue of Nature has two short articles on the future of science in the USA. The first one refers to Indentured Labour. It talks about the fact that the number of life science researchers in the universities (tenure and tenure-track) has leveled off at about 30,000 while the number of students earning degrees in the life sciences has doubled. The pejorative reference to graduate students as indentured labour is quite unnecessary. It declares a bias and prevents rational discussion.

The second article makes a similar point [More biologists but tenure stays static] about the job prospects of Ph.D. students.

Both Nature articles are based on statistics compiled by the Federation of American Societies for Experimental Biology (FASED). The original study can be found at [Education and Employment of Biological and Medical Scientists: Data from National Surveys]. The Nature articles have stimulated considerable debate on the blogosphere, See PZ's posting and the comments [The most daunting numbers I've seen yet].

Most of the postings have failed to ask the really hard questions so that's what I'm going to do. But first, let's look at the data from the powerpoint presentation on the FASEB site.

The first graph shows the number of Ph.D. graduates in life sciences over the past 40 years. The rate was about 4,000 per year throughout most of the 1980's then jumped up to about 6,000 per year in the late 1990's. Lately there has been a further increase to about 7,000 per year. Much of the increase is due to foreign students.


The second graph shows the increase in positions for researchers with a Ph.D. in life sciences. The number of jobs has almost tripled from 1973 to 2003. Most of the increase has been in industry as a result of the expansion of biotech firms. Most of the fuss is because the number of academic jobs seems to have flattened out at about 60,000. Of these, only 30,000 are tenure or tenure-stream positions. At our university the number of positions in hospital research institutes (non-tenured) has vastly outpaced the number on the campus (tenured) so this isn't a surprise to me.


One of the questions being debated is whether we should continue to graduate far more Ph.D's than the number of academic positions that need to be filled. The answer is yes and here's why.

Assuming (incorrectly) that our primary purpose in graduate education is to train our replacements and assuming (incorrectly) that all graduates want an academic position, we should still graduate more candidates than there are positions because we will want to choose the best candidates for a position and this means that there has to be a larger supply than the demand. How large should this supply be if we were to treat graduate students as a commodity? I don't know, maybe five or ten times the number of jobs?

Now, don't get me wrong. I'm not advocating that we behave this way. I'm simply pointing out to those who do want us to adopt this point of view that there should be many more Ph.D.'s than jobs. That's something that most people don't seem to understand. They seem to think that the number of Ph.D. graduate should approximate the number of jobs available. What this would mean in practice is that the selection for tenure-stream Professors would take place mostly on admission to graduate school and whatever happens afterwards is hardly relevant (i.e., no weeding out). (Some people even think that the candidates for tenure-stream positions are chosen from graduates of their own institutions. Those people are really out of touch.)

Is the "crisis" as serious as most people think? I don't believe it is for several reasons. First, many of the foreign students will return to their native countries. This means that the graduate students who are getting Ph.D.'s in America won't all be looking for jobs in America. Second, many students want to take jobs in industry because they pay better. They won't be competing for academic positions. Third, there's a considerable lag between the expansion of student numbers and the expansions of faculty. Many universities have plans for faculty expansion in the near future. Fourth, the steady-state level of faculty positions disguises the fact that faculty hired in the 1970's expansions are now retiring. Thus, for the short term there will be more new hiring than the graphs indicate.

But behind all this debate and discussion is a more serious issue. Why do students go to graduate school? Is it only because they want to be trained for a future job? Should Professors look upon every graduate student as a job trainee and behave accordingly? I'd like to think that there are still students out there who go to graduate school for the love of science. I did.

The graduate school experience is an end all by itself and not always a means to an end. Sure, it would be nice if things work out and the student gets a nice post-doc and an academic position—if that's what they want—but there's other things to do after graduate school. I've known lots of students who went into teaching, medicine, or law for example. I've known students who choose to be full-time parents even though they did well in graduate school and enjoyed the experience.

I'm very reluctant to fall into the mindset where I view every graduate student as a trainee for a job in industry and academia and not as a young inquisitive scientist. If Professors adopt the former mindset, and some do, then the goal of graduate research is not to answer important scientific questions but to churn out enough papers in respectable journals to ensure you get a good post-doc. The fact that this goal is sometimes compatible with the ambitions of the P.I. (more papers) makes for a deadly combination.

Hugh McLachlan on Cloning Humans

 
Last week I posted an article on cloning humans. It was a reference to a piece in New Scientist by Hugh McLachlan, a Professor of ethics at Glasgow Caledonian University in Scotland (UK). McLachlan does not oppose the cloning of humans and neither do I.

Here are some other articles on the same topic [Ignore The Boys from Brazil - say Yes to human cloning], [Poor reasons for making human cloning illegal].

McLachlan sent me the following message in response to some of his critics. It addresses some of the issues that have come up in the comments on Sandwalk. He has given me permission to post it.

I think that the risks to the embryos are irrelevant to the issue of whether or not human cloning should be illegal. (Whether public money should be spent on human cloning if it is a very inefficient technique is another matter.) The potential mothers should be informed about the known risks and they must, of course, give their consent. The risk to the mothers is not a justification for making the technique illegal in my view.

Consider an analogy. Imagine that 100 people were trapped, unconscious in a building. They might, for instance, be hostages. A bomb might be primed to explode shortly. If they are not rescued fairly soon they will die. Suppose that the only way they could be rescued is if they were snatched by SAS. The snatch might kill them all. It might result in some being injured, impaired and disabled. It might even result in some living a life that was not worth living. However, there is a chance that one or more might survive to live a normal life. Should we take the chance and snatch them? If we are thinking only about the interests of those 100 people, we must do it even if the chances are remote that any will be saved.

To say that it should be illegal to make the snatch because of the risk to the hostages would be absurd. It is similarly absurd to say that, because of the risks to the embryos involved, human cloning should be illegal.

There is a risk to the soldiers. However, since people volunteer to be soldiers and might even volunteer for particular dangerous missions it is generally judged acceptable that soldiers are exposed to such risks. I can see no reason why we should not allow potential mothers to accept the risks of delivering clones if that is what they want to do.

The objection about the risks to the embryos/clones involved looks at the issue of risk and uncertainly the wrong way round. Suppose that some technique or other were devised to reduce the suffering of those people who had some particular relatively minor ailment. The question of the risk of the technique to these potential patients might be relevant particularly if we assume that to live with the ailment is still pleasant and worthwhile even if not as pleasant and worthwhile as life without the ailment. Suppose that, with the technique, the likelihood is that X% of the patients will be cured completely of the ailment, Y% will end up with a worse case of the condition and that Z% will die in the course of treatment.

In a situation such as this, it is important to know what numbers X, Y and Z stand for to try to judge whether the risk involved in worth taking. Ideally, we would tell the patients and let them decide for themselves. However, human cloning is quite different from this imagined scenario. For the people who might be born as a result of cloning - whether, in the event, they actually are born - cloning is their only chance of birth and life. In the absence of cloning, they will not be born. Hence, cloning is not a risk for them but an opportunity - their only opportunity. To make cloning illegal in their interests on the grounds that, in the course of the technique, not all implanted embryos will become healthy mature human bodies is absurd.

Fool me once .... shame on you ...

 
See Can You Hear the Drums Beating?, Bush Flubs the Message and A Prelude to War.

There's an old saying in Tennessee — I know it's in Texas, probably in Tennessee — that says, fool me once, shame on — shame on you. Fool me — you can't get fooled again.
                                                   George W. Bush 2002

[Hat Tip: John Lynch]

Rationalism vs. Superstition: The Enemies of Reason (Part 2)

 
Here's part 2 of Enemies of Reason, Richard Dawkins' attack on superstition. This episode focuses on medical quacks and kooks. It's very entertaining. You'll certainly like the segment on how to increase the number of strands in your DNA!

Read Orac's review at Respectful Insolence. The point to remember is that the battle is between rationalism and superstition and the atheism vs. religion controversy is only a subset of the bigger battle. And evolution vs. creationism is an even smaller subset. You are missing the point when you ask people like Richard Dawkins to align themselves with moderate theists in order to combat the extreme versions of creationism.

Justice, Texas Style

 
Reuters is reporting that the State of Texas has just executed it's 400th convicted criminal since 1982 [Texas executes 400th person since 1982].

The Governor's office issued a statement in response to criticism of the large number of executions in Texas.

Texans long ago decided that the death penalty is a just and appropriate punishment for the most horrible crimes committed against our citizens.

I suspect this is true. Texans probably do support the death penalty. That's not the point. The point is why are there are so many more executions in Texas compared to other states with the death penalty and why is the USA one of the few "civilized" nations to permit executions of their own citizens?

I don't know the answers to these questions. Does anyone else?

Nobel Laureate: Earl W. Sutherland, Jr.

 

The Nobel Prize in Physiology or Medicine 1971.

"for his discoveries concerning the mechanisms of the action of hormones"

Earl W. Sutherland, Jr. (1915-1974) received the Nobel Prize in Physiology or Medicine for his work on the mechanism of action of hormones, particularly epinephrine. Sutherland was very much influenced by Carl Cori [Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori] who worked on the pathways of glycogen breakdown and glucose synthesis in mammalian liver cells. Sutherland is responsible for discovering how the hormone epinephrine regulates glycogen synthesis [Regulating Glycogen Metabolism]. Along the way, Sutherland discovered the second messenger cyclic AMP (cAMP), which was Monday's Molecule #39.

The presentation speech was delivered by Peter Reichard of the Karolinska Medico-Chirurgical Institute. Note the opening line that refers to Monod's famous quote"What is true of E. coli is also true of the elephant." It was 1971 and Chance and Necessity had just come out. For years scientists had thought that the action of hormones demonstrated that so-called "higher" organisms used higher-level processes to regulate metabolism. Hormones needed whole tissues and organs to show an effect. What Sutherland proved was that hormones work at the cellular and molecular level just like the molecules that regulated activity in bacteria.

Your Majesty, Your Royal Highnesses, Ladies and Gentlemen,

What applies to bacteria also applies to elephants. This free quotation after the French Nobel prize winner, Jacques Monod, illustrates with some exaggeration one important principle of biology: that of the identity of the fundamental life processes.

Yet one need not be a Nobel prize winner to know the difference between bacteria and an elephant. The latter is not only much larger. The decisive difference lies in the fact that bacteria are unicellular organisms and that all the functions of life are contained in a single cell. In higher organisms on the other hand, there occurs a division of labor between different types of highly specialized cells. Nevertheless, the elephant must function as an integrated unity. The cells in the different organs must be coordinated in such a way that they rapidly adapt to the changing requirements of the environment.

The hormones form part of such a coordinating system. Among other things, the difference between a bacterium and an elephant lies in the fact that the latter - as well as all of us here - for the sustainment of his life is completely dependent of the proper function of hormones, while bacteria can do without them.

What then is the function of hormones? Ever since the first hormone was discovered about 70 years ago this has been a central theme of research for many scientists. This question is also of considerable medical importance. Many diseases are hormone diseases, amongst them diabetes. In spite of this the mechanism of hormone action remained a complete mystery until recently. The answer did not come until Earl Sutherland started his investigations on the function of the hormone epinephrine.

This hormone is produced in the adrenal glands and is transported to different organs of the body by the blood. It is formed in increased amounts during stress and adapts the individual to new situations. One of its important functions lies in the liberation of glucose inside the cells for the production of energy. Epinephrine serves as a chemical signal, as a messenger, which is sent out from the adrenals to activate different organs essential for the defense of the individual.

Sutherland investigated the effect of epinephrine on the formation of glucose in liver and muscle cells. He discovered a new chemical substance which serves as an intermediate during the function of the hormone. This substance is called cyclic AMP. It transmits the signal from epinephrine to the machinery of the cell, and Sutherland therefore called it a "second messenger". Furthermore, Sutherland made the important discovery that cyclic AMP is formed in the cell membrane. This means that epinephrine never enters the cell. We may visualize the hormone as a messenger which arrives at the door of the house and there rings the bell. The messenger is not allowed to enter the house. Instead the message is given to a servant, cyclic AMP, which then carries it to the interior of the house.

Sutherland suggested already around 1960 that cyclic AMP participates as a second messenger in many hormone mediated reactions, and that its effect thus is not limited to the action of epinephrine. First this generalization was not willingly accepted by the scientific community, since it was difficult to visualize how a single chemical substance could give rise to all the diverse effects mediated by various hormones. By now Sutherland and many other scientists have provided convincing evidence, however, that many hormones exert their effects by giving rise to the formation of cyclic AMP in the cell membrane. Sutherland had discovered a new biological principle, a general mechanism for the action of many hormones.

How can one then explain the specificity of different hormones? A good part of the explanation lies in the fact that different cells in their membranes possess specific receptors for various hormones. The different messengers thus must find their way to the right door in order to deliver their messages.

Cyclic AMP was discovered in connection with investigations concerning the function of hormones. It came therefore as a big surprise when Sutherland in 1965 reported that cyclic AMP also occurred in bacteria which apparently had no use for hormones. It was soon found that cyclic AMP was produced by other unicellular organisms, too. In all these cases cyclic AMP was shown to have important regulatory functions which aid the cells in their adaptation to the environment. Maybe we can look upon cyclic AMP as the first primitive hormone, regulating the behaviour of unicellular organisms. We then may look upon the true hormones of higher organisms as components of an overriding principle which was added during the course of evolution. Thus the difference between uni- and multicellular organisms does not, after all, appear to be so great, and with respect to cyclic AMP we can turn around Monod's dictum and say that what applies to elephants also applies to bacteria.

Dr. Sutherland,

Hormones were known in biology and medicine for a long time. The mechanism for hormone action remained a mystery, however, until you discovered cyclic AMP and its function as a second messenger. In recent years it has become apparent that cyclic AMP also serves as an important regulatory signal in microorganisms, and that its action thus is not limited to the function of hormones. When you discovered cyclic AMP you discovered one of the fundamental principles involved in the regulation of essentially all life processes. For this you have been awarded this year's Nobel prize in physiology or medicine. On behalf of the Karolinska Institute I wish to convey to you our warmest congratulations, and I now ask you to receive the prize from the hands of his Majesty the King.

Google Sky

 
If you haven't updated your copy of Google Earth then you should do so right now. A new feature called "Sky" has been added [Celestial add-on points Google Earth at the stars.

The image on the right shows us what the sky will look like tomorrow night when Mercury, Saturn, and Venus are close together in Leo. Saturn is going to be very close to Regulus. Unfortunately, the program won't tell me if I can see this from where I live. I don't know if this feature is missing or if I just can't find it.

You can click on the galaxy icons to get more information and you can click on each star to find out it's name, distance, spectral type etc.

Pretty cool. I wonder if Phil Plait of Bad Astronomy will comment? I'd like to know what he thinks of the program.

Identity of the Product of Mendel's Green Cotyledon Gene

 
This posting has been replaced by Identity of the Product of Mendel's Green Cotyledon Gene (Update).


Another of Mendel's seven genes has been identified. This one is described in his 1865 paper Experiments in Plant Hybridization [MendelWeb] as character number 2.

2. To the difference in the color of the seed albumen (endosperm). The albumen of the ripe seeds is either pale yellow, bright yellow and orange colored, or it possesses a more or less intense green tint. This difference of color is easily seen in the seeds as their coats are transparent.

Mendel's reference to the color of albumin, or endosperm, is inaccurate. He was actually observing the color of the cotyledons—the "seed leaves" that surround the embryo in the pea seed. These tiny leaves are covered by a seed coat that is partially transparent.

In wild-type peas the seeds turn yellow as they mature (i) but certain mutants exhibit a "stay-green" phenotype where the peas retain their green color (I). The figure shows seeds from a plant with the II genotype (top) and the ii genotype (bottom). The seed coat has been removed from the lower pair of each group of four peas.

In a paper just published in the Proceedings of the National Academy of Sciences (USA) a group in Japan has identified the "stay green" gene that Mendel worked with (Sato et al., 2007). It turns out that the gene, called SGR (stay-green), encodes an enzyme that is localized to chloroplasts and plays a role in the degradation of chlorophyll during senescence and maturation of seeds. When the enzyme is defective chlorophyll isn't broken down and the tissue stays green.

This brings to three the number of Mendel's genes that have a known function. The wrinkled pea phenotype is caused by a defect in the gene for starch branching enzyme (Bhattacharya et al., 1990) [Biochemist Gregor Mendel Studied Starch Synthesis]. The tall/short phenotypes are caused by defects in the gene for gibberellin 3β-hydroxylase (Martin et al., 1997). Gibberellins are plant growth hormones.

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[Photo Credit: The photograph of mutant and wild-type pea seeds is taken from Figure 1 of Sato et al. (2007)]

Bhattacharyya, M. K., Smith, A. M., Ellis, T. H., Hedley, C., and Martin, C. (1990) The wrinkled-seed character of a pea described by Mendel is caused by a transposon-like insertion in a gene encoding starch-branching enzyme. Cell 60:115-122.

Martin D.N., Proebsting W.M., Hedden P. (1997) Mendel's dwarfing gene: cDNAs from the Le alleles and function of the expressed proteins. Proc. Natl. Acad. Sci. (USA) 94:8907–8911.

Sato Y., Morita R., Nishimura M., Yamaguchi H., and Kusaba M. (2007) Mendel’s green cotyledon gene encodes a positive regulator of the chlorophyll-degrading pathway. Proc. Natl. Acad. Sci. (USA) (early publication, [August 20, 2007]).

Monday's Molecule #39

 
Today's molecule is complex but it has a very simple common name. The common name is not sufficient—you must supply the formal IUPAC name to win the prize. There's a direct connection between this Monday's Molecule and Wednesday's Nobel Laureate.

The reward (free lunch) goes to the person who correctly identifies the molecule and the Nobel Laureate(s). Previous free lunch winners are ineligible for one month from the time they first collected the prize. There's only one (Marc) ineligible candidate for this Wednesday's reward since many recent winners haven't collected their prize. The prize is a free lunch at the Faculty Club.

In preparation for the beginning of classes in three weeks I'm going to start requesting email responses. Send your guess to Sandwalk (sandwalk(at)bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and the Nobel Laureate. All responses will be posted tomorrow along with the time that their message was received on my server. This way I may select multiple winners if several people get it right.

Comments will be blocked for 24 hours. Comments are now open.

Like a Broken Record ...

 
Matt Nisbet is at it again. His particular spin frame on the rationalism vs. superstition debate is that the rationalists are making too much noise. According to Nisbet, we atheists are hurting the "cause" (what cause?) by speaking out loudly against superstition in the form of religion. Apparently it would be better to tone down the rhetoric in order to avoid offending those who believe in superstition. This is the strategy that has been followed by Americans for the last 100 years or so. No matter how stupid the religious extremists are, whether from the pulpit or on talk radio, we mustn't say that they are stupid because that would hurt their feelings. Or rather, it would hurt the feelings of the moderate believers who tolerate and support the religious extremists.

Of course Matt doesn't recognize that this is just his personal opinion. Oh no, that wouldn't be right, would it? If you are going to attack Dawkins, Hitchins, and Harris then you'd better frame it make it sound like an attack based on solid scientific reasoning. Here's what Matt Nisbet says in his latest posting [Why the New Atheist Noise Machine Fails].

Everything we know from social science research on attitude formation and beliefs predicts that the communication strategy of the New Atheist noise machine will only further alienate moderately religious Americans, the very same publics who might otherwise agree with secularists on many social issues.

Everything we know from history predicts that social change is often stimulated and led by vocal "extremists" who dare to speak out even if it offends those who prefer the status quo. This was true of the women's movement, the civil rights movement, and the gay rights movement. In those cases it was the moderate male chauvinists, the moderate racists, and the moderate homophobes who were initially offended. They didn't like being told that their long-held beliefs were wrong. In all those cases I suspect there were Matt Nisbets who tried to silence the outspoken leaders because they were offending the average moderate citizen.

If social science "research" says that the cause of outspoken individuals always fails then that says a lot more about the so-called "research" of social scientists than it does about reality.

The Dawkins/Hitchens PR campaign provides emotional sustenance and talking points for many atheists, but when it comes to selling the public on either non-belief or science, the campaign is likely to boomerang in disastrous ways.

The experiment is under way. Up until 2005, atheism was pretty much hidden under a bushel and religious superstition was rarely confronted in public. The result is that America is the most religious country in the industrialized world and evolution isn't taught in schools. Let's see if there's any change in the status quo over the next decade as the Dawkins/Hitchens framing PR campaign continues. According the Nisbet, the country will become even more religious because of the backlash. I'm betting that religion will become less important to Americans when they realize that there are other options.

There are times when I wonder which side Nisbet is on. It sounds to me like he's perfectly happy with the way things have been for the past several decades.

Don't Mess with Canadians

 
I recently returned from spending a week in a foreign country. I did not behave like the Canadian in this video although there were times ...



[Hat Tip: Canadian Cynic]

The Cause of Variation in a Population

John Dennehy of The Evilutionary Biologist has posted a wonderful article on This Week's Citation Classic. The classics are two back-to-back papers on genetic variation in fruit flies (Hubby and Lewontin (1966), Lewontin and Hubby (1966)). That's Lewontin on the left.

Please get on over to The Evilutionary Biologist and read what John has to say. These were very important and groundbreaking papers when they came out and everyone needs to know why.

Here's some background.

In the olden days there were two competing theories to explain variation (heterozygosity) in a population. The classical theory said that mutations are constantly being removed from the population by positive natural selection or purifying selection. Variation is a transient phenomenon that would disappear entirely if it weren’t for new mutations that arise at a significant rate.

The balance theory maintains that variation in a population is often due to balancing selection. The best known example of balancing selection is the allele for sickle cell disease. In the heterozygous state it confers resistance to malaria but in the homozygous state it is often lethal. Both the sickle cell allele and the wild type allele are maintained in the human population by balancing selection.

Hubby and Lewontin (1966) discovered that there was a huge amount of genetic variation in fruit flies. Their data suggested that 50% of all loci had multiple alleles. This is difficult to reconcile with the balance theory and it was also a big surprise to those who supported the classic theory. It seemed unlikely that at any given point in the evolutionary history of a species that so many genes could be undergoing selection. Further work confirmed that other species contained a huge amount of variation.

The solution to this surprising observation was the recognition that most of the alleles were neutral. The variation is explained by fact that fixation by random genetic drift is much slower than fixation by natural selection. Thus, while the variation is transient in the sense that it is a snapshot of an ongoing process, the process is not selection but drift.

The results of Hubby and Lewontin (1966) led directly to Neutral Theory.

The neutral theory also asserts that most intraspecific variability at the molecular level (including DNA and protein polymorphisms) is selectively neutral, and is maintained in the species by the balance between mutational input and random extinction. In other words, the neutral theory regards protein and DNA polymorphisms as a transient phase of molecular evolution and rejects the notion that the majority of such polymorphisms are adaptive and actively maintained in the species by some form of balancing selection.
                M. Kimura

This explanation is also known as the Neoclassical Theory. Balancing selection is now thought to play only a minor and insignificant role in the cause of variation in a population.

... the neoclassical theory is not refuted by occasional observations of overdominance for fitness, because the theory does not deny that cases exist but only that they are common and explain a significant proportion of natural variation. So it is no use trotting out that tired old Bucephalus, sickle-cell anemia, as a proof that single-locus heterosis can exist. Anyone who has taught genetics for a number of years is tired of sickle-cell anemia and embarrassed by the fact that it is the only authenticated case of overdominace available. “If balancing selection is so common," the neoclassicists say, "why do you always end up talking about sickle-cell anemia?"
                R. Lewontin

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[Photo credit: The photograph of Richard Lewontin is from (Photographs of Participants in the Molecular Evolution Workshop)]

Where's the Evidence for Intelligent Design Creationism?

 
Denyse O'Leary has friend named David Warren. Warren writes articles for newspapers and he and Denyse are friends because they both worship at the church of anti-Darwinism. Over on Post-Darwinist Denyse brags about the latest article written by her friend [ Another Toronto journalist takes swat at Darwinists (or Darwinoids)]. Note the title of the blog article. It's more of the same old, same old, "Darwinist" baiting. Turns out that 99.9% of the IDiot movement is about attacking evolution (their version) and 0.1% is about presenting evidence for intelligent design. (And even that tiny amount of evidence has been refuted or shown to be irrelevant.)

So what about David Warren? Is he any different—don't hold your breath. Here's the article that he wrote for some Canadian newspapers [Panspermianism]. The main point of the article is supposed to be that panspermia is ruled out because scientists have shown that DNA won't survive in outer space (*yawn*). But the real purpose of the article is to whine about the evil atheist materialists and how they are suppressing the IDiots.

Much of the “star chamber” atmosphere, that has accompanied the public invigilation of microbiologists such as Michael J. Behe, and other very qualified scientists working on questions of design in organisms and natural systems, can only be explained in this way. The establishment wants such research to be stopped, because it challenges the received religious order, of atheist materialism. Any attempt, or suspected attempt, to acknowledge God in scientific proceedings, must be exposed and punished to the limit of the law; or by other ruthless means where the law does not suffice.

There's more, but you get the idea. The IDiot movement is scientifically bankrupt. They have no scientific evidence to back them up so the only thing they can do is lash out at their opponents. When is the last time you've seen an article from an IDiot that explains any evidence for the existence of an Intelligent Designer? That's right, hardly ever. Is there a reason why they don't support their case with real data? Yep, you bet there is. And that's exactly why they have to stoop to attacking "Darwinism" at every chance they get. They don't have any other option. Pathetic, isn't it?

[Image credit: The photograph is from one of my students, Zarna. That's her in the picture. She took it last December in India (Oh My God)]

Should Cloning Humans Be Legal?

 
In the July 21 issue of New Scientist, Hugh McLachlan thinks that we should legalize cloning of humans [Let's legalise cloning].

But why are we so against the idea of cloned human babies? As a bioethicist specialising in reproductive issues, I believe it has more to do with an irrational fear of cloning than any logical reason. All the arguments in favour of a ban describe risks that we accept quite easily and naturally in other areas of reproduction.

One argument against human cloning is the idea that it is morally wrong or undesirable to create replicas of people. But although a clone has the same gene set as the adult from which it was cloned, environmental factors will ensure that the resulting individual is not an identical copy, either psychologically or physically. What's more, we accept genetically identical people in the form of twins. If anything, clones would be less alike than twins because they would be different ages and be brought up in different contexts. Objecting to cloning on these grounds makes no sense.

I agree with McLachlan. Aside from the safety issue, there doesn't seem to be any good reason to forbid the cloning of humans.

This is a topic that's frequently discussed in "ethics" classes. I've never really understood what "ethics" actually means—but I'm working on it. The cloning of humans isn't an ethical issue for me personally because there isn't a conflict between two versions of what I think I ought to do. However, maybe it's an ethical issue for society as a whole because there are some people who think that it is unethical to clone people. Is that right? What's unethical about it?

Do we define "ethical" issues in terms of conflict between different groups? If so, is there a way of distinguishing between issues where the two sides are almost equally represented and those where one side has an overwhelming majority? For example, is the cloning of humans still an ethical issue in a society where 99% of the population is opposed? Does it cease to be an ethical issue if 99% are persuaded to accept human cloning?

Amazing Grace

 
Last night we saw a screening of the film Amazing Grace in a small cozy theater. At the end of the movie there was a fascinating talk by one of the producers Ken Wales. We learned a lot about how the film was made.

The film follows the efforts of William Wilberforce to abolish slavery in the British Empire at the end of the eighteenth century. Wilberforce and his close friend William Pitt the Younger, who became Prime Minister in 1783, finally succeeded in eliminating slavery by 1807.

There's mention of the fact that Wilberforce was a Christian and some of his allies were preachers but this isn't an important theme. The movie makes it clear that Pitt, who was a prime mover in social change, did not share Wilberforce's beliefs. During the discussion afterward it was clear that the religious motivation was important to some people.

The title of the movie comes from the song Amazing Grace whose words were composed by John Newton, an ex-slave trader who converted to Christianity. Newton, who has a significant part in the movie, influenced Wilberforce and served as his mentor.

One interesting scene depicts a debate in the House of Commons in 1778. The newly elected Wilberforce is advocating the withdrawal of British forces from America, thus abandoning the attempt to put down the rebellion. Wilberforce is attacked and challenged to distinguish between appeasement and surrender. "It's merely a question of timing," he says.

This scene, and many others, reveal that Great Britain was a functioning democracy at the time of the American Revolution. It contrasts markedly with the general impression of Americans who tend to think that this sort of representative democracy was invented by them in 1776.

William Wilberforce's third son was Samuel Wilberforce ("Soapy Sam") who became the Bishop of Oxford and debated evolution with Thomas Huxley in 1860.