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Darwinian Evolution Needs Randomness
Charles Darwin suggested that life developed,
and new forms of life arose, through what he called descent and
modification. He led the way in offering a mechanistic explanation
of descent as a natural phenomenon, a process that follows natural laws.
His approach motivated later attempts to explain even the actual origin
of life on a mechanistic basis.
To account for descent, Darwin strove to explain how the vast complexity of life could have arisen from some simple life form. If such an explanation could be achieved, there was hope that one could also discover how that simple living form could have arisen in a natural way from inert matter. The entire existence of life could then be accounted for as a purely natural phenomenon, not requiring supernatural intervention. Darwin's agenda, thus, called for him to find a natural process to account for descent.
Recognizing the need for a physical mechanism to account for descent, Darwin hit on the idea that many heritable variations normally exist in a population, and many new ones appear all the time. Some of these variations can affect the fitness of the organism in its environment. Organisms that are unfit will perish - only those that are fit will survive. His reading of Malthus led him to conjecture that animal populations produce far more offspring than could possibly survive, and they hover constantly on the edge of misery and starvation. Under these circumstances, Darwin saw living organisms experiencing a fierce struggle for survival from which only the fittest would emerge.
He was mistaken in this conjecture, however, because plants and animals do not hug the brink of disaster. Population size is not controlled by starvation, disease, or predation. In most animal populations mass starvation and disease are rare; they occur only as the result of extraordinary catastrophes, such as droughts or epidemics. Moreover, predators do not overexploit prey populations. Many animal colonies are known to adjust their birth rates to match the available resources. Plants also are known to adjust their seed production to the space and resources allotted to them.
Darwin suggested natural selection, acting
over a long time on the variations in a population under conditions of
a struggle for existence, could transform the population into a new species.
He admittedly did not know the source of the variation, but he knew it
was there. In the sixth edition of The Origin, Darwin was hesitant
about labeling the variations as random, even though he had earlier referred
to them as having occurred by chance. He explained that he used the word
chance only to indicate that their causes are unknown.
He did not refrain from speculating on their causes, however. He felt there were definite causes for the variations. They could be caused by environmental conditions or they could come from the use or disuse of organs. But he did not want to call them random.
In the first third of the 20th century Darwin's theory was overtaken by new discoveries in biology. By the end of the 1930s the theory was in disarray. There were unanswered riddles and the theory was in serious need of repair and updating. In 1941, at a meeting of a the Geological Society of America, a suggestion was made that geneticists join with morphologists, taxonomists, and paleontologists to try to synthesize, from the latest findings in these disciplines, a modernized and consistent version of Darwin's theory. Specialists in these fields responded to the call, and over the next few years, they developed a revised theory of evolution. They called it the modern synthetic theory of evolution. The theory gradually became known as the neo-Darwinian theory of evolution, and its framers and their followers became known as neo-Darwinians. Their agenda called for a theory that could explain the development of life in a natural way. If they could account for the development of all the present complexity of life from some sufficiently simple first organism, the way would be prepared for a theory of a fully natural account of the actual origin of life.
Neo-Darwinian theory rejected Darwin's suggestion of the environmental induction of heritable variation, and even more emphatically rejected the inheritance of acquired characteristics. Hereditary elements, known as genes, had by now been discovered, and, although their molecular structure was still unknown, the neo-Darwinians had accepted the separation of the somatic and the germ cells as suggested half a century earlier by Weismann. It seemed clear to them that neither environmental influences nor acquired characteristics could affect the germ cells, and that heritable variation could stem only from changes in the germ cells.
Unwilling to accept environmental influence as a cause of variation and unable to find a mechanism that could directly produce changes needed for descent, the neo-Darwinians rescued randomness from the rubbish heap which Darwin had relegated it, and assigned it to function as the source of the variations. Some variations are detrimental to the organism, but others may be beneficial. The neo-Darwinians hold that a heritable variation of the latter kind, even if rare. will spread by natural selection, and will eventually take over the population.
The neo-Darwinians thus built their theory on random variation, culled and directed by natural selection. They identified the heritable variations required by the theory with the mutations discovered and named by De Vries in the early 20th century. A decade after the establishment of the neo-Darwinian theory, Watson and Crick identified the heritable variation of the theory with random errors in DNA replication.
If the neo-Darwinian agenda had worked out, there would be no place for a Creator in the origin of life except to establish the laws by which the evolution had taken place. Even that position would not be an honorable one if the appearance of man were not inevitable, as Gould believes it is not.
The Motif Of Neo-Darwinism Is Incompatible With Randomness
Random variation, however, turns out to be inadequate to account for evolution, and this inadequacy calls for a reexamination of neo-Darwinian theory. There is no evidence that random variation can play a role in major evolution advances as postulated by the theory. Indeed, there is evidence to the contrary - that randomness does not, and even cannot, play such a role.
The vast majority of random changes in the genome that have any effect on the phenotype are detrimental to the organism. The mammalian genome is a sequence of about 4 billion nucleotides, and a single error in DNA replication could change one of these nucleotides into another. There are an enormous number of different sequences those nucleotides can assume, only a very small fraction of which can result in a viable phenotype, and only a smaller fraction still will have a positive selective value, yielding an improvement over an existing population.
Since DNA was discovered to hold the code of life, conventional wisdom has held that errors in copying DNA are the source of the random variation called for by the neo-Darwinian theory. These errors occur in prokaryotes with a probability of between 10-10 and 10-8 per nucleotide per replication. In eukaryotes the rate is even lower. The error rate in eukaryotes is between 10-11 and 10-9 per nucleotide per replication. These error rates are low because a special proofreading mechanism in each cell checks and corrects the replication. The rates are just below the level of intolerability to genetic damage. Some think the system may even operate with the accuracy it does so as to maintain this level. The error rates could not be much larger if a species is to survive.
Because of these low mutation rates, no more than one specific mutation of this sort can be expected in a population of 100,000 in 100,000 generations. Two specific mutations would require 1015 generations. Since there is not enough time for 1015 generations, a specific double mutation will almost never occur. The probability of a double mutation occurring, for example, in a population of 100,000 animals within 100,000 generations is only 10-10. This is to be compared with the probability of a single specific mutation occurring in the same population within the same time, which is 1/e, or about 0.37. Thus with higher organisms, such as mammals, evolution can make a specific change in the genome of no more than one nucleotide (or base pair) at a time. Moreover, even if such a mutation is beneficial, it is highly unlikely to be retained by natural selection to the point where it dominates the population. To raise this probability to 1/e one would need about 1,000 times as many generations, or about 108 generations.
If evolution is to proceed through random nucleotide substitutions, then an adaptive improvement in the genome must be possible at any stage by a change of just one base pair. A long chain of such steps requires that there be long sequences of such changes, one after the other, each leading to an adaptive improvement of the organism. Moreover, because of the low probabilities involved, such evolution requires that there be not one, but many, long potential sequences of this kind. Indeed, the number is so large that many of these paths, or portions of them, would have been observed in the many genetic experiments performed since genetics became a science.
Whenever probability calculations have been made, they have shown that random point mutations cannot account for major evolutionary change. Calculations on the evolution of the horse, as induced from the fossil record, bear this out. All calculations based on neo-Darwinian theory show that major evolutionary events are highly improbable. Events that a theory predicts to be very improbable cannot be said to be accounted for by that theory. If a theory can account for data only by declaring them highly improbable, then the theory must be rejected. This is a fundamental principle in the mathematics of hypothesis testing.
More than 30 years ago I predicted that contradictions to neo-Darwinian theory would emerge when probability calculations could be made of so-called convergences. Such calculations can now be made. From the assumed convergence of the lysozyme enzymes common to ruminating cows and ruminating langur monkeys, one can set an upper-limit probability of 1054 to the probability that they evolved independently through random point mutations. It is less than the probability of your winning the New York State Lottery seven weeks in a row. Most people would consider such an event impossible.
A striking identity has recently been found between a gene in Drosophila and a corresponding gene in many vertebrates that plays a role in the development of the eye. The same gene has been found to control eye development in insects and in vertebrates, including humans. These genes are 94% identical between Drosophila and humans. The conventional wisdom until now has been that the eye is an extraordinary example of convergence in that it has developed independently as many as three or four dozen times. This new finding makes convergence in eye evolution look so improbable that, even without making any probability calculations, one author suggests that: "the traditional view that the vertebrate eye and the compound eye of insects evolved independently has to be reconsidered."
The neo-Darwinians claim they can account for the development of life from some very simple form. They must, therefore, account for the buildup of the information found today in the genomes of mammals and birds, fish and reptiles, all the invertebrates, and all the plants that inhabit the earth. This information is supposed to have been built up from such a simple organism as a single cell. If this information was built up, as the neo-Darwinians claim, by long series of small steps of random errors in DNA replication directed by natural selection, then each of these steps had to add, on average, a small amount of information. Information had to be generated little by little to accumulate to the large amount that resides in living organisms today.
It is easy to believe that single-nucleotide
substitutions are random, but they are not known to have added any
information to the genome. They are known to have produced minor
changes, even some with selective advantage in special cases. Geneticists
have been studying mutations in the laboratory for nearly a century, and
on the molecular level for a third of a century. But they have not found
a single mutation that adds information to the genome! Yet these
are the mutations the neo-Darwinian theory calls for to produce major evolutionary
No Mutations Are Known That Add Information
Random mutations do occur, but they do not add information to the genome. Some of these mutations may, under special circumstances, even have selective value and benefit the organism. But because they do not add information, they cannot represent the typical mutations required by neo-Darwinian theory. Most of the mutations in a chain of cumulative selection must be ones that add information. If evolutionary theory is to account for the increase of information in living things from a very simple primitive form of life to the complexity we find today, then each of its component steps must, on the average, add a little information. If the theory is to account for the general buildup of information in life, then this information must be new - not just new to the genome of that organism alone, but new to the "global genome" of the entire biosphere.
I cannot prove that there are no mutations that add information. I cannot even exhibit all known mutations to show that none of them adds information. Indeed, in principle, there could be such a mutation, but it would be improbable. The best I can do is to exhibit some well-known mutations that have been said to demonstrate neo-Darwinian evolution and show that they do not add information. I shall pick two examples of mutations. The first is perhaps the most well known among nonbiologists. The second, although not well known outside professional circles, is, I think, the most dramatic of the mutations that appear to lead to evolution.
My first example is a single nucleotide substitution in the DNA of a bacterium giving it immunity to streptomycin. Most cases of acquisition of drug resistance in bacteria involve the transfer of whole genes from other microorganisms that already have the resistance. Although the acquisition of a new gene does add information to the bacterial genome, the information is not new to the biosphere. It has already existed in other organisms. This is not the case, however, when a single copying error in the DNA leads to drug resistance. Let us take a look at how a random mutation leads to the evolution of streptomycin resistance.
Bacteria normally sensitive to streptomycin can undergo a random change of one nucleotide, granting them resistance to the drug. Is this an example of new information added to the genome? Can this mutation be a prototype of the mutations called for by the neo-Darwinian theory? Can it be of the kind that produce a long sequence of evolutionary steps that together add large amounts of information to the genome? Do we have here an example of neo-Darwinian evolution in action? Does this example contradict the theoretical consideration outlined above?
The mechanism of how streptomycin stops bacterial growth has been known for some time. Mycin molecules attach to a matching site on the bacterial ribosome, preventing the correct assembly of amino acids into protein. The mycin molecule fits into the matching site on the ribosome like a key fitting into a lock, as shown schematically in Figure 1 . Because protein is incorrectly made, the cell cannot grow or replicate. Mammalian ribosomes do not have the matching site for the mycin molecule so, while the drug affects the bacterium, it does not affect its mammalian host. That is why mycin drugs are useful antibiotics.
A point mutation in the right place grants the bacterium resistance by losing information. Figure 2 shows schematically how a change in the matching site on the ribosome can prevent the mycin molecule from fitting onto the ribosome and interfering with its operation. The change makes the bacterium resistant to the drug.
As you can see from Figure 2, the change could be in any one of several places on the matching site to make the bacterium resistant. Any one of several changes in the attachment site on the ribosomal protein is enough to spoil its match with the mycin. That means that a change in any one of several DNA nucleotides in the corresponding gene can grant resistance. Indeed, several different mutations in bacteria have been found to result in streptomycin resistance. We see then that the mutation reduces the specificity of the ribosome protein, and that is a loss of genetic information. This loss of information leads to a loss of sensitivity to the drug, resulting in resistance. Since the information loss is in the gene, the effect is heritable, and a whole strain of resistant bacteria can arise from the mutant bacterium.
Although such a mutation has high selective value in the presence of streptomycin, the mutation decreases rather than increases the genetic information. It therefore cannot be typical of mutations that neo-Darwinian theory requires for macroevolution. The steps required by the neo-Darwinian theory must, on average, add information. Even though the bacterium acquires resistance to the drug, it acquires resistance not by gaining information, but by losing it. Rather than say that the bacterium gained resistance, we would more correctly say that it lost sensitivity. In genetic-information content, the mutation is a loss rather than a gain. The loss of information is, moreover, manifest in the mutant's loss of viability. In the absence of streptomycin the mutants are less viable than the wild type.
My second example is the most striking illustration I know of random mutations granting selective value to an organism. It is actually a series of three mutations in the soil bacterium Aerobacter aerogenes. Experiments with these bacteria have shown what seemed to some investigators to be an example of the basic processes of evolution -- namely, the evolution of new enzymes. Bacteria grown in culture have shown they can learn to live and grow on new substances that they originally could not use. Several experiments of this kind have been reported.
The experimenters tried to see if the bacteria could evolve an enzyme that would metabolize a nonnatural sugar, similar to their natural nutrients, but on which their repertoire of enzymes would not work. They put the bacteria under strong selection pressure. They denied them their normal pentose-sugar nutrients, ribitol or D-arabitol, and tried them instead on several artificial pentoses. When they gave them xylitol, they found that, although the wild-type bacteria could not grow, mutants appeared that could. The experimenters extracted these mutants, denoted them as X1, and grew cultures from them. They found that the X1 strain grew on xylitol, but its rate of growth was only one ninth that of the wild type on ribitol.
They isolated the X1 strain and continued it on xylitol. A new mutant appeared within the culture that could grow even faster on xylitol. The experimenters extracted the second mutant, cultured it, and named the resulting strain X2. The growth rate of X2 on xylitol was nearly 2.5 times that of X1, but still less than the rate of the wild type on ribitol.
They isolated the X2 strain from the X1 and continued it on xylitol. A third mutant appeared that grew still faster on xylitol than did the X2. They extracted the new mutant, cultured it, and called the resulting strain X3. They found that the X3 grew on xylitol about twice as fast as did X2; but its rate of growth on xylitol was still not much more than half that of the wild type on ribitol. The three mutations were all found to be single-nucleotide substitutions, and there is every indication that they were random.
These experiments show that bacteria can sometimes find other ways of getting what they need when their normal nutrients are denied them. Moreover, they did it through random single-nucleotide changes. These experiments surely looked like neo-Darwinian evolution in action. The experiments appeared to show bacteria evolving through a series of three small steps. Can this short series of steps be part of a potentially long chain of steps leading to cumulative selection? Can these three steps, performed in a few months under artificial selection, serve as a model for long series of millions of steps over geological times under natural selection that might lead to macroevolution? Could these steps show the sort of evolution that primitive bacteria might have undergone? Could this be how bacteria developed their enzymes for the first time?
If we examine these experiments in detail, we see no new information entering the genome. Each of the three mutations made a gene less specific and lost information. Therefore, none of them can serve as a prototype for the small steps that neo-Darwinian theory says lead to macroevolution. None of the above experiments show the evolution of enzymes -- enzymes cannot be built by mutations such as these.
The wild type of Aerobacter aerogenes normally feeds on ribitol. The cell takes in ribitol from the outside and breaks it down in a series of steps, using a special enzyme for each step. The first of these enzymes is ribitol dehydrogenase (RDH).
Ribitol is a pentose sugar normally found in the soil. Xylitol, on the other hand, is a pentose sugar not found in nature, but its structure is similar to ribitol. Xylitol and ribitol are made up of the same atoms in almost the same arrangement. The difference between them is slight, yet the cell's RDH enzyme is specific to ribitol and discriminates against xylitol as well as other substrates. Figure 3 shows the structures of ribitol, xylitol, and another nonnatural sugar residue, L-arabitol (which I shall get to shortly). The figure does not show the three-dimensional arrangement of the atoms, but it does give an idea of how small the differences are between these sugars. Because the two sugars are so much alike, the same RDH enzyme that works on ribitol works also on xylitol, but with less activity. RDH hydrolyzes xylitol to make the same product it makes from ribitol. After this one step, all other steps in the metabolism of ribitol and xylitol are identical and are effected by the same enzymes. But, because the RDH is highly specific to ribitol, it works but poorly on xylitol.
The genes responsible for the metabolism of ribitol are turned ON only when ribitol is present. The parts of this control system relevant to our present discussion are shown in Figure 4. The gene, denoted in the figure by Y and which encodes RDH, is normally repressed, and therefore the RDH enzyme is not normally made in the cell. The presence of ribitol will induce gene Y to turn ON, leading to the synthesis of RDH. Moreover, molecules cannot easily enter a cell unless they are brought in by a special permease enzyme in the cell wall. The cell is selective about what it brings in from the outside. The permease enzyme is also not normally found in the cell until it is synthesized by the gene denoted by Z in the figure. Gene Z is normally repressed, and therefore the permease is not present. The presence of ribitol will induce gene Z to turn ON to transcribe the permease.
In summary, there are three problems that
prevent the wild-type cell from using xylitol. They are:
1. Although RDH has a small activity on xylitol, that activity is much lower than it is on ribitol.
2. Since ribitol is absent, gene Y will not turn ON and RDH will not be synthesized.
3. There is no permease enzyme to bring xylitol into the cell.
The X1 mutant partially overcame the above
problems through a point mutation in the gene that regulates the synthesis
of RDH. This regulatory gene encodes the protein that represents RDH transcription.
The mutation, whose point of effect is shown labeled (1) in Figure
4, did not change the RDH molecule itself. What it did was to disable
the repressor protein. As a result, there was no repressive control and
RDH was synthesized constitutively. The gene transcribed RDH without having
to be induced, and it did so at its maximum rate. RDH was made in such
abundance that, in spite of its low activity on xylitol, it converted enough
xylitol to allow the cell to function. The cell could function because:
1. Since the mutation disabled the repression of the gene transcription, the cell synthesized the RDH constitutively.
2. Unrepressed, the gene synthesized the RDH enzyme at its maximum rate. The large amount of RDH that was made helped compensate for its low activity on xylitol.
3. Although the cell has no transport system to admit xylitol, a small amount does enter by diffusion.
The X1 strain did not have a perfect solution to the three problems. It therefore grew much more slowly on xylitol than does the wild type on ribitol. Nevertheless, X1 can grow on xylitol alone, and the wild type cannot. But the benefit of the mutation came through a loss of information. Note that the mutation that destroyed the activity of the repressor could have been one of several mutations. It did not have to be a particular one: it was not specific.
The second step in the chain of three single-nucleotide substitutions converted the X1 strain into X2. This mutation changed the enzyme itself and raised its activity on xylitol. The point of effect of this mutation is shown as (2) in Figure 4. Because of the higher activity of the enzyme, the growth rate of X2 on xylitol was about 2.5 times that of X1. Because the mutation made the enzyme more active on xylitol, one might think the enzyme became more specific, and that genetic information is increased. But it turns out that the mutation leading to the X2 strain is just another example of a mutation making the enzyme less specific. Brian Hartley and his group at Imperial College in London studied this enzyme. They compared its activity in the X2 mutant with that of the wild-type enzyme, and they measured the activity of the two enzymes on ribitol, xylitol, and L-arabitol, another unnatural substrate. They found that, compared to the wild type, the mutant enzyme was less active on ribitol, more active on xylitol, and more active on L-arabitol.
Figure 5 presents the Hartley group's results in graphic form, showing a comparison of the reaction rates of the two forms of the enzyme for the three substrates. The enzyme in the wild type and the X1 strain is denoted in the figure by A; the enzyme in the X2 strain is denoted by B. The vertical scale shows the relative rate of catalysis. Note that the mutation transforming the X1 strain into X2 broadened the range of substrates that the enzyme could catalyze. The enzyme of the wild type (A) has a reaction-rate curve higher and narrower than that of the mutated type (B). An enzyme that is very specific would show a high and sharp plot of reaction rate. One that is less specific would be lower and broader. Figure 5 shows that the reaction rate of B is less specific than that of A. The new enzyme could accept a wider range of molecules as substrates than the old one; thus the mutation made the enzyme less specific, not more, and reduced the information in the genome.
One might have thought that if a mutation
causes an enzyme's activity to increase on a particular substrate, it must
be because the enzyme has become more specific to that substrate; but here
we see that this is not necessarily true. If an enzyme were really to become
more specific to one particular substrate, it should become not only more
active on that substrate, but it should become less active on all other
Figure 5 shows the wild-type enzyme's activity (A) with a high sharp plot, indicating high specificity, and the mutant enzyme's activity (B) with a lower and broader plot, indicating a lower specificity.
The specificity of an enzyme to its substrate is no less important to the cell than its level of activity. An enzyme that accepts any molecule as its substrate can be harmful. For an enzyme to be useful to the cell, it must limit its activity to its proper substrate.
The mutated enzyme of X2 also turns out
to be less stable than that of the wild type. Typically, when an enzyme
loses information, its function is degraded. The mutation leading to the
X2 strain is a point mutation and is indeed an example of a small random
change; it is an example of microevolution, but it cannot be typical
of a step in macroevolution. The typical step must gain some information.
The steps of macroevolution must, on average, add information to the genome.
The third mutation, which converted strain X2 into X3, improved the cell's ability to metabolize xylitol. This mutation was a single-nucleotide substitution in a regulatory gene controlling the synthesis of a permease enzyme for D-arabitol. The point of effect of this mutation is shown as (3) in Figure 6. Although the permease normally functions to transport D-arabitol into the cell, it turns out also to be able to transport xylitol. Normally the transport enzyme is not synthesized unless its gene is induced by the presence of D-arabitol. In the absence of D-arabitol a repressor protein keeps the gene OFF. So, even though the D-arabitol transport enzyme can work on xylitol, it is not normally present in the cell in the absence of D-arabitol. The mutation leading to strain X3 disabled the gene encoding a repressor protein that normally represses the gene encoding the permease. As a result the permease was synthesized constitutively. It was synthesized at the maximum rate and in large amounts without regulation. There was no need for its induction by D-arabitol.
Xylitol then gets a free ride into the
cell on the transport enzyme intended for D-arabitol. Much more xylitol
could then enter the X3 cell than could enter the X1 or X2 cell. Therefore,
X3 could grow on xylitol better than X2 could. As with the X1 and X2 mutations
before it, the mutation leading to X3 also reduced the specificity of an
enzyme and therefore caused a loss of information.
There Are Nonrandom Mutations That Can Lead To Evolution
I have indicated that it is highly improbable for random variation in the form of DNA replication errors to lead to any sizable amount of information getting into the global genome of life. I have also declared that I know of no example of mutations that have been alleged to add such information. In each case, even though the mutation is beneficial to the organism under special circumstances, I have shown that it actually leads to a loss of information from the genome. The important feature of these examples is that even though they can offer the organism a selective advantage, they cannot serve as prototypes of the mutations called for by the neo-Darwinian theory.
But there is a large and ever-growing body of evidence that heritable changes do occur in living organisms that adapt them to their environments, and that these changes do not stem from simple errors in DNA replication. In the last decade and a half, we have seen mounting evidence on the molecular level of large genomic changes that confer selective advantage and occur just when they are needed. These observations have so far been made only on bacteria. Directed mutations are also known to occur in plants, and there is evidence that they occur in animals as well. These mutations are not random, but are apparently induced by the environment. They are not merely errors in DNA replication, but seem to be mutations of a totally different kind.
In 1982 Barry Hall reported on an experiment in which he prepared a strain of E. coli bacteria lacking the beta-galactosidase gene lacZ, which normally hydrolyzes lactose. When these bacteria grew and multiplied on another nutrient, but in the presence of lactose, they gained the ability to metabolize lactose, an ability that proved to be heritable. The gained ability was found to be due to the presence of a new gene. The new gene encodes a new enzyme that can perform the function of the beta-galactosidase, enabling the mutant bacteria to metabolize lactose. The gene was present all the time, but in a dormant state. It was turned ON by two mutations that occur in the presence of lactose and do not appear in its absence. Hall declared that the "normal function" of this gene is unknown, and he called it a "cryptic" gene.
Neither of these two mutations alone gives the bacterium any advantage, so there could not have been any selection for them separately. For the cryptic gene to become active, both mutations have to occur. In the absence of lactose, these two mutations are independent. They can occur together only by chance, and will do so with a probability of only about 10-18 per replication. If they occur at random and independently, the expected waiting time for one of these double mutations to occur in Hall's population would be about 100,000 years. But in the presence of lactose, he detected about 40 of them in just a few days! One can conclude that the lactose in the environment was inducing these mutations.
In 1981 Ann Reynolds and her coworkers reported experimenting with E. coli, which cannot normally metabolize salicin because they lack an enzyme to catalyze the first step. They found that a mutation involving a DNA rearrangement occurs in the presence of salicin and turns ON what they called a "cryptic" gene, permitting the bacterium to metabolize salicin.
Hall later also grew bacteria in the presence of salicin. He found that Reynolds's cryptic gene encodes an enzyme that can catalyze the first step in the metabolic pathway of salicin. The cryptic gene is normally repressed by a regulatory gene, and it will become active if one of a few mutations occurs in the regulatory gene.
He used a strain of bacteria whose cryptic gene did not work. The cryptic gene did not work because there was an insertion sequence (IS), known as IS103, sitting upstream of the cryptic gene. The IS keeps the gene OFF because it shifts the coding frame and garbles transcription to mRNA.
For a bacterium of Hall's strain to metabolize salicin, two mutations had to occur. First, the sequence IS103 had to be precisely deleted. Then, a base substitution had to occur that would make the regulatory gene stop repressing the cryptic gene. He tried to measure the spontaneous rate of the precise deletion of IS103, and found it too low to measure. He could do no more than assign an upper limit of 2*10-12 to its probability. In the absence of salicin, the probability that the necessary two mutations would occur in a particular cell in a single replication is less than 10-19. That they occurred many orders of magnitude more frequently in the presence of salicin indicates that salicin may be inducing the mutations.
Cairns and his coworkers described another experiment with bacteria. They used a Lac- strain of bacteria, so called because the bacteria had a defective lacZ gene. The strain could not synthesize beta-galactosidase, and therefore could not metabolize lactose. Cairns's team fed lactose to these bacteria and looked for the appearance of mutants that could metabolize it. They found such mutants, and from the statistics of their appearance they concluded that the mutations appeared only in the presence of the lactose. They wrote:
The cells may have mechanisms for choosing which mutations will occur... Bacteria apparently have an extensive armory of such 'cryptic' genes that can be called upon for the metabolism of unusual substrates. The mechanism of activation varies... E. coli turns out to have a cryptic gene that it can call upon to hydrolyze lactose if the usual gene for this purpose has been deleted. The activation of (this cryptic gene) requires at least two mutations... That such events ever occur seems almost unbelievable.
When these experiments were first reported, they were met with skepticism. Their results brought into question the status of the principle of the independence of mutations from the environment. There were many attempts to explain the phenomena as resulting from the same kind of random mutations called for by the neo-Darwinian theory. Although some have suggested that Cairns's results indicate the failure of the principle, others have offered explanations that leave the principle intact. Further experiments, however, have dispelled these notions. Recent studies have shown that, in the presence of lactose, adaptive mutations activating a dormant gene encoding an enzyme that will hydrolyze lactose in E. coli are different from mutations that occur in the absence of lactose.
In addition to these recent observations of nonrandom mutations in prokaryotes, there has long been evidence of nonrandom variation in eukaryotes, including plants and animals. Seventy-five years ago Victor Jollos experimented with Paramecium aurelia, and found an environmentally-induced variation that was heritable. When the environmental stimulus was removed, the variation persisted in subsequent generations. An interesting feature of this work is that the original state of the organism returned after 40 generations without the environmental stimulus.
Many other examples can be given of environmentally-induced variations in plants and animals observed over the past hundred years. Taken together, the evidence indicates nonrandom variation, induced by the environment, may play an important role in evolution. These varied examples share a common feature: namely, that an adaptive variation can appear in large numbers in a population when it is needed. When adaptive nonrandom variation does occur, it is far more frequent than chance, and it appears in a large fraction of the population.
Proposed Mechanisms
On the one hand, the kind of evolution envisioned by Darwin and the neo-Darwinians cannot occur. Genetic information cannot be built up by random variation even with the directive force of natural selection. Yet we see that plants and animals can change when stimulated by environmental changes. We have even seen molecular details of such changes occuring in bacteria in response to environmental stimuli. Permit me to speculate on how the phenomena of environmentally-directed mutations observed in bacteria might be generalized and extended to multicelled organisms.
Living organisms respond to their environment on several levels. As Jacob and Monod have shown, the genetic control system senses the presence of an enzyme's substrate and turns ON the gene that encodes the enzyme. The cell's control system turns genes ON or OFF as they are needed, but makes no heritable change in the genome. This kind of control permits the organism to operate efficiently through specific short-term changes in the environment.
I have suggested that a straightforward extension of such controls, making their results heritable, can lead to changes in the long-term -- on an evolutionary time scale. Moreover, if the control is in the development process, even a small change of the "right" kind can lead to a large adaptive change in the phenotype. The "right" kind of change is unlikely to occur by chance. If the changes are random, the probability of a "right" change occuring is a function of the fraction of "right" changes among all possible ones. The number of "wrong" changes is so much greater than the number of "right" ones, that a "right" change is unlikely to occur by chance even in large populations and over immense periods of times. But, if the genome had the built-in ability for an adaptive change to be triggered by an environmental cue, then chance would not be a factor -- the right adaptive change would be elicited when it is needed.
What physical mechanism can produce environmentally-induced heritable variations? How could large amounts of genetic information be generated quickly? Environmental influence on the variation does not have to imply that it generate a substantial amount of information in the DNA. Indeed, if the environment merely triggers the genome to switch between n potential states, it generates no more than log2n bits of information. I suggest that most of the information necessary for organisms to adapt to their environment is already present in the organism, and no mysterious or ill-defined mechanism need be invoked to account for the generation of the few bits of information needed to switch.
As has been shown with the bacteria, the environmental trigger induces a change to an adaptive phenotype with no apparent role left to chance. There may, however, be some role here for chance. The environment may trigger not one, but a set, of genetic switches leading to a set of potential phenotypic outcomes. The trigger may be to one switch in some individuals, and to different switches in others. The resulting phenotype would then vary from one individual to another. Natural selection may then favor one of these types. The switch, triggered by the environment, may be seen as a coarse adjustment to adaptivity, and natural selection among the outcomes as a subsequent fine adjustment.
As with many bilogical phenomena, there is, I suggest, more than one mechanism that can lead to nonrandom adabtive variation. Nonrandom variations in the genome induced by the environment can be divided into two types, which I shall call Type I and Type II. Type I produces a change in the DNA base-pair sequence, and Type II produces only a change of state of the genome, but leaves its nucleotide sequence unchanged.
An environmental trigger that could produce a change in the genome was suggested about a decade ago by Wanner. Any change in the genome can be called a mutation, and all mutations have been conventionally assumed to be random and unrelated to the environment. Although many mutations apparently are random in the sense used here, there are many that are not. Single-base substitutions resulting from uncorrected random errors in DNA replication are indeed random. Their effects on the phenotype are independent of environmental influences, and they occur without regard for the organism's needs. They are simply errors.
As opposed to errors in the working of the complex cellular mechanism, there are mutations that are not errors, but that are directed by that cellular mechanism. They are called up when they are needed, and they are executed under tight cellular control. Genetic rearrangements, including insertions, deletions, amplifications, and inversions, have been observed to be under strict cellular control. An insertion sequence sometimes enters a gene and prevents it from transcribing its protein. The cell can also remove the sequence with perfect precision, allowing the gene to return to working order. Until recently, genetic rearrangements were thought to have no known functions and, therefore, were considered to be random. The experiments of Hall, Cairns, and others, however, have shown that through insertions, deletions, and point mutations, a bacterium can turn ON a cryptic gene, permitting the cell to metabolize a carbon source that was otherwise denied it.
A transposon is a large mobile genetic element that can transpose itself from one place to another in the genome. It carries within itself genes encoding some of the enzymes needed for its transposition, and the cell provides several others. Some transposons serve their host bacterium by carrying genes granting resistance to antibiotics. The jumping of a transposon is one of several kinds of genetic rearrangements. Deletion, amplification, and inversion are others.
Three adaptive deletions have been found in prokaryotes that are triggered by environmental cues. Two of them are found in the cyanobacterium Anabaena. If these cells are deprived of a nitrogen source, a DNA sequence is deleted from the genome. Deletions of sections 11 kilobases (kb) long and 55 kb long have been found. These deletions lead to the cell becoming dormant, presumably in an effort to conserve nitrogen. An adaptive deletion of 42 kb has also been found to occur in the bacterium Bacillus subtilis. Environmentally-induced DNA changes have also been reported in plants. The mechanisms of these inductions, however, are as yet unknown.
Many important genetic rearrangements are known to be nonrandom. Some are nonrandom in time, and all are nonrandom in their position on the genome. Some occur when they are needed, and seem to be environmentally induced (as in the bacteria in Cairns's and in Hall's experiments). And some, which are always needed and therefore do not require environmental induction, occur at random times in just the right place on the genome where they can be effective (as in Salmonella and in Trypanosoma). These nonrandom mutations are executed with precision and are under elaborate cellular control. Although genetic rearrangements have until now been thought of as random, to dismiss them as nothing more than chance events in an attempt to preserve the neo-Darwinian theory would be to ignore what nature is telling us. Various forms of genetic rearrangement help make up the set of Type I environmentally-induced adaptive variations.
Type II variations are different. They are environmentally-induced changes in only the state of the genome and they do not change the DNA sequence. Genetic states that dictate the current metabolic activity of the cell through enzyme synthesis are usually not heritable. A gene that is normally OFF needs a signal to turn it ON. It will be ON only as long as the turn-ON signal is present. Take that signal away, and the gene turns OFF. Similarly with a gene that is normally ON. The state of a gene or an operon depends on the presence of inducing or repressing signals, and is usually not heritable.
But some altered genetic states are known to be heritable. The most outstanding examples of heritable genetic states are the programmed changes that occur in embryonic development. As cells differentiate, genes are selectively turned ON and OFF, and their ON/OFF states are passed from mother to daughter cell: the state is heritable. Not every method of turning genes ON and OFF lends itself to being heritable. How cells during development pass on their genetic state to daughter cells is not yet well understood.
One way the cell has of establishing a genetic state and making it heritable is to attach a methyl group to one of the carbon atoms of the cytosine bases in the DNA. Methylation serves to keep the gene OFF by preventing regulatory proteins from attaching. When the cell wants to turn ON selected genes, it first has to remove the methyl groups, and then apply the regulatory protein. Methylation has been suggested as one of the ways in which the organism might control gene activity during development. The oattern of methylation is made heritable through an enzyme that acts during DNA replication. The enzyme copies the methylation pattern from the template strand of DNA onto the daughter strand as it is being constructed.
Another way of making a genetic state heritable is to have the gene (or operon) turn ON and OFF with a locking trigger. A trigger that turns ON an operon will lock it ON, if the operon's activity itself leads to the synthesis of a control protein that keeps it ON. Once such an operon is turned ON, it will remain ON even after the trigger is removed. Such a state can be heritable.
So far I have indicated only how an environmental cue can enter an exposed cell and cause a heritable effect on its genome. How could an environmental cue produce a heritable change in a plant or animal? Having the environment cause a heritable effect on an exposed cell is one thing. But creating a heritable effect on a multicelled organism, where the reproductive cells are isolated from the somatic cells, seems to be something entirely different.
Environmentally-induced changes seem more difficult to achieve in plants or animals than in single cells. For one thing, in multicelled organisms the environmental cue has to penetrate to the reproductive cells, or gametes. Second, the environmental stimuli that have been seen to trigger bacteria are relatively simple, while those that would trigger plants or animals would have to be complex. Can complex environmental cues get into the organism? We know they can because animals, for example, adjust their birth rate to match available resources. Plants are known to adjust their seed production to the available space. We know that complex stimuli can enter through the sense organs and be processed by the brain to produce appropriate physiological or psychological states such as stress. These states stimulate the production of hormones, which travel throughout the bloodstream to reach their targets in any part of the body. The target sites of some of these hormones could well be the reproductive cells, and there they could make a heritable change. These suggestions must remain speculative for the present until more is known of how environmental cues act. But herein lies a possible mechanism for observed evolution.
Nonrandom Evolution And Torah Hashkafa
I have here described the important role neo-Darwinian theory assigns to random variation. I have also noted that random mutations are unable to play that role, and that all the evidence points to the absence of a major role for randomness in evolution. I have suggested, instead, that any significant evolutionary change that occurs does so principally through nonrandom variations induced by environmental cues. A role has been left open for randomness and for natural selection, but this role is much attenuated from that assigned to randomness by neo-Darwinian theory. I suggest that changes in the environment drive the evolution of living organisms by triggering a switch to alternative genetic programs. The organisms have the built-in capability to adapt to a wide variety of environments.
How does this suggestion fit with Torah hashkafa? Is there room for such evolution, or for any evolution at all, within Torah? It turns out that the suggestion made here is derivable from Talmudic sources. Rabbi David Luria (RaDaL) indeed made such a derivation in his commentary to the Midrash Pirkei D'Rebbi Eliezer. From Talmudic and Midrashic sources he derived the necessity of animals to evolve. As Rabbi Luria interpreted the Midrash, there were 365 basic species (minim) of beasts created, and the same number of birds. All the others were derived from these. As each basic species moved into a different environment and found itself a new niche, it changed. The changes were dictated by the conditions under which it lived, including the food it ate. Rabbi Luria's conclusion is very much like the suggestion presented here.
The basic species, according to Rabbi Luria, can transform into new species as they are influenced by the conditions under which they live. The Sages of the Talmud (Tanaim, Amoraim) as well as the medieval commentaries (Rishonim) were aware of the phenomenon of domestic animals changing their characteristics in a heritable way when they become feral and vice versa. There is discussion in the Talmud, and in subsequent rabbinical literature, on whether the domestic ox (shor) and the wild ox (shor habar) are of the same or different species. One opinion is that the wild ox was originally a domestic ox that became feral, and therefore they are the same species (min). Another opinion is that the two animals belong to two entirely different species (minim).
It is well known that feral animals change on domestication. Darwin noted that domestic cattle undergo changes when they become feral. Some of the pigs given to the Maoris by DeSurville in 1769 and by Captain Cook in 1773 became feral. They were observed to have become very wild, cunning, and speedy. They were very different from the domestic pigs from which they descended. These wild pigs were indistinguishable from wild pigs elsewhere. It has also been observed that whenever wild pigs become domesticated the tusks of the boars become very much reduced, they lose their bristles, and the young are no longer striped. These changes are hereditary but the animals gradually revert back if they again become feral. Moreover, the changes from domestic to feral are always the same. They are not random.
Lurian evolution is the change of an organism under environmental influence. It is not the neo-Darwinian kind, but rather the kind I have just described. Conventional wisdom in biology states that characteristics aquired by an organism cannot be inherited. The environment may change an animal, but these changes have conventionally been held not to be heritable.
According to the central dogma of molecular genetics, the environment cannot cause an organized change in the genome. There is no way an outside influence can alter the genetic program in such a way as to make the organism adapt to that influence. There would have to be some way of reversing the genetic coding, and that seems difficult to do. One biologist has recently speculated how such an influence might be possible, but no one else seems to accept his speculation. The heritable variations appearing in living creatures are conventionally thought to be random in the sense that their effects on the phenotype are independent of the environment.
If living organisms had within their genes not just one development program, but several alternative programs that could be called up by a cue from the environment, then we could see how the environment can influence the genes. The environment can change the structure of the genes, or it can change their state. It can turn genes ON and others OFF in such a way that the new state is heritable.
The randomness of the variations claimed by neo-Darwinian theory, and which is essential to it, stands in major contradiction to Torah hashkafa. The neo-Darwinians need the randomness to arrive at a "natural" explanation for the development of life from a simple beginning. Had it worked, they would have reduced the development of life to a simple natural law. Much like the way the law of gravity accounts for a falling rock, so neo-Darwinian theory would have accounted for the development of life, from a simple unicellular organism to the great complexity of life we see today. Had they done that, they would have made the appearance of man a mere chance event.
Had the neo-Darwinians succeeded in establishing their case, the Torah believer would have had two choices: (1) he could simply reject the theory, believing that no matter how good the logic seems to be, there must be something wrong with it; or (2) he could engage in apologetics to show how the Creator and creation could be accommodated by smuggling Divine control into the randomness.
The first of these choices has been the one favored over the centuries. It is a robust choice, and has proved its merit as one scientific theory after another has fallen by the wayside. The second choice would be unsatisfying to any but the most commited accommodationist. If the theory works well, then a creation explanation is superfluous. But the Torah believer is not faced with this dilemma. I have shown that the neo-Darwinians have not successfully established their case, and randomness therefore cannot play the important role they have assigned it.
Evolutionists will not easily accept my solution. The suggestion that living organisms have within themselves the ability to be switched ON or OFF by a cue from the environment may be satisfactory as an explanation of special cases of evolution, but evolutionists will not accept it as the explanation of evolution in general. They will ask for my explanation (on scientific, not on supernatural, grounds) how such a built-in capability arose. How could such a general capability have arisen in the development of life from a simple beginning? How could my suggestion fit the neo-Darwinian agenda?
I reject the neo-Darwinian agenda. I do not attempt to explain on a scientific basis how the built-in capabilities arose. I do not attempt to explain the development of life from a simple beginning; nor do I attempt to explain the buildup of complexity from a simple beginning to the forms of life we find today. Such development and buildup have never been observed, and there is thus no imperative for a theory to account for them. The inability of my hypothesis to account for the spontaneous origin and development of life, events that have never been observed, is not a valid criticism of it. If the hypothesis can account for observed adaptations, it will be doing all that should be asked of it.
To read more about these topics check out the book Not By Chance
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Downton Abbey's fourth season hasn't even begun in the United States, but PBS is already looking ahead to the fifth. The British series was officially renewed for a fifth season on Sunday.
"Like millions of other Downton fans, I can't wait to see what's next for the Crawley family," PBS boss Paula Kerger said in a statement. "We're proud to be the home of this extraordinarily entertaining series and, along with our stations, we look forward to sharing Season 5 with U.S. audiences."
25 totally unnecessary TV spin-offs
Downton is the most-watched series in PBS' history. It has already concluded its fourth season in the U.K., where it is the highest-rated TV drama.
"We are thrilled to produce a new series of the show next year," added executive producer Gareth Neame."We promise all the usual highs and lows, romance, drama and comedy played out by some of the most iconic characters on television. All the actors and makers of the show continue to be humbled by the extraordinary audience response and want to take the show from strength to strength next year."
Downton Abbey's fourth season kicks off Jan. 5 in the United States. Are you looking forward to more Downton?
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355 Mr R. G. Casey, Minister to the United States, to Department of External Affairs
Cablegram 199 WASHINGTON, 14 March 1941, 7.29 p.m.
From Naval Attache [1] to Chief of Naval Staff. [2]
With reference to my telegram No. 159. [3] Progress report 6.
(1) Probable date of completion of conversations, March 25th.
(2) United States have accepted the responsibility for strategical direction in the Pacific area defined as follows:
(a) Area North of Equator to the East of longitude 140 degrees East.
(b) Area North of latitude 30 degrees North [to] [4] the West of longitude 140 degrees East.
(c) Area South of equator to East of longitude 180 degrees.
(3) They have refused responsibility for strategical direction in the Far East area and they have refused to place the Commander-in- Chief of the United States Asiatic Fleet under British direction until after the fate of the Philippine Islands has been settled.
(4) United Kingdom delegation have agreed as follows:
(a) The commanders of Associated and Allied Military Forces win collaborate in formulation of strategic plans for operations in that area.
(b) Defence of Territories of Associated and Allied Powers will be the responsibility of the respective commanders of the Military Forces concerned. These commanders will make such arrangements for mutual support as may be practicable and appropriate.
(c) Responsibility for strategical direction of Associated and Allied Naval Forces, except of Naval Forces engaged in supporting the defence of the Philippines, will be assumed by the British Commander-in-Chief China. Commander-in-Chief of the United States Asiatic Fleet will be responsible for the direction of Naval Forces engaged in supporting the defence of the Philippines.
(d) For the above purposes die Far Eastern Area is defined as the area between latitude 30 degrees North and 11 degrees South and between longitude 140 degrees East and 92 degrees East. Northern boundary of area is a line from a position 020 degrees North, 092 degrees East to boundary between India and Burma. [5]
(e) British Commander-in-Chief China is also charged with the responsibility for the strategical direction of Associated and Allied Forces which may operate in Australia and New Zealand stations west of longitude 180 degrees.
(5) This is the best the [U.K.] delegation can get in the way of an agreed solution to the problem of [unified strategic] control in the Pacific and Far East and appears acceptable.
(6) Group Captain Isitt [6] has been in close touch with the United Kingdom delegation for a short period during last week and will return to Washington before the conversations end.


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For about 3 weeks I have been working out 6 times a week and rest on Sunday. What I've been doing is M-W is hypertrophy and T-S is Strength days. Is this ok? How many of you workout 6 times a week. And will I be overtraining?
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Alumni Chapters
Alumni chapters provide St. Mary's alumni with the opportunity for professional and social interaction, and volunteer opportunities that benefit both the College and the individual. Through alumni chapters, graduates from St. Mary's are able to maintain and develop friendships and associations with other alumni, participate in the ongoing progress and life of the College, and continue to nurture the important education-for-life experience.
Each alumni chapter will have a chapter committee led by a chapter president. The president works hand-in-glove with the alumni director and represents the chapter at quarterly Alumni Council meetings. Chapter committees should be comprised of alumni from various ages, interests, and backgrounds. These committees support the chapter president in the planning and execution of alumni chapter activities and initiatives. There is no term limit for chapter presidents or committee members as long as they are actively involved in fulfilling the duties outlined in the Chapter Handbook.
Interested in getting involved with current chapter or starting one in your area? Contact Dave Sushinsky '02, Director of Alumni Relations, at (240) 895-3381 or email email@example.com.


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Moxibustion by Li Tang, Song dynasty
Moxibustion (Chinese: 灸; pinyin: jiǔ) is a traditional Chinese medicine therapy using moxa made from dried mugwort (Artemisia argyi). Available scientific evidence does not support claims that moxibustion is effective in preventing or treating cancer or any other disease,[1] but it plays an important role in the traditional medical systems of China (including Tibet), Japan, Korea, Vietnam, and Mongolia. Suppliers usually age the mugwort and grind it up to a fluff; practitioners burn the fluff or process it further into a cigar-shaped stick. They can use it indirectly, with acupuncture needles, or burn it on the patient's skin.
The first Western remarks on moxibustion can be found in letters and reports written by Portuguese missionaries in 16th-century Japan. They called it "botão de fogo" (fire button), a term originally used for round-headed Western cautery irons. Hermann Buschoff who published the first Western book on this matter in 1674 (English edition 1676) used the Japanese word mogusa. As the u is not very strongly enunciated, he spelled it "Moxa". Later authors blended "Moxa" with the Latin word combustio (burning).[2][3]
The name of the herb Artemisia (mugwort) species used to produce Moxa is yomogi (蓬) in Japan and ài or àicǎo (艾, 艾草) in Chinese.[4]
The Chinese names for moxibustion are jiǔ ( 灸) or jiǔshù ( 灸術), Japanese use the same characters and pronounce as kyū and kyūjutsu. In Korean the reading is tteum (뜸). Korean folklore attributes the development of moxibustion to the legendary emperor Dangun.[5]
Theory and practice[edit]
Practitioners use moxa to warm regions and meridian points[6] with the intention of stimulating circulation through the points and inducing a smoother flow of blood and qi. Some believe it can treat conditions associated with the "cold" or "yang deficiencies" in Chinese Medicine.[7] It is claimed that moxibustion militates against cold and dampness in the body, and can serve to turn breech babies.[8]
Practitioners claim moxibustion to be especially effective in the treatment of chronic problems, "deficient conditions" (weakness), and gerontology. Bian Que (fl. circa 500 BCE), one of the most famous semi-legendary doctors of Chinese antiquity and the first specialist in moxibustion, discussed the benefits of moxa over acupuncture in his classic work Bian Que Neijing. He asserted that moxa could add new energy to the body and could treat both excess and deficient conditions. On the other hand, he advised against the use of acupuncture in an already deficient (weak) patient, on the grounds that needle manipulation would leak too much energy.[citation needed]
Practitioners may use acupuncture needles made of various materials in combination with moxa, depending on the direction of qi flow they wish to stimulate.
There are several methods of moxibustion. Three of them are direct scarring, direct non-scarring, and indirect moxibustion. Direct scarring moxibustion places a small cone of moxa on the skin at an acupuncture point and burns it until the skin blisters, which then scars after it heals.[9] Direct non-scarring moxibustion removes the burning moxa before the skin burns enough to scar, unless the burning moxa is left on the skin too long.[9] Indirect moxibustion holds a cigar made of moxa near the acupuncture point to heat the skin, or holds it on an acupuncture needle inserted in the skin to heat the needle.[9] There is also stick-on moxa.
In traditional Chinese medicine there is a belief that moxibustion is effective at increasing the cephalic positioning of fetuses who were in a breech position before the intervention. A 2012 Cochrane review stated that there is "some evidence" that moxibustion may be useful for reducing the need for external cephalic version, but well-designed randomised controlled trials were needed to evaluate the safety and efficacy of moxibustion.[10]
Medical research[edit]
The first modern scientific publication on moxibustion was written by the Japanese physician Hara Shimetarō who conducted intensive research about the hematological effects of moxibustion in 1927. Two years later his doctoral dissertation on that matter was accepted by the Medical Faculty of the Kyūshū Imperial University.[11] Hara's last publication appeared in 1981.[12]
According to the American Cancer Society, "available scientific evidence does not support claims that moxibustion is effective in preventing or treating cancer or any other disease".[1]
Although some positive results have been reported from studies in China, concern has been expressed that publication bias may result in a falsely positive impression.[13][14]
Parallel uses of mugwort[edit]
In many religions of North and South America that pre-date European colonization, mugwort is regarded as a sacred plant of divination and spiritual healing, as well as a panacea.[citation needed] Mugwort amongst other herbs was often bound into smudge sticks. The Chumash people from southern California have a similar ritual.[15] Europeans placed sprigs of mugwort under pillows to provoke dreams; and the herb had associations with the practice of magic in Anglo-Saxon times.[citation needed]
See also[edit]
- ^ a b "Moxibustion". American Cancer Society. 8 March 2011. Retrieved August 2013.
- ^ Wolfgang Michel (2005). "Far Eastern Medicine in Seventeenth and Early Eighteenth Century Germany". Gengo bunka ronkyū 言語文化論究 (Kyushu University, Faculty of Languages and Cultures) 20: 67–82. ISSN 1341-0032.
- ^ Li Zhaoguo (2013). "English Translation of Traditional Chinese Medicine: Theory and Practice". 上海三联书店. p. 11. ISBN 978-7-5426-4084-0.
- ^ There is a great variety of further Chinese names (bingtai 冰台、ecao 遏草、xiang'ai 香艾、qiai 蕲艾、aihao 艾蒿、jiucao 灸草﹑yicao 医草﹑huangcao 黄草﹑airong 艾绒)
- ^ Needham, J; Lu GD (2002). Celestial lancets: a history and rationale of acupuncture and moxa. Routledge. pp. 262. ISBN 0-7007-1458-8.
- ^ Not all acupuncture points can be used for moxibustion. A few of them are preferred in both classical literature and modern research: Zusanli (ST-36), Dazhui (GV-14).
- ^ https://www.yinovacenter.com/chinese-medicine/moxibustion/
- ^ American Journal of Chinese Medicine, Winter, 2001, Yoichi Kanakura, et al.; also see Cochrane Library
- ^ a b c "Moxibustion, Acupuncture Today". Acupuncturetoday.com. Retrieved 2011-05-17.
- ^ Coyle ME, Smith CA, Peat B (2012). Coyle, Meaghan E, ed. "Cephalic version by moxibustion for breech presentation". Cochrane Database Syst Rev 5: CD003928. doi:10.1002/14651858.CD003928.pub3. PMID 22592693.
- ^ English summary of S. Hara's findings
- ^ S Watanabe; H Hakata; T Matsuo; H Hara; S Hara (1981). "Effects of Electronic Moxibustion on Immune Response I". Zen Nihon Shinkyu Gakkai zasshi (Journal of the Japan Society of Acupuncture and Moxibustion) (Japan Society of Acupuncture and Moxibustion) 31 (1): 42–50.
- ^ Lee, MS; Kang, JW; Ernst, E (2010). "Does moxibustion work? An overview of systematic reviews". BMC research notes 3: 284. doi:10.1186/1756-0500-3-284. PMC 2987875. PMID 21054851.
- ^ Coyle ME, Smith CA, Peat B: Cephalic version by moxibustion for breech presentation
- ^ Timbrook, Janice (2007). Chumash Ethnobotany: Plant Knowledge among the Chumash People of Southern California. ISBN 978-1-59714-048-5.
External links[edit]
|Look up moxibustion in Wiktionary, the free dictionary.
- W Michel: Far Eastern Medicine in Seventeenth and Early Eighteenth Century Germany
- Hermann Buschoff, The gout, more narrowly searcht, and found out; together with the certain cure thereof. London 1676. W Michel ed. Fukuoka, March 2003. (Japanese introduction by the editor, English text)


text:
Hardly surprising given the number of Tegra 4 devices
Review: Bay Trail on a budget
First two parts coming this month
But you won't see them in any phones or tablets
Rogue mid-life kicker
Still falls short of 2012
Quarter off select models
There's actually a market for them?
Jaguar to thank for bucking industry trend?
Some people just love fake slides


text:
RubyMine helps create Gemfile, when the bundler gem is installed.
- On the main menu, point to .
- On the submenu, choose . RubyMine generates the stub Gemfile in the project root directory. Later you can add more gems if required.
Thecommand is only available, when the Gemfile doesn't exist.
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Current Articles
From Idaho Fish and Game
-- Big game hunters whose names were drawn in controlled hunt drawings have until Aug. 1 to buy their tags. Any tags not purchased by that date will be forfeited. After a second drawing, any leftover tags are sold over the counter.
The rules have changed for controlled hunt permits. Hunters who were successful in a controlled hunt drawing no longer have to buy a separate permit. All hunt information is included on the tag.
Hunters are responsible for checking whether they were drawn in the controlled hunts they entered. Results of deer, elk, pronghorn and fall black bear controlled hunt drawings are available on the Fish and Game website at http://fishandgame.idaho.gov/apps/ch/results.cfm.
Hunters can buy those tags at any Fish and Game office, license vendor, by telephone at (800)554-8685 or online at https://id.outdoorcentral.us/. For information on rules and dates for specific hunts consult the regulations brochure or the Fish and Game website.
Those lucky enough to draw can use Fish and Game's Hunt Planner at http://fishandgame.idaho.gov/ifwis/huntplanner to plan those fall hunts.
For hunters who weren't drawn, big game general season tags also are available in many big game units. For details contact license fishandgame.idaho.gov vendors or local Fish and Game offices.
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Homeowners Association MeetingsThe Roosevelt Gardens' Home Owner Association (HOA) hosts a community meeting every third Monday of the month.
Eligha Lewis III, Roosevelt Gardens HOA President
Code Compliance
Click here to learn what Broward County's code violations are and how to report them.
Bulk Trash Pick Up
Residents north of NW 13th StreetService Day: Second Thursday of every month
Residents between Sunrise Blvd and NW 13th StreetService Day: Third Thursday of every month
Bulk waste items may be placed outside NO MORE than 24 hours prior to collection day.
For additional bulk waste collection guidelines visit: www.broward.org/wasteandrecycling/pages/default.aspx and click the Unincorporated tab
Community Information
Roosevelt Gardens Park Amenities include: There is a 4,500-square-foot community center with an assembly hall (capacity 125), a game room, a warming kitchen, a computer lab, and park offices. The back patio features full-size rocking chairs where parents can relax and watch their children play.Location: 2841 N.W. 11th St., Fort Lauderdale, FL 33311 Phone: 954-327-3888 Website: www.broward.org/Parks/RooseveltGardensPark/Pages/Default.aspx
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Spotted around the media universe
The Calendar Boys of BuffPost - Posted June 6, 2013
You've heard of The Beltway Boys -- how about the BuffPost Boys? Sam Stein and the guys over at HuffPost (dubbed "BuffPost" by MSNBC's Joe Scarbor... [FishbowlDC]


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Welcome to the home page of the Office of Institutional Assessment, Planning & Effectiveness at Texas Southern University. We hope you find the information here useful for your department and research. We are also interested in your experiences, good or bad, please send us feedback on your experience with the program. Our office is located in Hannah Hall – Main Entrance - Room 143.
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Institutional Assessment, Planning & Effectiveness
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Executive Director
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Phone: 713-313-1066
Fax: 713-313-4317
Email : firstname.lastname@example.com


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This bed is elegant and stylish. However I had to replace the two stakes holding the middle of the bed with steel poles because the original stakes were made of hard plastic and one broke, after this minor fixing no more issues to be concerned. The color is more cream/beige than white. I am happy with this purchase and can stop admiring it.
The bed was very easy to put together. I did it myself, but I recommend two people because the bed is heavy. It came in two separate shipments. I received the headboard 5 days before the rest of the bed arrived. It is sturdy and attractive. As you can tell from the picture, the bed is very low to the ground. I can't get my hand under it, let alone storing anything under there. I am looking into risers to bring the bed up. At this height, it's better for a child than an adult. Also, the full size bed frame is bigger than my mattress. But this is a good bed for the money.
Overall, I'm very satisfy with the purchase from this vendor and will do business again.. thanks
This bed looks very elegant and it fit perfect in my daughter's room, delivery was quick and very secure.
I love this new bed I purchased from Overstock! It's absolutely beautiful and just the perfect design! Assembly was fairly easy :-) Material is well made. Im just really pleased. It's a highly recommended product!
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Down 1.4% to $58.62, CVR Energy (NYSE:CVI), is one of today's notable movers. The S&P is trading fractionally lower to 1,550 and the Dow is trading fractionally higher to 14,402.
CVR Energy (NYSE:CVI) is currently priced 1.3% above its average consensus analyst price target of $57.88. The stock should discover initial support at its 50-day moving average (MA) of $53.80 and subsequent support at its 200-day MA of $38.78.
CVR Energy, Inc. is an independent refiner and marketer of transportation fuels. The Company, also through a limited partnership produces ammonia and urea ammonia nitrate, or UAN, fertilizers.
In the past 52 weeks, CVR Energy share prices have been bracketed by a low of $23.54 and a high of $62.50 and are now at $58.62, 149% above that low price. Over the last five market days, the 200-day moving average (MA) has gone up 2.0% while the 50-day MA has advanced 2.2%.


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Scroll through other Ipswich Real Ale pubs
This pub dates from 1689, though the building is older. It offers gaming areas and various seating areas including an outside patio. It's believed that Cardinal Wolsey was born either here or in the Black Bell.
It is believed to be the oldest pub of this name in East Anglia.
listed building grade II
Local licensing authority for Ipswich is Ipswich Borough Council
last updated 07/12/2014
(Most pub, location & historic details collated by Nigel, Tony or Keith - original sources are credited)
(detailed information from Old inns of Suffolk by Leonard P Thompson)
(information from Dudley Diaper)
(** historic newspaper information from Bob Mitchell)
(*** historic newspaper information from Stuart Ansell)
(**** information supplied by Neil Langridge)


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Analog Devices' broad portfolio of solutions for power supply sequencing has now grown even larger with the addition of two new families of sequencing IC's. The ADM1062, ADM1063, ADM1064, ADM1065, ADM1066 , and ADM1067 Super Sequencers™ are the newest programmable devices offering more channels, greater accuracy and smaller size.
The ADM1085, ADM1086, ADM1087, and ADM1088 Simple Sequencers™ are cascadeable analog supply sequencers that enable a capacitor adjustable time delay between the enabling of Voltage Regulators all in an SC70 Package.
The ADM1060 combines power supply sequencing with monitoring/supervising in a single chip on multi-power supply systems.
|Content Type
|File Type
|ADM1060: Communications System Supervisory/Sequencing Circuit Data Sheet (Rev B, 01/2004) (pdf, 451 kB)
|Data Sheets
|AN-897: ADC Readback Code (pdf, 65 kB)
|Application Notes
|AN-667: Up/Down Sequence of Supplies Using the ADM1060 (pdf, 950 kB)
|Application Notes
|AN-722: Watchdog Detection Using the ADM106x (pdf, 179 kB)
|Application Notes
|AN-755: EEPROM Checksum Information for the ADM1060 (pdf, 98 kB)
|Application Notes
|AN-723: Interrupt Generation Using the ADM106x (pdf, 262 kB)
|Application Notes
|analogZone Reviews the ADM1060 (htm)
|Technical Articles
|Single Chip Supervises and Sequences Power Supplies (pdf, 842 kB)
|Technical Articles
Temperature monitor measures three thermal zones
by Susan Pratt, Analog Devices, Inc. (EDN, 12/11/03)
|Technical Articles
Solving Power-Management Problems with a Single Chip that Handles up to 7 Channels of Sequencing, Monitoring, and Supervision
by Peter Canty, Analog Devices, Inc. (Analog Dialogue, Vol. 37, June 2003.
|Analog Dialogue
|Supervisory Devices Complementary Parts Guide for Altera FPGAs (pdf, 664 kB)
|Product Selection Guide
|Supervisory Devices Complementary Parts Guide for Xilinx FPGAs (pdf, 661 kB)
|Product Selection Guide
|Power Supply Sequencing Bulletin (2007) (pdf, 5188 kB)
|Solutions Bulletins
|Voltage Monitoring and Sequencing (2009/2010) (pdf)
Optical and High Speed Networking
(pdf, 2236 kB)
Analog Devices' optical and high speed networking ICs solve a depth and breadth of challenges faced by today's designers of datacom and telecom systems, optical modules, and subsystems. Analog Devices products address a wide range of networking applications from O/E/O conversion, clock recovery, and backplane transmission to monitoring and control of optical power, power management, and clock generation and distribution.
|Power System Management (Spring 2007) (pdf, 1170 kB)
|RAQs index
|Rarely Asked Questions
|Glossary of EE Terms
|Content Type
|File Type
ADM1060 Evaluation Software
Supports Windows XP only, it does not support any later versions of Windows such as Windows Vista or Windows 7. It supports the parallel port to I2C dongle, CABLE-SMBUS-3PINZ, but does not support the USB-SMBUS-CABLEZ or USB-SDP-CABLEZ interfaces.
|Evaluation Software
Symbols and Footprints— Analog Devices offers Symbols & Footprints which are compatible with a large set of today's CAD systems for broader and easier support.
The USA list pricing shown is for BUDGETARY USE ONLY, shown in United States dollars (FOB USA per unit for the stated volume), and is subject to change. International prices may differ due to local duties, taxes, fees and exchange rates. For volume-specific price or delivery quotes, please contact your local Analog Devices, Inc. sales office or authorized distributor. Pricing displayed for Evaluation Boards and Kits is based on 1-piece pricing.


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Avenue Silver Plated Champagne Flutes, Set of 2
Use code: MC2014
The graceful stylings of the tapered bowls are accented by dazzling cuts in the superior-quality crystal. Vertical and horizontal cuts combine to form an elegant and sophisticated geometric pattern in the crystal. Majestically ascending from base to rim, the vertical cuts sweep upward in sleek, clean lines. Standing in dramatic counterpoint to the vertical cuts, horizontal cuts around the base of the flutes form a stylish geometric pattern that will compliment any table setting or décor. Elegantly crafted from superior-quality crystal. Hand wash with warm water and a mild detergent; rinse and dry immediately. Set of 2 silver plated champagne flutes, each holds 8 ounce.


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By Rob Morris on May 19, 2010
From the Aydlett resident who feared losing a way of life to the local leaders who said it was past time to build the bridge, about a dozen speakers offered their views at the first of three hearings on the project.
More than 60 people attended the session at the Ramada Plaza in Kill Devil Hills.
The hearings are required as part of the process of studying the bridge, an idea that dates back to the 1980s. Its stated purpose is to relieve massive backups at the Wright Memorial Bridge, ease hurricane evacuations and cut the driving time to the Currituck Outer Banks.
Before the hearing, an information open house with an array of maps and officials available to explain them provided details on five alternatives in a draft environmental impact statement.
Although the hearing room was nearly full, only eight people had signed up to speak, and one of them left before making a statement. After they were finished, seven more volunteered their opinions.
Yvonne Avery, who lives in Aydlett, noted that the North Carolina Turnpike Authority had assured property owners and businesses that they would be made whole with fair compensation if the bridge displaced them. The small mainland community with expansive views of the Currituck Sound would be at the western terminus of the bridge.
"When you change a community's way of life, how can you make that whole again?" she asked.
But political and business leaders from Duck and Southern Shores said traffic has been affecting their communities for years. Because the Wright Memorial Bridge is the only way across the sound, vacationers heading to Corolla have to cross there, then head north along N.C. 12 through the two towns.
Mayor Hal Denny said Southern Shores has "long been the victim of weekend traffic jams."
Denny and Mayor Pro Tem Don Kingston of Duck both voiced strong support for the turnpike authority's recommended alternative, which calls for building the bridge and not widening N.C. 12 except for a short stretch near the eastern terminus north of the Currituck Club in Corolla.
Variations of that alternative will cost in the range of $600 million and and $816 million. Tolls have not been determined, but they would be from $6 to $12. Construction could start as soon as early next year, and the bridge could be open to traffic by late 2014.
Several speakers voiced concerns about what they saw as the potential negative effects of the 5-mile bridge on the Currituck Outer Banks.
Andrew and Michael Meredith, the owners of Corolla Watersports near Timbuck II said the bridge would spoil what makes the area attractive: its remoteness.
"It's so desirable because it's so hard to get to," Andrew Meredith Jr. said.
Michael Meredith said that one of two options for the eastern terminus could block his business' access to the sound. He asked the turnpike authority to consider that impact or choose the second alternative, which is farther north near Corolla Bay.
Other speakers warned of overdevelopment, higher crime and dangers to children who might have to cross the four-lane stretch of N.C. 12 near the bridge. At least one suggested that the state put more of its efforts into building a replacement for the Bonner Bridge over Oregon Inlet.
Wally Davis of Aydlett asked for a show of hands of the people who had read the entire draft environmental statement. After a few responded, he contended that some of the information seemed tailored to supporting the bridge option rather than alternatives that include widening U.S. 158 and N.C. 12 rather than building the span.
"The problem is mostly in Dare County," he said.
But Gene Gregory, a Currituck County commissioner, said the traffic problems affect mainland businesses, some of which choose to shut down on weekends, and force duplication of police protection. With a bridge, Currituck sheriff's deputies could get to Corolla in 10 minutes, he said.
"We desperately need this bridge," he said.
Hearings at 7 p.m. will be preceded by information sessions from 3:30 to 6:30 p.m. at the Currituck Center for Wildlife Education in Corolla today and at the Currituck County Center in Barco on Thursday.
more information and the draft environmental impact statement »
Join the discussion


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What does VLL mean in US Government?
This page is about the meanings of the acronym/abbreviation/shorthand VLL in the Governmental field in general and in the US Government terminology in particular.
Virtual Law Library
Find a translation for VLL in other languages:
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Use the citation below to add this abbreviation to your bibliography:
"VLL." Abbreviations.com. STANDS4 LLC, 2014. Web. 21 Dec. 2014. <http://www.abbreviations.com/term/221630>.
VLL also stands for:
- former code for Valladolid Airport, Valladolid, Spain
- Oakland/Troy Airport, Troy, Michigan USA (formerly 7D2)
- Vehicular Laser Locator
- Vestal Little League
- Video Layered Library
... and 14 more »
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Riding is always more fun when you can bring a buddy along, and that's easy to do with the Yakim Superjoe 2 trunk rack. It packs a lot of premium punch into an incredible value package. It's got plenty of space to securely store two road or mountain bikes and it easily sets up on most car models. The frame is made of bomb-proof steel tubing, so it can stand up to some serious abuse. It's a great way to transport a lot of bike for just a little bit of cash.
Item No. » YR-YAKSJ2-BASE
Nashbar No price available.
Sorry, this item is Out of Stock. You can still order it and we will ship it to you as soon as it comes in.


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As a ten-year-old growing up in a rural enclave, John...
John John In The Sky movie trailer - starring Randy Travis, Matt Letscher, Rusty Schwimmer, Romy Rosemont. Directed by Jefferson Davis. Genre: Drama
Rating: PG-13
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Title: i2c.resource Description: The i2c.resource provides access to the I2C bus 0 found on Sam440ep and Sam460ex boards. I2C devices may be connected to the bus via the J10 connector on Sam440ep and the J9 connector on Sam460ex. Check your board user manual for the I2C connector pinout. How to use: * copy i2c.resource.kmod into your kickstart directory * add the following line in the Kicklayout file: MODULE Kickstart/i2c.resource.kmod * copy the SDK directory into SDK: (if installed) * check the SDK directory for include files, autodoc and example Notes: Currently bus 1 (I2C/SPI) is not supported. History: 14-Apr-2011 - Version 53.2 - added I2C_Probe() 19-Dec-2010 - Version 53.1 - Initial version for Sam440ep and Sam460ex board
|Copyright (c) 2004-2014 by Björn Hagström All Rights Reserved
Amiga OS and its logos are registered trademarks of Hyperion Entertainment


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The Round Rock Public Library's Teen Book Club will meet from 6:30 to 7:30 p.m. Tuesday, Feb. 19.
This month's book is Watership Down, by Richard Adams, a classic novel "set in England's Downs, a once idyllic rural landscape, this sirring tale of adventure, courage, and survival follows a band of very special creatures on their flight from the intrusion of man and the certain destruction of their home." (Publisher's Description)
A limited number of FREE copies of the book will be available at the Reference Desk (2nd Floor). First come, first served!


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Gilbert eyes ways to get its tuition School considers default by town
WINSTED — The Gilbert School Corp. is exploring its legal options should the town be unable to make future tuition payments to the quasi-public junior-senior high school.
In a letter to Gilbert Head of School Anthony Serio dated Feb. 7, Gilbert's lawyers, Gregory J. Bezz and Peter A. Janus, state that the corporation has two options — file a lawsuit for breach of contract or demand for "adequate assurance" of payment.
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"......I wanted to tell you how wonderful our eRL-FE595 lock is doing! I never have to worry about passing out entry codes and having them floating around! The unique code concept is wonderful and I have peace of mind! Our renters have found it easy to open and reset their own code....... " Read more eResortLock testimonials
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9 Yellow Kitchens You'll Love
Give your kitchen a burst of energy with these bright decorating ideas from some of our favorite designers.
French Brasserie Kitchen
Designer John Oetgen spent a lot of time in French brasseries, which inspired the kitchen in this Atlanta house, complete with blue-and-green bistro stools. Working with Ann Sullivan Kitchens, he installed a range hood, done in hand-hammered zinc, made to look like a fabric canopy. Zinc range canopy and island ironwork by Calhoun Design & Metalworks. Wall and ceiling trellis paper from Cowtan & Tout. Marly stools from T & K French Antiques.