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THE COURT: Be seated, please. You can pick it up where you left off, Mr. Muise.
Q. Thank you, Your Honor. Dr. Behe, before we broke we were talking about how proteins aren't simply colored squares or hexagons, that they are far more complex than that, including what makes them stick together in any particular order, and I want to return back to that. We put up a slide which has some indication I believe of proteins, and I'd like you to explain what you meant, that they're more complex than just these colored hexagons.
A. Yes, sure. Let me preface my explanation by saying this, that in talking about these matters there's kind of, an intelligent design proponent and a Darwinian theorist who have different goals.
A Darwinian wants to persuade his audience that evolution isn't all that difficult, it's doable, and so will not always attend to all the complexity of a system, whereas in order to show the difficulties for undirected unintelligent processes, an intelligent design proponent has to show all of the very severe complexity of systems, and that's often times hard to do because people often times don't have the patience to attend to it, but I apologize in advance but I have to attend to some of the complexities here.
So on this slide there are three figures taken from a biochemistry textbook by Voet and Voet of the protein, of the same protein, a protein named hemoglobin. Hemoglobin is the protein that binds oxygen and carries it from your lungs and dumps it off in peripheral tissues such as your fingers and so on. Now, this is a rendering of the structure of hemoglobin, and actually this rendering itself does not show the full complexity of hemoglobin. Let's focus --
Q. You're referring to Figure 8-63 on this slide?
A. Yes, that's correct. Let's focus on this yellow glob here. You'll notice a number of circles. They represent atoms in one of what are called the protein chains of hemoglobin, but the amino acids in that protein chain are actually different. So if it was actually rendered in more detail you would see a lot of different colors of atoms, indicating different groups and so on, and the identity of all these amino acids is also frequently very critical to the function of a protein.
Hemoglobin itself consists an aggregate of four proteins designated here by the blue and the green and the light blue colors, and it is the aggregate of the four protein chains, that is the active molecular machine in this cell that carries oxygen from your lungs to your tissues. Nonetheless, a drawing like this of such a complex system is often times bewildering to students, and so artists with the proper purpose of getting across some conceptual points to students will draw simplified renditions of the same figure.
For example, in the lower left here this is also supposed to be a rendition of the same protein hemoglobin. But in here the only atoms that are represented are things called the alpha carbons of each amino acid, and the artist has kind of shaded it to show the different directions in which the protein chain is heading. One can also to make a legitimate point to students simplify the drawing even further, and here's another rendering of hemoglobin in Voet and Voet.
Here each very, very complex protein chain is rendered as a simple square, and the O sub 2 represents the oxygen that each protein is supposed to be carrying. Now, all of these are legitimate renderings of the protein hemoglobin, but when we discuss these matters and we discuss difficulties with evolution and we discuss arguments for intelligent design, we have to keep in mind that this is the actual protein, this is the actual machine in the cell, and so these are the things that we have to deal with.
Q. Again that last figure you're referring to is 8-63?
A. That's right, uh-huh.
Q. And the two previous, the one just previous to that was Figure 10-37 and the one prior to that 10-13?
A. That's correct. Now, let's consider a further point. We have this yellow conglomeration of circles representing the atoms of the protein chain, with this blue one and this green one and this light blue one. Why do they stick together? Why don't they just float away? How come they are in the arrangement they are? Why don't we have the yellow one over here? The green one down here?
Well, it turns out that proteins arrange themselves. Molecular machines are actually much more sophisticated than the machines of our common experience, because in our common experience with things like say outboard motors, an intelligent agent assembles the parts of those machines. But in the cell the molecular machines have to assemble themselves. How do they do that? They do it by having surfaces which are both geometrically and chemically complementary to the proteins to which they're supposed to bind, and I think --
Q. Do you have a slide to demonstrate that for us?
A. Yes, I do. I think it's the next one. Okay, remember here's another little cartoon version which gets rid of some complexity of the system in order to make an important point to students. This is also a figure taken from the biochemistry textbook Voet and Voet. This is meant to convey why two molecules, why two proteins bind to each other specifically in the cell. This one up here is supposed to represent one protein. The second one is supposed to be this greenish area, and it's supposed to have a depression in it in which the yellowish protein binds to and sticks.
Now, let me point out a couple of things. You'll notice that the shapes of the proteins are matched to each other. They're geometrically complementary, kind of like a hand in a glove. But not only are they geometrically complementary, they're also chemically complementary. You see these little circles and NH and this thing here? Well, these are chemical groups on the surface of the two binding proteins, and they attract each other. Certain groups attach other groups.
I think the easiest to understand is the one right here, there's a red circle marked with a minus sign in it. That indicates an amino side chain of a protein that has a negative charge. When it binds to the larger one, notice that on the surface of the larger protein there's this blue circle with a plus sign in it. That is taken, that is meant to indicate an amino acid side chain with a positive charge. Negative and positive charges attract. So therefore these guys stick together.
If this were a negative charge these two proteins would not stick together. They would float away from each other. It's not sufficient to have just one group in the protein be complementary to another group in a protein. Usually proteins have multiple amino acids that stick together and cause them to bind to each other. For example, look up here, this little circle labeled H. H is supposed to stand for something called hydrophobic, which essentially means oily. It doesn't like to be in contact with water.
It lines up with another H on the green protein so that the two oily groups can stick together and avoid water. So it's kind of like oil, you know, oil and water, they don't mix. If they're in this configuration the two oily groups can stick together and be away from water, and there are other groups, too, which I won't go into which exhibit things call hydrogen bonding which also help the proteins stick together.
So in molecular machines, in aggregates of proteins, all of the proteins which are sticking together have to have all these complementary surfaces in order for them to bind their correct partners. If they do not have the complementary surface, they don't bind and the molecular machine does not form. Now, interestingly, remember Darwin's theory says that evolution has to proceed in small steps, tiny steps.
Well, one way something like this might form is by, you have to have mutations that might produce each of these interactions at a time. For example, I think there's a quotation from an article in Nature which kind of make this point, and I'll explain it after I quote it, it's from an article by a man named John Maynard Smith, who is a very prominent evolutionary biologist who died about a year ago I believe, and he wrote in a paper called Natural Selection and the Concept of a Protein Space, which was published in Nature in 1970, "It follows that if evolution by natural selection is to occur, functional proteins must form a continuous network which can be traversed by unit mutational steps without passing through nonfunctional intermediates," and by unit mutational steps, we mean each of those pluses, each of those H's, each of those OH's and so on that I showed you in that little cartoon drawing on the previous slide.
If for example a mutation came along that changed a positive into a negative charge and disallowed an interaction that needed to occur, that would be a detrimental one. John Maynard Smith is saying that we need to proceed, you know, one step at a time. So the point is that those little colored squares are enormously complex in themselves, and further the ability to get them to bind specifically to their correct partners also requires much more additional information. It is not a single step phenomenon. You have to have the surfaces of two proteins to match.
A difficulty of getting two changes at once?
A. Yes, that's exactly right. If you can do this one tiny, tiny step at a time, then Darwinian evolution can work. If you need to make several changes at once, two, three, four, there were multiple interactions that were required for those two proteins to bind. If you need multiple interactions, the plausibility of Darwinian evolution rapidly, rapidly diminishes.
Q. And have other scientists made similar observations?
A. Yes. On the next slide an evolutionary biologist by the name of Allen Orr, who's at the University of Rochester, published an article in a journal called Biology entitled A Minimum on the Number of Steps Taken in Adaptive Walks in which he makes this similar point. He says, "Given realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying and substituting one mutational step neighbors. Thus, if a double mutant sequence is favorable, but all single amino acid mutants are deleterious, adaptation will generally not proceed," and translating that into more colloquial English it means that you have to change again those groups one at a time, and if you need to change two at a time in order to get a favorable interaction, then you are running into a big roadblock for Darwinian processes.
Q. Now, have you done any writing or research that emphasizes this particular point?
A. Yes. On the next slide I believe is a copy of an article that I published with David Smoke which was published last year in the journal Protein Science, which is entitled Simulating Evolution by Gene Duplication of Protein Features that Require Multiple Amino Acid Residues, and in this paper we were addressing exactly that problem. What happens if you need to change a couple of amino acids before you get a selective effect?
And the gist of the conclusion is if you need to change two at once or three at once, then again the expectation that that will happen at a probability becomes much smaller, the length of time one would have to wait for such a mutation to show up is much longer, the population size of a species would have to be much, much longer to have an expectation of such a mutation occurring.
Q. And this particular article, the one you wrote with David Smoke, you testified to previously?
A. Yes, that's the same one.
Q. I believe we have a diagram to further make this point?
A. Yes. Here again is a little simplified cartoon version of how proteins might interact, simply to point out the problem that is not apparent in the earlier drawings. Now I've made the shapes of those colored proteins, I've altered the shapes. Now the A is a circle and what's that, a C, the C is a rectangle, and the other proteins have other shapes. How do we get those to bind into a conglomerate molecular machine?
In order to get them to bind to each other we have to alter their surfaces to be geometrically and chemically complementary, and that is a large and long, tall evolutionary order. As a matter of fact, it's so tall that one can reasonably conclude that something like this would not be expected to occur. So the point I want to make here is that even if one was to have parts in the cell which if they could develop binding sites to bind to each other, and if that binding together would produce a new selectable property, that still does not help in Darwinian processes, because you still have the problem of adjusting many, many different things before you get the final result.
Q. And this diagram is a figure from the chapter that you wrote in Debating Design, is that correct?
A. Yes. That's Figure 2.
Q. And that's the chapter that you've already testified to previously?
A. Yes, that's correct.
Q. And I believe we have a slide with the figure legend?
A. Yes, that's right. I make this point exactly in my article in that book Debating Design. Let's just look at the bold and underlined text. It's says, "Thus, the problem of irreducibility remains even if the separate parts originally had individual functions." So even if the parts can do something on their own, that does not explain how one can get a multipart molecular machine in a cell.
Q. I just want to point out that that figure legend in the figure is from pages 352 to 370 in your chapter?
A. No, that's the whole chapter. The figure legend is on one of those pages.
Q. As well as that previous diagram?
A. Yes, that's correct.
Q. Dr. Behe, if I understand you correctly, so even if there are similar separate parts are in the cell, that doesn't explain irreducible complexity?
A. That's correct.
Q. Dr. Miller testified about something called the Type 3 secretory system, the TTSS, and he said that that showed that the flagellum was not irreducibly complex, do you agree with that assessment?
A. No, I disagree. That's a mischaracterization.
Q. Why do you disagree?
A. Well, I think we have some slides from Professor Miller's presentation, and he said that, let us start with the bacteria flagellum, and he has a drawing of the flagellum from a recent paper. Let me just make another similar point. You see these little three, four-letter abbreviations all over here? Each one of those is of the complexity of a hemoglobin molecule that I showed on an earlier slide. Each one of those has all the sophistication, all the needs to have very complex features to bind together that hemoglobin had.
Can you press the slide again to advance the figure on this same thing of Professor Miller's? Professor Miller says that well, okay, you start with the bacterial flagellum, and if you remove the pieces, then he says, press again, please, he says, "That leaves just ten," and he says, his characterization, his mischaracterization of my argument is that what's left behind should be non-functional.
And if we go to the next slide of Professor Miller's, he says, "But it's not. Those ten parts are fully functional as a protein secretion system," but again I tried to be very careful in my book to say that we are focusing on the function of the system, of the bacterial flagellum, and while a subset of the flagellum might be able to be used as something else, if you take away those parts it does not act as a rotary motor. So it is irreducibly complex as I tried to carefully explain. I'm sorry.
Q. So is it fair to say that Dr. Miller makes a misrepresentation of what your claim is by his representation?
A. This is a mischaracterization, yes, that's correct, and I think I pointed that out on the next slide. I pointed this out, as I said earlier we've debated this back and forth for a while. I pointed it out recently in my book chapter. I write, "Miller asserted that the flagellum is not irreducibly complex because some proteins of the flagellum could be missing, and the remainder could still transport proteins perhaps independently.
"Again he was equivocating, switching the focus from the function of the system to act as a rotary propulsion machine to the ability of a subset of the system to transport proteins across a membrane. However, taking away the parts of flagellum certainly destroys the ability of the system to act as a rotary propulsion machine as I have argued. "Thus, contra Miller, the flagellum is indeed irreducibly complex."
Q. Dr. Behe, even if that is true, doesn't the Type 3 secretory system help us to explain the flagellum, the development of the flagellum?
A. No, it does not help in the least. And that may be surprising to some people, so let me take a second to explain. Most people when they see an argument such as Professor Miller presents will naturally assume that well, perhaps this part, this system that had fewer parts, the Type 3 secretory system, maybe that was a stepping stone, maybe that was an intermediate on the way to the more complex bacterial flagellum.
But in fact a number of scientists have said that's not true, and perhaps we could see the next slide. Yes, thank you. For example, in a paper published by Nguyen, et al. five years ago they investigated the Type 3 protein secretion system, and they said the following, "We suggest that the flagellar apparatus was the evolutionary precursor of Type 3 protein secretion systems."
In other words, they're saying that from their investigation it looked like the more complex type or more complex flagellum came first, and then the system with fewer parts, the Type 3 secretory system came second and perhaps was derived from that. Exactly what the opposite of what one might first expect.
Q. Have scientists reached different conclusions?
A. Yes, and it turns out that other groups have reached different conclusions from those of Nguyen at all. For example, in a paper published by Gophna, et al. recently in 2003 in the journal Gene they write, "The fact that several of the Type 3 secretory system proteins are closely related to flagellar export protein has led to the suggestion that the TTSS has evolved from flagella. Here we reconstruct the evolutionary history of four conserved Type 3 secretion proteins and their phylogenetic relationships with flagellar paralog." And then they say, "The suggestion that Type 3 secretory system genes have evolved from genes and coding flagellar proteins is effectively refuted." In other words. They say that the conclusion of the first group was incorrect. Instead they suggest that the Type 3 secretory system and the flagellum developed independently of each other, perhaps from the same precursor gene. And I think on the --
Q. We have another study on this issue, correct?
A. Yes. I think that's right. In the year a man named Milton Sayer, who was the one of the authors, the senior author actually on the study by Nguyen, et al. that I referred to a couple of slides ago, wrote an article in a journal called Transient Microbiology called Evolution of Bacterial Type 3 Protein Secretion Systems, he says the following, "It is often not possible to prove directionality of an evolutionary process. At present, too little information is available to distinguish between these possibilities with certainty. As is often true in evaluating evolutionary arguments, the investigator must rely on logical deduction and intuition.
"According to my own intuition and the arguments discussed above, I prefer pathway for the Type 3 system deriving from the flagellum. What's your opinion?" So I think you can see from this the very tentative nature of the results regarding the Type 3 secretory system and the flagellum that in fact what is going on is very much up in the air.
Q. And again I believe we have another result from --
A. Yes. Let me apologize that again this is a complex subject, and so you really have to delve into it to come to a firm conclusion. This is a quotation from a review article by a man named Robert Macnab who was a professor of biology at Yale University who died in the year 2003, and this article was actually published posthumously. It's entitled Type 3 Flagellar Protein Export and Flagellar Assembly. It was published in journal Biochemica Biophysica Acta, and I underlined words that emphasized the tentativeness and the speculative nature of discussions on this topic.
Robert Macnab wrote, "It has been suggested that the Type 3 virulence factor secretion system evolved from the Type 3 flagellar protein export system since flagella are far more ancient, existing in very diverse genre than the organisms which are targets for Type 3 virulence systems. However, it is possible that the original targets were other bacteria. Also, the possibility of lateral gene transfer cannot be ruled out.
"Finally, one could argue that evolution from a less complex structure, the needle complex, to a more complex one, the flagellum, is more probable than the other way around," and he continues I think on the next slide, and I think I'll pass over much of this quotation and just go to the last line of his article, and he says, "As the above discussion indicates, there is much about the evolution of Type 3 systems that remains mysterious."
So let me point out that in the past couple of years we've had investigators suggest that in fact the flagellum came first and the Type 3 secretory system came after it. We've had other investigators suggest that the Type 3 secretory system came first and the flagellum came after it. We've had other investigators suggest that the Type 3 secretory system and the flagellum arose independently, perhaps from similar genes, so --
Q. Dr. Behe, so what do these widely different opinions mean?
A. Well, maybe we could go to the next slide. To me it means this. We see the little cartoon drawing of the flagellum here, and this is a cartoon drawing of the Type 3 secretory system.
Q. I'm sorry, this is one of Dr. Miller's slides?
A. I'm sorry, yes. This is Dr. Miller's slide. Science knows a lot of information about the structure of the Type 3 secretory system, a lot of information about the structure and function of the flagellum. It knows the sequences of proteins of the flagellum. It knows the sequences of the proteins of the Type secretory system. It sees many similarities between them, both in the amino acid sequence and function, and it still can't tell how one arose or whether one arose first, the other second, or whether they arose independently.
So this to me drives home the point that such information simply does not come out of Darwinian theory. Much like our discussion of Haeckel's embryos earlier in the day, Darwinian theory can live with any result that experimental science comes up with on this question and then goes back and tries to rationalize the results afterwards post hoc, and so to a person like myself this exemplifies the fact in fact these results have nothing to do with Darwinian theory. They are no support at all for the claim that natural selection could have produced them. Quite the contrary.
Q. I just need to backtrack for one moment. If I may approach the witness, Your Honor?
THE COURT: You may.
Q. Dr. Behe, I handed you what's been marked as Defendant's Exhibit, 238 correct?
A. Yes.
Q. Is that the study from Nguyen that you referenced in your testimony on the section of the Type 3 secretory systems?
A. Yes, that's correct.
Q. It was inadvertently left out of your book, but I just wanted to make sure you identified it as an exhibit. You can just keep that with you and I'll retrieve it later.
A. Thank you.
Q. I want to see if I can get you correct, Dr. Behe. It's your opinion that this also shows that even knowledge of the structure and sequences of two systems doesn't necessarily give a clue as to how these systems might have arisen, is that true?
A. That's exactly right.
Q. And could you explain that further? And I believe we have some additional slides for that.
A. Yes, I think some text with actually Professor Padian wrote as part of his expert report illustrates this problem, and I'd like to quote you several sections from that report. On the next slide Professor Padian said the following. He said that, "Darwin's main concern, however, was with the mechanism of natural selection, which cannot be observed directly in the fossil record."
So to me this means you cannot see natural selection. You see fossils, and how you classify those fossils and what explanations you come up with them is not based directly on the evidence. Rather, it's provided by your theory. And I think we have a further quote from Professor Padian. He said the following, and this is a long quote, so --
Q. If you could read it a little bit slower for our court reporter when you are reading these quotes, please? Thank you.
A. Okay. "Molecular biology has produced tremendously powerful tools to compare the DNA sequence of all manner of living organisms, and a few extinct ones, and so help to derive their evolutionary relationships. However, molecular systematics can say nothing about the relationship or role of fossil organisms to each other or to living lineages," and he gives an example.
"For example, several recent molecular analyses agree that whales and hippos are each other's closest relatives. From this conclusion some authors have suggested that because both kinds of animals spend time in the water, their common ancestors would have been aquatic. Only the fossil record could show that this inference is incorrect. Therefore, hippos and whales, even if they are each other's closest relatives among living animals, did not have a common ancestor that lived in the water, but that was terrestrial. Only paleontological research and materials could demonstrate this."
And let me make a point about this. Professor Padian is saying that molecular studies of DN A sequence of whales and hippos suggested or led to the suggestion that both animals had aquatic ancestors. But they didn't. They had terrestrial ancestors. That means that the molecular information is compatible with either result, with the ancestors being aquatic or the ancestors being terrestrial.
That means that the molecular information can't decide what the ancestors were and therefore it can't tell what the selective pressure was or other factors of what might have caused an ancestor of those organisms to produce what we see in the modern world. So that means that does not speak to Darwin's claim that natural selection drove evolution, okay? Well, molecular data can't decide the question.
But nonetheless, Professor Padian told us that paleontology did. Paleontology discovered what seemed to be ancestor of both hippos and whales, and saw that they are terrestrial organisms. So can paleontology tell us whether it was natural selection that drove the evolution of these organisms? Well, no. On the previous slide he said explicitly natural selection is not shown directly in the fossil record.
That means that there is nothing that can show from the fossil record or from molecular data that current organisms derive by a process of natural selection from organisms in the past or how such a thing might have happened. That means that in fact the inference that such a thing did is simply a theoretical construct in which we try to fit that data into our current theory. The current theory either predicts it, does not predict it, and may be consistent with such evidence, but a lot of theories might be consistent with the same evidence.
And I think that, bring it back to the flagellum, I think that's illustrated in the flagellum and Type 3 secretory system 2. We know all the molecular data, we know lots of structural and functional studies, and yet we still can't tell how natural selection could have produced them.
Q. So are you saying then at best the evidence, and you were talking about sequence comparisons and in particular the fossil record, at best they may be consistent with natural selection but they also may be consistent with any number of mechanisms that might be derived?
A. That's exactly right. Perhaps intelligent design, perhaps complexity theory, perhaps something else. But consistent does not, is not the same thing as evidence for a theory.
Q. And the next slide we have is another quote from Dr. Padian that I'd like you to comment about.
A. I think this also throws light on this topic. Professor Padian said in his expert statement, he said, "Darwin was not talking about how major new adaptive change took place. He was talking about how minor variations could be selected. He was really talking about the baby steps of evolution. He made only the most passing references to how new major adaptive types might emerge," and I could comment that no one disputes or certainly no one I'm aware of disputes that Darwinian processes, Darwinian mechanism, can explain some things in life. And certainly nobody disputes that baby steps could be explained by random mutation and natural selection. It is exactly the new major adaptive types and new molecular systems for myself as a biochemist that is the focus of dispute.
Q. So again though when you say nobody refutes, is that saying that intelligent design does not refute this notion of baby steps that Dr. Padian is referring to?
A. That's right. It is very happy to say that Darwinian processes are consistent with those.
Q. Here I believe is a continuation of that particular statement from his report.
A. Yes, this is Professor Padian continued, referring to Darwin, he said, "Though he was convinced that would happen in the course of time," and let me just comment on that. Well, that's interesting that he was convinced that would happen, but another way of saying that is that Darwin assumed that these small changes would add up to larger changes, or to major new adaptive features, but that is exactly the point of contention. And for a point of contention an assumption is not evidence, let alone proof. So I see this as very pertinent to the question of things like the flagellum Type 3 secretory system and other things as well.
Q. So is it clear, I guess in summarizing you think that the flagellum is in fact irreducibly complex, correct?
A. Yes, that's right.
Q. Does that affect necessarily the positive argument for intelligent design?
A. Well, yes. Let's perhaps we can look at another slide here that I just wrote out some text to make this point clear. It's this. For the past number of, past hour or so we've been talking about the argument against Darwinian processes, but I want to re-emphasize to say that it is important to keep in mind that the positive inductive argument for design is in the purposeful arrangement of parts.
Irreducible complexity, on the other hand, is an argument to show that Darwinism, the presumptive alternative to design, is an unlikely explanation. However, one also has to be careful to remember that Darwinism isn't positively demonstrated by attacks on the concept of irreducible complexity. Darwinism can only be positively supported by convincing demonstrations that it is capable of building the machinery of the degree of complexity found in life. In the absence of such convincing demonstration it is rationally justified to think that design is correct.
Q. So an argument against irreducible complexity is not necessarily an argument against design?
A. An argument against irreducibly complexity is not an argument against design, and more importantly it's not an argument in favor of Darwinian evolution.
Q. Have other scientists agreed that Darwinian theory has not yet explained complex biochemical systems?
A. Yes. I recall there on that slide that I say Darwinism can only be positively supported by convincing demonstrations, and almost everybody agrees that such demonstrations have not yet been forthcoming. For example, on the next slide these are quotations taken from a number of reviews of my book Darwin's Black Box, most of these are by scientists. The first one James Shreeve, a science writer, but all of them making the point that we do not yet have Darwinian explanations for such complex structures.
For example, James Shreeve, the science writer, writing the New York Times said, "Mr. Behe may be right that given our current state of knowledge, good old Darwinian evolution cannot explain the origin of blood clotting or cellular transport," and James Shapiro, who is a professor of microbiology at the University of Chicago, wrote in a review that, "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations."
Jerry Coyne, who's a professor of evolutionary biology at the University of Chicago wrote in a review of the book in the journal Nature, "There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. We may forever be unable to envisage the first protopathways."
And Andrew Pomiankowski, who is an evolutionary biologist I believe at the University College London, wrote in a review in New Scientist, "Pick up any biochemistry textbook and you will find perhaps two or three references to evolution. Turn to one of these and you will be lucky to find anything better than 'evolution selects the fittest molecules for their biological function.'"
So this is a sampling of writings by scientists agreeing with the point that no, we do not have these demonstrations yet that Darwinian processes can produce complex biological systems.
Q. And these were scientists, and in one case a science writer, who are commenting on your particular book, correct?
A. Yes.
Q. And have scientists in other contexts made similar claims?
A. Yes, another good comment on this was by Franklin Harold, who I mentioned before, he's an emeritus professor of biochemistry at Colorado State University, and in his book The Way of the Cell published by Oxford University Press in 2001 he kind of echos James Shapiro. He says, "We must concede that there are presently no detailed Darwinian accounts of the evolution of any biochemical system, only a variety of wishful speculations," and perhaps I might add that besides these people one can add also complexity theorists, who also like Stuart Kauffman who also deny that such things have been explained in Darwinian theory.
Q. Sir, have some scientists argued that there is experimental evidence that complex biochemical systems can arise by Darwinian processes?
A. Yes, there have been a total of two such arguments which I regard to be very important, because these were claims that there had been experimental demonstrations, not just speculations, not just stories, but experimental demonstrations that either irreducible complexity was incorrect or that complex systems could be built by Darwinian processes.
Q. And one of those claims was raised by Dr. Miller, is that correct?
A. That's correct. I think on the next slide we see that he wrote in his book Finding Darwin's God ,which was published in 1998, he said, " A true acid test used the tools of molecular genetics to wipe out an existing multipart system and then see if evolution can come to the rescue with a system to replace it."
So here he was making the point well, here one test of this claim of irreducible complexity and the ability of Darwinian processes to make complex systems, well, is to find a complex system in a cell, destroy it, and then see if random mutation and natural selection can come back and replace it. And I have to say I agree that's an excellent test of that claim. However, I disagree with Professor Miller's further comments and conclusions.
Q. What was the particular system that he was looking at?
A. Well, he was referring to what is shown in a little cartoon version on the next slide. This is a figure again taken from that biochemistry textbook by Voet and Voet discussing a system called the lac operon. Now, an operon is a little segment of DN A in a bacteria which codes for a couple of genes, and genes code for proteins, and the proteins usually have related functions or function as a group, and one of them is called the lac operon which is used to, the proteins of which are necessary for the bacterium Escherichia coli to metabolize a sugar called lactose, which is a milk sugar.
And it consists of a number of parts. No, let's go back one slide, please, I'm sorry. All these little squares here, this little green thing represents a very complex protein called a repressor, which will bind to the DNA, and when it binds there it stops another protein called an RN A prelimerase from binding to the same spot, and therefore the information carried by these genes is not expressed, and that's important because the sugar lactose is usually not present in the bacteria's environment, and making proteins that metabolize lactose in the absence of that sugar would be wasting energy.
So the bacterium wants to keep that turned off until lactose is around. So the repressor turns off the operon, and that means that the genes for these three proteins here are not turned on, not expressed. This first one, which is labeled Z, codes, is the gene for a protein called a beta galactosidase, okay? That's actually the enzyme which chops up lactose. We don't have to go into the detail of how that happens.
This little thing marked Y codes for something called a permease. Now, a permease it turns out is a protein who is job it is to allow the lactose to enter the bacterial cell. The bacterial cell is surrounded by a membrane which generally acts as a barrier to largish molecules, and there's this specialized protein, this specialized machine called a permease which, when lactose is around, grabs the lactose from outside the cell, turns it around, and allows it to enter to the inside of the cell.
In the absence of that permease the lactose might be present in abundance in the bacteria's environment, but it can't get inside the cell. And so the bacterium can't use it. One other detail of this before I go on is that this repressor kind of sticks to the beginning of the gene and turns it off, but when lactose is present in the environment a small molecule which is a derivative of lactose can bind to the repressor, and that, and again start thinking in terms of the complex shape and structure of hemoglobin, when that happens it interacts in specific ways in order and causes the shape of the repressor to change, and that changed shape makes it now no longer geometrically and chemically complementary to the site that it bound on the lac operon, and it falls off. So in the presence of the inducer the repressor falls off, this prelimerase can come along and those proteins get made in the cell.
Q. Would you like the next slide?
A. Yes, thank you. Now I'm going to simplify, after that discussion I'm going to try to simplify nonetheless. So let me just list some parts of the lac operon. There's the galactosidase, the repressor, the permease, all three of which are proteins, and something that I've written IPTG/allolactose. That is the small molecule which can bind to the repressor and cause to it fall off of the operon, allolactose is something, is a metabolite of lactose itself, and that's the substance which usually binds to the repressor in the cell, but there's also an artificial chemical called IPTG, which stands for isopropyl thiogalactoside, which is sold by chemical supply companies, which mimics the action of the allolactose, and when a scientist comes and dumps some IPTG into the beaker, that binds to the repressor and causes those genes to be expressed, to be turned on.
Okay, those are the parts of the lac operon. Now, for purposes of further illustration let me just mention that in E. coli there are thousands of genes, and many of them are grouped into operons. Unbeknownst to the experimenter, whose name is Barry Hall, there also existed in the E. coli another operon called the EBG operon, which he called it that because it stands for evolved beta galactosidase. He thought this protein evolved in response to the selective pressure that he put on it, and it turns out that that operon also codes for a galactosidase, another galactosidase and another repressor as well.
Q. So this was the system that Dr. Miller was talking about in --
A. Yes, I'm afraid this is the background for the system that he started to discuss in his book.
Q. Which he sees it as experimental evidence to refute the irreducible complexity claim?
A. Yes, that's right, and if you look on the next slide you'll see the part of his book where he discusses that. He says of the system, he says, "Think for a moment. If we were to happen upon the interlocking biochemical complexity of the re-evolved lactose system, wouldn't we be impressed by the intelligence of its design. Lactose triggers a regulatory sequence that switches on the synthesis of an enzyme that then metabolizes lactose itself.
"The products of that successful lactose metabolism then activate the gene for the lac permease, which ensures a steady supply of lactose entering the cell. Irreducible complexity, what good would the permease be without the galactosidase? No good of course." And he continues that same discussion on the next slide, he continues, "By the very same logic applied by Michael Behe to other systems, therefore, we can conclude that this system had been designed, except we know that it was not designed. "We know it evolved, because we watched it happen right in the laboratory. No doubt about it, the evolution of biochemical systems, even complex multipart ones, is explicable in terms of evolution. Behe is wrong."
Q. Is Dr. Miller right?
A. No. Dr. Miller is wrong. Now, Professor Miller is always enthusiastic and he always writes and speaks with great excitement, but I say that when you examine his arguments closely, under close inspection they simply don't hold up and this is enormously exaggerated, and the results of researcher Barry Hall that he is describing here I would happily have included as an example of irreducible complexity in Darwin's Black Box.
So let me please try to explain why I say that. Reading Professor Miller's prose one would get, and I certainly did get when I first read it, the impression that this system was completely knocked out in that it completely came back under the experiments that Barry Hall conducted. But it turns out of this multipart system, only one part, the protein beta galactosidase, was knocked out by experimental method.
Everything else, the repressor, the permease, and we'll see later IPTG, and importantly as well other proteins which did very, very similar jobs in the cell, were left behind. And the worker Barry Hall himself was always very careful to say that he was only knocking out that one protein.
Q. The galactosidase?
A. Yes, that's correct. I think on the next slide he makes that point. This is a quotation from a paper by Professor Hall recalling his experiments that he did earlier on the lac operon. He says the following, "All of the other functions for lactose metabolism, including lactose permease and the pathways for metabolism of glucose and lactose, the products of lactose hydrolysis, remain intact. Thus, reacquisition of lactose utilization requires only the evolution of a new," and this should be a beta, "beta galactosidase function."
So let me point out that what he did in his laboratory was to take an E. coli bacterium and using molecular biological methods to knock out or destroy the gene for that one part of the loc operon, the beta galactosidase. He left the permease intact, he left the repressor intact, everything else was intact. He just had to get one more component of the system.
And what he saw was that he did get bacteria that were again able to use lactose. And when he did the experiments in the 1970's, that's all he saw. He saw he had bacteria that could grow when they were fed lactose. But years later after methods had developed and after he had the ability to do so, he asked himself what protein was it that took over the role of the beta galactosidase, and he named it EBG, evolved beta galactosidase.
But when he looked at it further he found it to be a very similar protein to the one that he had knocked out. Essentially it was almost a spare copy of the protein that had been destroyed. So this slide makes a couple of points. Let me just point to a couple. The EBG protein that took the place of the beta galactosidase is homologous to lac proteins. That's a technical term, that means they're very similar. Their protein structures, their sequences are pretty similar, and odds are good that they have the same sort of activity.
What's more, after further investigation Professor Hall showed that even the unmutated, even the EBG galactosidase before he did his experiment, the unmutated galactosidase could already hydrolyze, although it was inefficient. So again this was almost a spare copy of the protein, and I think on the next slide, I'll skip that last point on the next slide to drive home the point I want to show you what are the amino acid sequences of the area around what's called the active site of the protein, which is kind of the business end where the lactose binds and where the chemical groups reside which will cause it to be hydrolyzed into two component parts.
Notice this. Look at these sequence of letters. Now, I know that they don't mean much to most people in here, but notice the sequence of letters, these are the amino acid sequences, abbreviations for the amino acid sequence of various beta galactosidase enzymes found in E. coli and a related species. Notice here, let's start in here, there's an R here, HEHEMYEHW. Look up top, there's RHEHEMYEHW, the same thing on the lower one, too. They're active sites, their business ends are almost identical. Like I said, these are essentially spare copies of each other.
Q. So in fact it wasn't a new evolved element to this system. It was a spare part that was already existing?
A. Well, it was there and it did undergo small changes. But nobody, nobody denies that Darwinian evolution can make small changes in preexisting systems. Professor Miller was claiming that a whole new lactose utilizing system had been evolved in Barry Hall's laboratory, and that's, you know, that's very, very greatly exaggerated.
Q. Again do you have additional slides to emphasize the point?
A. Yes. This might be hard to explain, but Professor Hall says in one of his papers that, "The evidence indicates that either AS-92 and sys trip 977," these are the same of some amino acids, "are the only acceptable amino acids at those positions, or that all of the single based substitutions that might be on the pathway to other amino acid replacements at those sites, are so deleterious that they constitute a deep selective valley that have not been transversed in the two billion years since those proteins emerged from a common ancestor." Now, translated into --
Q. Yes, please into English.
A. -- more common language, that means that that very similar protein could only work if it became even more similar to the beta galactosidase that it replaced, and if you then also knock out that EBG galactosidase, no other protein in Professor hall's experience was able to substitute for the beta galactosidase. So the bottom line, the bottom line is that the only thing demonstrated was that you can get tiny changes in preexisting systems, tiny changes in preexisting systems, which of course everybody already had admitted.
Another interesting point, another interesting point is shown on that figure from Voet and Voet, the inducer, this little red dot, this little red dot actually stands for this chemical that binds to the repressor which changes its shape which causes it to fall off of the operon and allow the prelimerase to come in and transcribe that information. Well, it turns out that the EBG operon, this place in the DN A and E. coli that had that spare beta galactosidase, did not have a spare permease.
So the system was stuck, because it didn't have its own permease. When the repressor binds to this operon, the normal lac operon, if there weren't any lactose around then the repressor would be essentially stuck there indefinitely. And even if lactose were present outside the cell, it had no way to get inside the cell. So what Barry Hall did to allow his experiment to continue was that he added the inducer. He added that artificial chemical IPTG that he can buy from a chemical supply house, and he took some and sprinkled it in the beaker for the specific purpose of allowing the bacteria to survive so that it could take these small little steps to produce a new beta galactosidase.
Q. You have a slide to demonstrate that?
A. Yes. And Barry Hall was always very careful to explain exactly how these experiments were performed, and he brought it directly to the attention of readers when he described his system. For example he writes, "At this point it is important to discuss the use of IPTG in these studies. Unless otherwise indicated, IPTG is always included in media containing lactose," and that italics is Barry Hall's emphasis. He wanted to make sure his reader understood exactly what he was doing.
"The sole function of the IPTG is to induce synthesis of the lactose permease and thus to deliver lactose to the inside of the cell. Neither constitutive nor the inducible of all strains grew on lactose in the absence of IPTG." In other words, if this intelligent agent, Barry Hall, had not gone to the store and gotten some IPTG to help the bacteria survive, they would not have lived. This would not have occurred in the wild. This tells us virtually nothing about how Darwinian evolution could produce complex molecular systems.
Q. So again this system would not have worked in nature but for Barry Hall interjecting the IPTG to make this system work?
A. Yes. I should point out that Professor Miller does not mention this aspect of Barry Hall's experiments in his discussion, in his book Finding Darwin's God.
Q. Is that a significant oversight?
A. Well, I certainly would have included it.
MR. MUISE: Your Honor, we're about to move into the blood clotting system, which is really complex.
THE COURT: Really? We've certainly absorbed a lot, haven't we?
MR. MUISE: We certainly have, Your Honor. This is Biology 2. It's a quarter past, and if we're going to go until 4:30, it's probably not worthwhile to start up on the blood clotting because it's fairly complex and heavy and a lot of it is going to be --
THE COURT: Well, we don't have an issue as to his availability through the day tomorrow I assume?
MR. MUISE: He's available, Your Honor, for as long as we need him.
THE COURT: Any objection if we --
MR. ROTHSCHILD: No. He started it.
THE COURT: I was just waiting to see what you'd say.
MR. MUISE: We've gone from Biology 101 to advanced biology. So this is where we get.
THE COURT: We will recess then for today, and we'll reconvene at 9:00 tomorrow and we will pick up with Mr. Muise's direct examination at that time. So have a pleasant good evening, and we'll see you tomorrow.
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text:
Quoting from Ralph and Carter Stanley with the Clinch Mountain Boys from their 1963 album, "Good Old Camp Meeting Songs,"Who will sing for me?" The whole stanza goes like this:
Oft I sing for my friends
When death's cold hand I see
When I reach my journey's end
Who will sing one song for me
I wonder (I wonder) whoThis is likely a common concern of all of us mortals. Part of the answer lies in the work we are doing as genealogists. We not only sing, we write the songs. Its time we realize and help others realize where the songs come from, and the stories and the pictures. They come from us; the ultimate collectors; the genealogists. Let's get some genealogy pride going here.
Will sing (will sing) for me
When I'm called to cross that silent sea
Who will sing for me

subset: commoncrawl


text:
Ken Burns Exciting Digital News
Innovative App to Premiere February 2014
New Companion Website, "Ken Burns America," Featuring Resources For All of Burns's Films, Also Launches in February on pbs.org
(New York, NY) – February 10, 2014 – The Ken Burns App, launched for iPad on February 10, 2014, sets the stage for an innovative look at more than two centuries of American history from a curated look at selected excerpts from the entire library of Ken Burns and Florentine Films programs seen on PBS stations nationwide. The app can be found in the Apple app store at: https://itunes.apple.com/us/app/ken-burns/id723854283?mt=8
Marking the filmmaker's first complete catalog foray into the digital space, the Ken Burns App is one part of a digital initiative that will enable fans to experience and explore the films as never before. Also in February PBS, Burns's broadcasting network since his first film, THE BROOKLYN BRIDGE aired in 1982, and WETA, the Washington, DC public television station, will officially launch a newly created website dedicated exclusively to the work of Burns and Florentine Films — a comprehensive destination culled from Burns's more than 25 documentary films.
A short video about the app is available here: http://youtu.be/97onxUHpxjY
The Ken Burns App was conceived, directed and produced by his longtime friend Don MacKinnon. Florentine Films producer Sarah Botstein, who worked with Burns on JAZZ, THE WAR and PROHIBITION, worked closely with MacKinnon to produce and curate content for the project. The digital agency Big Spaceship collaborated with the team to create a platform on which to view Burns's work and experience his films in a new way.
Burns also added his own voice in exclusive interviews and created six thematic playlists — with selected scenes from his films — that illustrate how a specific theme shaped American history. For each playlist — Race, War, Innovation, Art, Hard Times and Politics — Burns has provided extensive filmed introductions, putting the selected stories in context, telling behind-the-scenes stories, connecting the moment to the larger theme. As a result, users see how, as Burns describes it, "the collisions of free electrons of a scene from this film and a scene from that film made 20 years apart suddenly interrelate in a new way."
"Our films are made in a small town in New Hampshire over many years, with images and stories woven together in a way that we hope brings experiences of the past into the present," Burns continues. "Working with some of the most talented people in tech today, we've tried to rethink how we can tell the story of America using our films and technology. Apple has long used an element of my filmmaking in its programs, which they call the Ken Burns Effect. I'm so excited to now be using Apple's platforms to create a radically new way to present my work and reach new viewers."
The app — developed exclusively for the iPad — seamlessly integrates with other platforms to let users further explore specific films they discover. Users can watch curated scenes inside the app. They can tap a button to be directed to where they can acquire an entire film via shopPBS, iTunes or Netflix. Each scene is also linked directly to dedicated pages on the newly launched PBS website, Ken Burns America (pbs.org/kenburns), where users will find a rich resource of information about each film.
MacKinnon, who first met Burns and Botstein 1999 when they collaborated on the music release for JAZZ while MacKinnon was head of Starbucks Entertainment, remarks, "Through his films, Ken Burns reinvented how we experience the stories of our history. With this app, we're able to bring his films together in a way that allows them to cross-pollinate one another, revealing the most relevant themes of the American story."
The Ken Burns America website, created in partnership with PBS and WETA and developed by Kapow, Inc., will officially launch in February. Through the generous support of The Better Angels Society, a non-profit dedicated to helping Burns tell America's stories, and PBS, the Ken Burns America website was created to serve as an integrated online presence for the films. The web site and educational materials will be free. While the Ken Burns app is free and has free content, there is a $9.99 charge to access all of the app's content. The app will also be discounted for educators.
On this new website, users have access to hundreds of photographs, primary source materials, interview excerpts and media spanning the entire body of Ken Burns's work, organized both chronologically and geographically. The site features essays, biographies and a screening room, as well as information about each film and the filmmakers.
A rich resource for educators, the website was designed to allow teachers to access more than 75 classroom lessons, as well as search through film clips, resources and assets by theme and topic. The lessons were developed for use in grades 7-12, but are adaptable to other grade levels and include complete background information, discussion questions, extension activities and objective evaluation measures.
All educational materials address key curriculum subjects such as social studies, U.S. and world history, civics and government, and geography and were designed to support critical thinking and reasoning, problem-solving, creativity and innovation, media literacy, communication and collaboration, and other life skills.
Burns further remarks, "The iPad app and the PBS website allow me to talk about and present my work in an entirely new way — one that reveals how my films interrelate. I could not be more excited by this opportunity to engage everyone through these ongoing, evolving platforms, using the flexibility of the digital world."
Burns noted that his films will continue to premiere on PBS, with "THE ADDRESS" scheduled for April 15, 2014 and "THE ROOSEVELTS: AN INTIMATE HISTORY" airing September, 2014.
Burns's 1994 film BASEBALL remains the most-watched series on PBS with a cume of 43.1 million, followed by the premiere broadcast of THE CIVIL WAR in 1990, which had a cume of 38.9 million. Rounding out the top five Burns premieres of all time are NATIONAL PARKS in September 2009 with a cume of 33.4 million, the encore of THE CIVIL WAR in September 2002 with a cume of 32.1 million and finally JAZZ in January 2001, with a 30.6 million cume.
Other Burns films include THE DUST BOWL (2012), PROHIBITON (2011), THE WAR (2007), JAZZ (2001) and LEWIS AND CLARK: THE JOURNEY OF THE CORPS OF DISCOVERY (1997) .


text:
Chinese stimulus hopes give markets a boost
LONDON Chinese stocks led the way Wednesday as investors grew more confident that policymakers in the world's second-largest economy would back another batch of stimulus measures.
The catalyst to the optimism across the markets was a Chinese government pledge to maintain policies intended to strengthen the economy and an expression of willingness to "fine tune" them and make them more effective.
China's main Shanghai Composite Index jumped 2.9 percent to 2,031.91 while the smaller Shenzhen Composite Index soared 3.8 percent to 771.72. Hong Kong's Hang Seng joined in on the act too, ending 2.2 percent higher at 22,270.91.
Those gains helped shore up stock markets in Europe despite an unexpectedly big 1.2 percent monthly decline in retail sales across the 17 European Union countries that use the euro in October. However, the euro fell on the news, and was trading 0.1 percent lower at $1.3086.
"As we saw following the global recession in 2008, a strong Chinese economy could help drive the recovery once again, with growth currently sluggish at best in most major economies," said Craig Erlam, market analyst at Alpari. "Any news which is pro-growth in China is always going to be well received in Europe and the U.S."
In Europe, the FTSE 100 index of leading British shares was up 0.2 percent at 5,881 while Germany's DAX rose the same rate to 7,447. The CAC-40 in France was 0.3 percent higher at 3,589.
Wall Street was poised for a solid opening too with Dow futures up 0.4 percent and the broader S&P 500 futures 0.3 percent higher.
The focus in the U.S. though will likely remain on the progress of negotiations between the White House and Congress on a deal to avert the so-called "fiscal cliff" of automatic spending cuts and tax increases at the start of the new year. Without a deal, the U.S. could well fall back into recession and push much of the world down with it.
Despite political posturing and a deep divide on critical issues, most analysts think a deal acceptable to both President Barack Obama and congressional Republicans will be cobbled together before the end of the year.
Investors are also focusing on a raft of U.S. economic data due for release over the coming days. Later Wednesday there's a monthly non-manufacturing survey from the Instititute for Supply Management and the private payrolls survey from ADP. Both could impact upon expectations for Friday's official nonfarm payrolls report for November. The figures could be distorted by the impact of Superstorm Sandy, which battered much of the eastern seaboard.
"Fiscal cliff uncertainties and the impact of Hurricane Sandy may subdue jobs growth in the month," said Neil MacKinnon, global macro strategist at VTB Capital.
Earlier in Asia, the gains weren't just confined to China. Japan's Nikkei 225 index rose 0.4 percent to 9,468.84, its highest close since April 27 while South Korea's Kospi added 0.6 percent to 1,947.04.
Oil prices tracked equities higher, with the benchmark New York rate up 28 cents at $88.78 a barrel.


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A chronic illness can cause many changes in your life. It may affect your independence, challenge you financially and affect personal relationships. It may also be stressful to maintain and establish treatments or lifestyle habits necessary to keep you well. With these stresses plus the worry of the illness itself, it is not surprising that depression is a common complication in people with chronic illnesses. Type 2 diabetes is a common chronic illness that previous research has linked to increased risk of depression.
Researchers from the United Kingdom conducted a review of previous studies to look for a pattern of depression in patients with type 2 diabetes. The review published in Diabetologia, found that people with type 2 diabetes had 24% higher risk of developing depression.
About the Study
The systematic review included 11 previous studies. These studies had all looked for the development of depression in patients with diabetes type 2 compared to those without diabetes. A total of 48,808 patients with diabetes but without depression were compared to 123,713 people without diabetes or depression. Researchers followed the patients for 2-10 years and noted the development of depression.
The review found that patients with diabetes had a 24% greater risk of developing depression than those without diabetes.
How Does This Affect You?
The individual studies are observational studies which are considered less reliable than other study types. However, because the review includes such a large number of patients, the results are more reliable. In addition, many studies have shown that chronic illnesses, such as diabetes, are often risk factors for the development of depression. Given all of these factors, it is reasonable to believe that diabetes is a risk factor for depression.
Diabetes treatment should not only include steps to help manage blood glucose levels, but it should also include assistance in making necessary changes and managing stress. Support groups in person or online with other people with diabetes may help you learn strategies to decrease stress. Be aware of the signs of depression, including loss of interest in daily activities, fatigue, problems with concentration, sleep disturbance, or weight gain or loss. Talk to your doctor if you feel you may be depressed.
- Reviewer: Brian P. Randall, MD
- Review Date: 09/2010 -


text:
BREAKING: PDP Wins At Sanwo-Olu's Polling Unit #NigeriaDecides2019
The Peoples Democratic Party defeated the ruling All Progressives Congress at the Femi Okunnu polling unit, Lateef Jakande, Ikoyi where the APC governorship candidate in Lagos State, Babajide Sanwo-Olu, voted in the presidential poll.
The PDP presidential candidate, Atiku Abubakar, polled 52 votes to defeat President Muhammadu Buhari of the All Progressives Congress, who got 48 votes.
Details soon…
Interesting Times Ahead In Kogi As Dino Melaye Picks Guber Nomination Form
The Senator representing Kogi West Senatorial District, Dino Melaye, has picked the People's Democratic Party (PDP) nomination forms for the Kogi State governorship election.
Similarly, another aspirant, Abubakar Suleiman, also picked the nomination documents for the Kogi election billed to hold on November 16.
The duo picked their nomination documents at the Abuja national secretariat of the PDP on Thursday.
Addressing journalists shortly after the nomination formalities, Melaye his decision to contest the election was informed by the agitation, clarion call and passion from people of Kogi state.
"The ambition is not mine but that of the people of Kogi state. There is the dire need to recover our state which has been completely battered, shattered and destroyed.
"Today, the magnitude and intensity of killings in Kogi State surpassed any other time in the history of our state. The state has never experienced such insecurity before.
"I have looked for people who believe that the welfare of workers of Kogi State is the basic priority of government and people who believe that security and the welfare of the people shall be the primary purpose of government and all these we will achieved
"Unemployment is on the high side. Retrenchment, sack and non-payment of salaries and pension are now a tradition in Kogi State. The economy and the economic activities in Kogi State have completely depleted. I have heard the loud cry from the Almighty and he said,: who do I send and I said, send me," Melaye said.
The controversial senator vowed to defeat Governor Yahaya Bello in the coming poll, saying, "We are resolutely determined to chase the mediocre in Lugard House.
"We are too sophisticated to have Yahaya Bello as a governor. We are too intellectually mobile to have a classless character like Yahaya Bello as governor.
"He never won an election. He is a coronated governor. Now for the first time, he is attempting to contest to be the governor through electioneering process. This is his first time and we will prove to him that we are masters in the game and we will separate the boys from the men"
Also speaking with journalists after picking his forms, Suleiman said Kogi is in dire need of change in leadership, stressing that things have deteriorated in the three-and-a-half years that Governor Yahaya Bello has been in the saddle.
Bemoaning the poor state of infrastructure and economy in the Kogi, Suleiman said workers have been reduced to beggars while victimisation and intimidation of the people had become the order of the day.
Stating his mission for joining the race, Suleiman said, "I have a priority policy document that I have worked on, which include: social infrastructure, fundamentals of government, physical responsibility and economic development.
"The policies are intertwined. For example economic development includes job creation; empowerment is related to physical infrastructure. My social infrastructure plans include health, schools and roads. All these will be given serious consideration".
Recall that another aspirant, Dr Joseph Ameh had obtained his nomination documents for the Kogi governorship race on Tuesday.
Judgement Day: Oyetola, Adeleke In Final Battle At The Supreme Court
The Supreme Court will today (Friday) give judgment in the four appeals filed by the Peoples Democratic Party (PDP) and its candidate in the last governorship election in Osun State, Senator Ademola Adeleke.
A seven-man panel led by Acting Chief Justice of Nigeria (CJN), Justice Ibrahim Muhammad had, after hearing the appeals on June 17, 2019 fixed July 5, 2019, for judgment.
Adeleke and the PDP are, by their four appeals, marked: SC/553/2019; SC/554/2019; SC/555/2019 and SC/556/2019, challenging the May 9, 2019 judgments of the Court of Appeal, Abuja which affirmed the election of Adegboyega Oyetola of the All Progressives Congress (APC) as the Governor of Osun State.
The Court of Appeal also set aside the majority judgment of the election tribunal which had allowed Adeleke's petition and declared him winner of the election.
By agreement of lawyers in the appeals, the court on June 17, 2019 took arguments from Onyechi Ikpeazu (SAN), for the appellant, and Wole Olanipekun (SAN), for the 1st respondent (Oyetola), in respect of appeal marked: SC/553/2019.
The court said its judgment in the main appeal – SC/553/2019 – will be applied to two other similar one, filed by Adeleke against the Court of Appeal's decision in relation to the appeals filed by the Independent National Electoral Commission (INEC) and the APC,marked: SC/554/2019 and SC/555/2019.
The court also took arguments from Ikpeazu (for the appellant), Yusuf Alli (SAN) for INEC; Bode Olanipekun (SAN) for Oyetola and Olumide Olujinmi, for APC in relation to the fourth appeal, marked: SC/556/2019.
In their arguments, lawyers to the respondents – INEC, Oyetola and the APC faulted the appeals and prayed the court to dismiss them for lacking in merit.
The respondents prayed the court to uphold the judgments as given onMay9, 2019 by the Court of Appeal in Abuja, which affirmed Oyetola of the APC as the winner of the governorship election held in september 2018.
In relation to the first set of appeals – SC/553/2019; SC554/2019 and SC/555/2019, ikpeazu urged the court to set aside the judgements of the Court of Appeal and restore the majority judgment given in his client's favour by the election tribunal.
In a counter-argument, Wole Olanipekun, Alli and Olunijmi faulted the competence of the appeals and urged the court to dismiss them for lacking in merit.
They prayed the court to uphold the May 9 judgments given in favour of the respondents by the Court of Appeal.
In arguing the fourth appeal: SC/556/2019, Ikpeazu urged the court to set aside the two concurrent judgments of the election tribunal and the Court of Appeal, in which both courts rejected Adeleke's request to void the supplementary election held after INEC declared the Osun governorship election inconclusive.
Ikpeazu said his client's contention was that INEC lacked the powers to have cancelled elections in some pooling units and order a rerun.
He argued that the supplementary election was unnecessary because his client had won the election and met the constitutional requirement to be declared winner.
Ikpeazu prayed the court to set aside the Paragraph 44 of the INEC's Guideline,on which basis the supplementary election was held,on the grounds that it conflicted with the Constitution.
Olanipekun's son, Bode Olanipekun (SAN) argued the fourth appeal for Oyetola, urged the court to disregard Ikpeazu's contention that the supplementary election was unnecessary.
He argued that Paragraph 44 of INEC Guidelines was not in conflict with the Constitution.
Olanipekun, who noted that Section 178(4) of the Constitution provides that the entire state is the constituency for a governorship election.
He argued that "where elections have not held in the entire state, the appellant cannot contend that he won the election, as against the 2nd respondent (Oyetola), who won the election as conducted across the whole of the state," Olanipekun said.
He urged the court to dismiss the appeal for lacking in merit.
Lawyers to INEC and the APC argued in similar vein, with Alli (for INEC) arguing that Ikpeazu's submission on reliefs 8and 9 of his client (Adeleke's) petition,overlooked the fact that election tribunal are special tribunal with limited jurisdiction to determine whether somebody was properly returned in an election.
"The quarrel of the appellant is against a concurrent findings of two lowers courts. There is no compelling reason to make this court interfere with the concurrent findings of the two lower courts," Alli said.
Olujinmi urged the court to be guided by its earlier decision in the case of Faleke v. INEC 2016 8 NWLR, prt 1543 pg 61, in which this court affirmed the limited scope of the jurisdiction of the election tribunal.
He noted that even though Adeleke and his party, the PDP are aware of this court's decision in that case (Faleke case), but have failed to approach the court for departure on its position on that issue.
Other members of the panel that heard the appeals Justices Olabode Rhodes-Vivour, Kumai Aka'ahs, Kudirat Kekere-Ekun, Amiru Sanusi, Paul Galunmje and Uwani Abbah-Aji.
(The Nation)
Nigeria Senate: Tension As 9th Assembly Elects Principal Officers Today
As the election of Nigeria's 9th Senate President and his Deputy comes up on (today) Tuesday with Senator Ahmed Lawan and Ali Ndume locking horns for the position, both former 8th Senate leaders are still gripped with tension.
It's particularly so, because the Clerk to the National Assembly, who is the administrative head has adopted a secret ballot system of Tuesday's election of principal officers of the Senate.
Initially, there was conflict of 'modus operandi' with skepticism from the Ahmed Lawan Campaign Group headed by Senator Yahaya Abdullahi that if secret ballot was adopted, there might be shocked despite Ahmed Lawan's adoption by the ruling All Progressives Congress.
While the Presidency's intervention has made the former Governor of Gombe State, who is also a ranking Senator, Danjuma stepped down for Lawan, his rival, Ali Ndume representing Borno South has insisted that it was late stepping down for anyone.
Between Ahmed Lawan and Ndume, no one has had the pendulum swung in his favour yet despite the acclaimed endorsement of some Senators-elect.
What further makes the situation looks gloomy is the dead silence of the Senators-elect of the Peoples Democratic Party (PDP).
Among PDP Senators-elect, most are still indecisive. Their silence is not only grooming, but heightening tensions all over the places.
Prodded to talk on the situation of things ahead of today, Senator Emmanuel Bwacha representing Taraba South Senatorial district confirmed that the party would take a unanimous decision on who to vote.
Speaking on reasons for PDP's silence even in few hours to the election, the ranking lawmaker said, "there is dignity in silence."
He further ruled out open ballot, stating that secret ballot has always been a tradition, insisting that Tuesday's election would not be different.
With PDP having 44 Senators-elect, they play a commanding decision as to who emerges as Senate President on Tuesday.
Meanwhile, PDP had scheduled a meeting last0 inviting all Senators-elect, House of Representatives-elect and governors at the instance of Rivers State Governor, Nyesom Nwike to hold at Rivers House As Okoro.
Sources close to the venue explained that the party would take a position ahead of Tuesday's election of principal officers of the upper and lower legislative Chambers. It also said, "the party would roll out conditions for supporting any candidate especially the Senate President."
The source added that the party became uncomfortable over the ruling APC's decision not to allow Chairmanship of Committees to any of its member irrespective of ranking or not. It added that so many factors would shape PDP's decision at the meeting today.
I'll Retrieve My Senate Mandate And Become Kogi Governor …Dino Melaye Reacts To Tribunal Sack Order
BREAKING: Tribunal Sacks Dino Melaye As Kogi West Senator, Orders Fresh Election
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Staff writer
The Centre High School girls' basketball team lost just one starter to graduation last year, so prospects look good for another successful year.
The team won 10 of its last 12 games in 2011-12, including the substate tournament, and went to the state tournament for the first time in many years.
Returning starters include two girls — Ellie Miller and Bryanna Svoboda — who did not play most of the season last year because of injuries but did letter and start in 2010-11.
"With four returning starters from the 2011-12 season and two more from 2010-11, as well as two top substitutes from last year, we return a lot of experienced players for this season," coach Allen Stahlecker said. "We are fairly tall up front and very athletic in the backcourt. We have a number of players who are capable of providing the scoring offense we need."
Three returning letter winners and starters are seniors, two are juniors, and one is a sophomore.
Beka Basore, a 5-foot, 10-inch senior, returns in the post position. She received all-league honorable mention last year.
Genesis Rudolph, a 5-5 senior, returns as a guard.
Cacey Simons, a 5-10 junior, will be a forward. She received all- league honors last year.
Shelby Makovec, a 5-5 sophomore, will be a point guard. She also received all-league honors last year.
Miller, a 5-7 senior, will return as a forward and will also play post.
Svoboda, a 5-7 junior, will be a point guard.
Letter winners Amy Makovec, a 5-2 junior, and Brenna Shields, a 5-5 sophomore, will play the guard position.
The 21-member squad includes five other sophomores — Cassidy Hill, Nellie Kassebaum, Callie Riffel, Kailyn Riffel, and Cassy Thompson — and five freshmen — Ally Basore, Taylor Peterson, Carissa Shields, Abigail Svoboda, and Kristin Vinduska. Two exchange students — senior Olesya Opanasyuk and junior Sualeha Mustafa — also are members of the team.
"We have a lot of young players who are still developing their skills for high school basketball," Stahlecker said. "Many of them have the potential to be contributors in the future."
Maintaining a healthy squad and developing skills and teamwork are his concerns for a successful season.
After a 3-7 start in 2011-12, Stahlecker is hoping the team's trip to state, along with its experience, will create the momentum for a better early season.
"The Herington Pre-season Tournament always provides some tough, competitive games," he said. "With a couple of new opponents on the schedule, there will also be some unknowns."
Stahlecker expects the teams in the Wheat State League to be balanced and therefore quite competitive. He expects his team to be in contention for the Wheat State League title.
He is in his fourth season as the head coach after five years as an assistant. His record as a head coach is 31-34. His team tied for third in the league last year and had an overall record of 13-10.
Stahlecker is assisted by Kim Shannon Shields, who is in her second season. Shields has a lot of experience working in a variety of sports. Stahlecker said that experience is helpful in dealing with various athletic abilities and personalities.
The season begins Nov. 30 with a home game against St. Xavier.


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diy lace Archive
Creative DIY T-shirt Ideas
As we can all notice, tees with cool graphics are standing out again this season. Not only is it an inexpensive way to achieve this look, but you can use your favorite brand and style of tee and have it feature whatever quote you want. You can even put a cool drawing on it. We
DIY Bow Back T-shirt Refashion
What you need most for this unbearable summer days is something that will make you feel comfortable. In our 100th article of the 365 DIY T-shirt project we will be showing you how to DIY Bow Back T-shirt Refashion. The DIY Bow Back T-shirt Refashion is created exactly for the hot summer days. You will
DIY T-shirt refashion: Crochet Trim Seam
Today we have the 99th article out of a 365 DIY T-shirt project. Since it's already all about summer here is another easy to do T-shirt refashion. Scroll below to see the new DIY T-shirt refashion: Crochet Trim Seam article. There are many designs to choose from, but I believe this DIY T-shirt refashion: Crochet
Off-the-Shoulder Ladder V-neck Tee
With this article we are continuing the series of 365 DIY T shirt project. Today is the 98th project, in which we'll be showing you how to refashion your old T-shirt into a lovely Off-the-Shoulder Ladder V-neck Tee. It's an easy DIY Off-the-Shoulder Ladder V-neck Tee with just a little bit of sewing. Nothing hard.
Easy Off-the-Shoulders dress
We should keep a special spot in our closet for old clothes and accessories because they will be stylish again at some point in our lives. So, in case you are wondering what to do with it, remember that what goes around comes around. Fashion comes back too. And of course there are too many


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CLO Ambassadors to Hold 16th Annual Wine Tasting & Silent Auction, 3/1
The Pittsburgh CLO Ambassadors hosted a Wine Tasting and Silent Auction preview party for sponsors and members of the press on January 29, at the Sheraton Station Square in Pittsburgh. The preview party was held to raise awareness for the Ambassadors' 16th Annual Wine Tasting and Silent Auction, which will take place Friday, March 1, 2013, at the Duquesne Club, and will feature wines from Capital Wine & Spirits.
Event guests will have the opportunity to sample premier wines as well as bid on unique silent auction packages. This year's packages include a walk-on role in a Pittsburgh CLO production, tickets to local cultural and sporting events, autographed memorabilia, fabulous getaways and once-in-a-lifetime experiences.
"Since its inception, the Wine Tasting and Silent Auction has raised more than $800,000 to benefit programs including the Pittsburgh CLO Academy, the New Horizons Program, Creative Vision and the Gene Kelly Awards," said Wine Tasting and Silent Auction Co-Chair, Lisa Woods of Burns White, LLC. "The CLO Ambassadors are pleased to have this opportunity to support quality arts education for young people in our communities."
"Lisa and I would like to invite and encourage everyone who recognizes the critical role the arts play in children's lives to attend this wonderful event on March 1st. Pittsburgh CLO Education programs reach more than 50,000 students in the region every year," added Co-Chair Stephen Bloomburg of Post & Schell.
This annual event sells out quickly. Tickets for the Wine Tasting and Silent Auction are available at two price levels and can be purchased online at pittsburghCLO.org or by phone at 412-281-3973 ext. 234.


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Program Evaluation
Overview of the Review Process
The program evaluation process at Excelsior College is intended to guide and support a culture of continuous quality improvement in the provision of student services and academic programs. By providing an ample body of evidence, program evaluation contributes to the assessment of institutional goals, provides useful information for data-driven strategic planning and decision-making, and guides the improvement of academic programs.
The College employs a multiple measures approach in its program evaluation, gathering data from multiple sources to triangulate and inform judgments about program effectiveness. The information collected and the reports produced through the process of program evaluation are also used to provide evidence to regulatory bodies, accrediting organizations, and other groups external to the College. Program evaluation at Excelsior College is congruent with the "Characteristics of Excellence in Higher Education Eligibility Requirements and Standards for Accreditation" as set forth by the Middle States Commission on Higher Education.
A. Each academic program at Excelsior College shall undergo program evaluations at no more than five-year intervals. The nature of this program evaluation is twofold: to provide the School and the administration a clear assessment of the program's strengths and weaknesses; and to provide the School with an opportunity for periodic self-examination.
B. The specific unit of analysis for each program will be the major or area of specialization of the degree or certificate program.
C. Due to the nontraditional nature of the College, there will be two levels of program evaluation. Programs in which Excelsior College offers 50 percent or more of the courses and/or examinations required for the major will undergo a comprehensive program evaluation. Other programs in which students must transfer in the majority of the credits required for completion of the degree or certificate will undergo a modified program evaluation.
D. All programs leading to a degree or certificate will be governed by the following program evaluation plans.
Programs undergoing a comprehensive evaluation must meet the following Excelsior College standards:
- Congruence with the Excelsior College mission and strategic plan
- Congruence with the School's mission
- Well-defined, measurable learning outcomes by which all program graduates are evaluated
- Commitment of adequate resources to achieve program goals
- Adequate student support services that are unique to the needs of the program
- Qualified, professional faculty
- Current, rigorous, and achievable program curriculum
- Financial profile
- Use of assessment results for program improvement
- Attention to environmental factors, societal need and demand, occupational and market considerations
- Evidence of student satisfaction
1. The evaluation report includes, but is not limited to, aggregated data collected, analyzed and summarized from reviews of the curriculum and student outcomes, end-of-program assessments, program success data over a five-year period (e.g., retention and graduation rates), course evaluations, graduate follow-up surveys, and employer and/or graduate school advisor follow-up studies.
2. Academic programs that are accredited by a specialized national accreditor conduct program evaluations as part of their accreditation process. Working together with the Institutional Effectiveness office (IE), these programs periodically create a program evaluation report that is submitted to the specialized accreditor. If the accrediting agency does not require a report at least every five years, the program should still conduct internal evaluations on a cycle of at least every five years. Therefore, programs that fall under this category may wish to adjust the timing of their program evaluation to coincide with the accreditation review or they may, with the approval of the provost, have the accreditation self-study serve as a portion of the internal program evaluation. However, all of the above criteria must be addressed; any significant program changes since the last external review must also be identified.
3. Each academic program which is not accredited by a specialized national accreditor is formally evaluated at least once every five years. All of the above standards must be addressed. The provost reserves the right to require an external review of any program in this category at any time.
4. Programs where students must meet 50 percent or more of the requirements for the major through external courses or examinations will undergo a modified program evaluation that includes a complete curriculum review as well as a review of the program's financial health (including enrollments) and a review of the program's end-of-course assessment, e.g. capstone. The program evaluation report will include, but will not be limited to: reviews of the curriculum requirements, student outcomes, end-of-program assessments, program success data over a five year period (e.g., retention and graduation rates), graduate follow-up surveys, and employer and/or graduate school faculty follow-up studies.
Programs undergoing modified programs evaluations must meet the following Excelsior College standards:
- Congruence with the Excelsior College mission and strategic plan
- Congruence with the School's mission
- Well-defined, measurable learning outcomes by which all program graduates are evaluated
- Commitment of adequate resources to achieve program goals
- Current, rigorous, and achievable program curricular requirements
- Financial profile
- Use of assessment results for program improvement
- Attention to environmental factors, societal need and demand, occupational and market considerations
- Evidence of student satisfaction
E. All degree and certificate programs undergo program evaluation on a continual basis. Ongoing review procedures related to the assessment of student learning are more fully documented in the Institutional Assessment Plan for Student Learning (IAPSL).
F. A multi-year schedule for formal program evaluation, self-studies, and accreditation reviews is determined by the provost in consultation with the Deans and is maintained by the IE office. The procedure for all program evaluations is as follows:
1. IE will contact the school at least 12 months prior to the due date of the formal evaluation. At that time, a schedule for the program evaluation will be agreed upon by the program and IE. In accordance with the practice of collaborative and participatory evaluation, this schedule will include communication needs between the participants (school representatives, IE staff, Center for Online Education, Learning, and Academic Services (COELAS), Enrollment Management, Marketing, Budgets and Financial Analysis, etc.) and an outline of deliverables by all parties involved.
2. The School in which the program is housed is responsible for preparing the self-study which must include recommendations for program improvement. IE can assist in conducting curriculum reviews and will provide reports on the results of alumni, employer and graduate faculty surveys.
3. The dean responsible for the program under evaluation will prepare the final report in an electronic format and send the self-study, plus any supporting documents/electronic files, to the provost office by the agreed-upon due date.
4. The provost will convene a meeting with the dean of the program under review to discuss the self-study.
5. The provost will prepare a summary report on the program evaluation. The summary report will include:
- A response to the recommendations in the self-study
- A review of the financial profile of the program
- A determination whether to continue, revise or eliminate the Program
- Any additional recommendations from the provost.
6. The provost's summary report will be sent to the dean within 30 days of the receipt of the self-study.
7. The provost will share the results of the program evaluation with the Executive Staff and the Board of Trustees.
G. Continuous Quality Improvement Process: An agreed-upon schedule for implementation and follow-up regarding any appropriate program revisions will be created. The report and the recommended program improvements will then be communicated to the Academic Affairs Council (AAC), the academic staff (for implementation), the college president and the Academic Affairs Committee of the Board of Trustees. Should it be determined that the program, for whatever reason, no longer meets the standards or needs of Excelsior College, the program will be referred for program elimination. The policy and procedures for the elimination of academic programs is covered under Policy 001 Program Evaluation.
H. Once the program evaluation process is complete, the report plus related materials will be available through the Program Evaluation Repository on the Excelsior College SharePoint site.


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The Green Question
"Here's a silly question," says Jack Schultz: "Why does the world remain green? Why don't the insects eat everything every year?"
Schultz, an entomologist who finds himself working on plants as often as on insects, likes to pose apparently simple questions — perhaps because he's been led into many an intriguing problem that way. Now he races headlong into the puzzle, pulling me after him in a sort of intellectual tag.


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This Week
An interesting research challenge is presented in "Divining faiths" at Nolichucky Roots: How to learn whether or not certain ancestors were Catholics, especially in places where public Catholic worship was not allowed?
At Roots and Rambles, Marian Pierre-Louis passes on an important lesson she learned from a CD history course: "Prove Genealogy Backwards, Read History Forward."
Many ethnic churches have been closed or will soon be closed, and others are losing their ethnic nature. Jasia at Creative Gene has been writing a series highlighting the background of some of these beautiful churches, "The Polish Catholic Churches of Detroit."
Some information we should all know and give some consideration to is presented in the post "Wisdom Wednesday: Top Ten Considerations for Donating Your Family Papers" at Sassy Jane Genealogy.
At Karen About Genealogy, Karen Packard Rhodes discusses "When it is Difficult to do Family History" – inspired by a tragedy that compels us to take a different perspective on black sheep ancestors.
And finally, presented for your consideration:
"Intentional Acts of Genealogical Terrorism with an Accomplice" at Hayley.
"Intentional Acts of Genealogical Terrorism" at Genea-Musings
"Intentional Acts of Genealogical Terrorism" at The Research Journal
Oh frabjous day, hoorah, hooray! Terry Snyder, The Desktop Genealogist Unplugged, is back at it!
Happy Second Blogoversary to Regina at Kinfolk News!
For more suggested genealogy blog reading, check out Randy Seaver's Best of the Genea-Blogs at Genea-Musings and John Newmark's Weekly Genealogy Picks at TransylvanianDutch.
This week I started following these blogs:
Day's Days
Gems of the Past
Kith and Kin Research: The Blog
The Canty Quest
Walking My Tree
Friday, October 15, 2010
Follow Friday: 15 October 2010
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