Chapter 7: The Wave Model for Capping and Cell Motions
This file describes the wave model for capping, particle movement and cell motility - which the author believes to be correct. It reviews the evidence for cell waves and for their involvement in these phenomena. It notes how published reviews in the field have failed to consider that evidence.
7.1 The Wave Model
7.2 Waves and Motility: Ciliated Cells
7.3 Waves on Mammalian Cells
7.4 Oscillations and Waves
7.5 Calcium Waves
7.6 Evidence Relating Particle Behaviour to Cell Waves
7.7 Saltatory and Reverse Movements of Particles
7.8 Evidence From Genetics
7.9 Criticism of the Wave Model
7.10 My Reaction to Such Criticism
7.11 The Present Situation of the Wave Model
Summary
But I believe in natural selection, not because I can prove in any single case that it has changed one species into another but because it groups and explains well (as it seems to me) a host of facts. (Charles Darwin, 1861)
7.1 The Wave Model
Darwin could not prove natural selection, because science never proves any claim. The wave model now to be described is likewise unproven but the grounds for affirming it are exactly those with which Darwin justified his belief in evolution. As it seems to this author, the wave model groups and explains well a host of facts, while being compatible with the evolutionary principles expounded by Darwin himself. By contrast, the models described in the preceding chapters achieve no grouping or explanation and are not so compatible.
Waves tend to entrain objects, carrying them along in their flow - the surf-rider is the most familiar example. Large objects tend to be carried along by waves better than smaller ones and very small objects are simply left behind. On water, these facts are well known and can be confirmed in a wave tank or even at the beach. Large surface objects (patches and particles) move on cell surfaces, while small objects (protein and lipid molecules) do not. These bare facts could be explained by cell-surface waves that might entrain patches and adherent particles but leave smaller objects unmoved, just as waves do on water.
Accordingly the wave model proposes that, indeed, there are waves travelling along the cell surface. Particles and patches are large in the way they interact with them and are carried along, they entrain with the wave motion. This entrainment is observed in the microscope as capping or as particle movement. Individual lipid or protein molecules are small compared to particles or patches, so they do not interact so strongly with waves and are left unaffected. Only when brought together into a patch, will receptors in the membrane cap.
These properties give the wave model a number of general advantages over the alternatives, particularly the cytoskeletal models.
- Direct contact between cytoskeleton and moving object is not required.
- All large enough, surface objects should move, regardless of their chemical nature explaining the reported lack of specificity.
- Capping and particle movement become related to other known facts about the cell surface and motility, explaining why they are so widespread.
The next sections support the wave model by reviewing the positive evidence for its metaphysical elements, thus building a prima facie case for it. Even so, remember logical force goes with disproof and feel free to be convinced or not. Unconvinced readers are encouraged to put their counter-arguments on record. Let the rebuttal of the wave model be known, to be examined by all, and criticised alongside the prima facie case.
In nature evolution has often achieved motility through a wave mechanism. Fish swimming, snakes moving, intestinal function, paramecia swimming etc.; merely watching natural history programmes on television, enables the construction of a very long list. Waves on such organisms are an evolutionary adaptation reflecting the survival advantages of an ability to move. Often creatures achieve movement because the waves act by peristalsis, the wave catching the surrounding fluid in its motion and pushing it backwards in the opposite direction to motion. Waves do not always move in the opposite direction to motion. For example, the waves on the upper surface of a maggot move in the same direction as motion.
Among the unicellular protozoa three forms of motility are commonly recognised. The amobae, of course, display amoeboid motion. Many protozoa, for example the trypanosome, causative agent of sleeping sickness, move using wave-like whipping of one, or a few, flagella. Other species move using visible waves of hair like cilia beating on their surfaces, paramecium is the classic example. The waves are easily visible because of the cilia on the surface of the organism. An example is shown in Fig. 7.2. The picture is a modern scanning electron micrograph and, remarkably, the waves have survived the complex fixation procedures used. These waves are also visible through the light microscope and have been documented for centuries. The cilia on such protozoa pass through the membrane of the cell and contact the underlying cytoskeleton, indeed the cilia may be seen as outgrowths of the cytoskeleton. The cilia beat in synchrony, so their beating must be coordinated through the membrane and cytoskeleton. Much is known about how the membrane and cytoskeleton are involved in the control of cilial waves and it involves waves of calcium ion concentration. (See Lauren and Fleury (1995) for a review.) It will be noted that, although waves on amoebae are far less obvious, they too display calcium waves.
The various cell types of a mammalian body exhibit all three of the motile mechanisms described in protozoa. Flagella are seen most notably in sperm cells, while ciliary wave patterns occur among several cells of the body, including the lung. An epithelial tissue forms the boundaries of an organ and that forming the inner lining of the upper respiratory tract, comprises a sheet of cells provided with large numbers of cilia, very similar to those in paramecium. These cilia engage in rhythmic beating to produce a wave, which in this case passes from cell to cell in the sheet. Again, waves of calcium ion concentration are involved in control of the wave. The cilial waves of the lung do not cause the cells to move, they are fixed in the sheet, but instead provide the motive force for the mucociliary escalator or mucociliary transport system. (Described in many textbooks on mammalian physiology, and Gray's Anatomy.) This system provides a defence mechanism against dust particles that would otherwise lodge in the lungs and damage them. The epithelium, including the ciliated cells, is coated by a sticky mucous to which particles in inhaled air become attached. The peristalsis of the beating cilia drives the resulting mixture, mucous and dirt, upwards and out of the lungs. The mixture, once driven from the lungs, is swallowed following a clearing of the throat. The mucociliary escalator is unusual in that the movement of particles is itself the function of the waves. Although this book arises from consideration of particle movement on cell surfaces, this system is the only situation known to the author where such movement is actually a biological function.
"A Habit of Lies" is concerned with amoeboid cells, which have no cilia, but like ciliated protozoa are eukaryotic. Although their membranes and cytoskeleton differ in many respects from amoeboid cells, the underlying principles seem the same. Lung epithelial tissue is a cell type genetically identical to amoeboid cells from the same organism - the two cell types are merely different developmental forms of the same organism. Most proteins and lipids of epithelial tissue will be exactly the same as the corresponding structures in amoeboid cells of the same animal. It is very likely indeed that the membrane and cytoskeleton of amoeboid cells will be as capable of generating and transmitting waves, as are those in lung epithelial tissue. Thus the evolvability criterion is not broken by the wave model. Known facts about the cytoskeleton of similar eukaryotic cells enable the assumption that the cytoskeleton and membrane of amoeboid cells will be excitable, able to produce waves.
Waves on cells without the cilia that make them obvious are hard to observe but have been reported on amoeboid cells. Some such reports were
cited in Hewitt, (1979). Waves on amoeboid eukaryotic cells are normally seen to move from front to back, for examples see Durham (1974) for a review or the "wave motility" described by Forscher & Smith (1988)). Kucik et al. (1990) described their waves as moving "centripetally." This seems best interpreted as toward the nucleus and, in practice, means much the same as front to back as the nucleus is at the rear of the cell. On at least one occasion waves near the leading edge of the cell have been observed to move in the other direction, forward (Couchman, Lenn & Rees, (1985)). Their photographs are most impressive, and example is reproduced in Fig. 7.3. There have been occasional observations of particles moving forwards also, (Kucik, Elson & Sheetz (1989)).
"A Habit of Lies" mentions recent papers but readers should not think waves on amoeboid cells are a recent discovery. In 1967, Berrill wrote this in a beginning college text on biology
Under these conditions (time lapse photography) wavelike movements of the membrane are seen to take place continuously. The movements, which are generated on the leading edge of the cell and travel rearward, are probably produced by the flow of cytoplasm beneath the surface. As the waves travel along the surface of the cell they make intermittent contact with the surface on which the cell is moving, contacts which continually change as the waves move back and the cell moves forward. This is clearly important to the mechanism of movement as a whole, not only of amoebae, phagocytes, and fibroblasts, but of sheets of tissue, i.e., epithelia, which form layers of the skin and other tissues. When such a sheet is examined in the phase-contrast microscope, wavelike movements of the membrane are seen to take place over the whole area of the sheet, again with intermittent contacts with the external surface. Such membrane movements are of great importance in processes such as wound healing and in connection with the development of embryos, and must be fully taken into account in any consideration of the mechanics of cell movement as a whole.The wave generating capabilities of the cell surface have been known for some time. The surface of an amoeboid cell is an excitable structure, that is capable of generating waves. Observations of such waves are not peculiar rarities.
For many years, physiologists, chemists and physicists have studied the characteristics that make systems excitable. Their general conclusion is that if a system can oscillate, change backwards and forwards between two states, it can also produce waves based on those states. Oscillations in cells are common and have been easier to study than waves but it is inevitable that the two phenomena will have much in common. There are a very few chemical reactions that oscillate, the most famous is called the Belousov-Zhabotinsky reaction, and the necessary chemical kinetic conditions have been carefully studied. The kinetic requirements are the same for both waves and oscillations, a parallel implying that systems giving rise to oscillations will also produce waves, that is, should be excitable. An oscillation is, more or less, a wave with time replacing lateral displacement. The expectation is fulfilled in practice and, although very few chemical reactions are known to oscillate, those that do can also produce waves.
These kinetic requirements, so rare in simple chemistry, are the commonplace of biological systems. Biochemical pathways oscillate because of the feedback by which they are controlled but no discussion of this will be given here (See Winfree (1980) for more information.) Oscillations are very widely documented in cells; one article (Rapp (1979)) catalogues several hundred examples but many have been reported since. Waves, especially those of short wavelength, are more difficult to observe than oscillations, but are likely to be similarly widespread. The many observations of oscillations in cells, implies the existence of similar numbers of undocumented waves. Many early reports of oscillations were of fluctuating calcium ion concentration and the associated waves are now well known.
While there is evidence to support the existence of waves on cells, their study is not an active field, probably because observations on amoeboid cells seem difficult to make. Through the light microscope there is a very low contrast between different components of the cell. Nearly everything in the cell is colourless and variations in refractive index are not large. As a result, it seems waves must become fairly gross to be observed.
However, in one field, that of calcium waves, much has been achieved to overcome the contrast problem. Waves of calcium concentration in the cytoplasm can be visualised using calcium sensitive dyes or a luminescent protein called aequorin. These agents report calcium concentration and make calcium waves visible, by changes in dye colour or light emission from aequorin. In many cases, waves develop because regions of membrane become permeable to calcium ions (Ca2+). These regions form waves passing along the membrane and producing locally high calcium concentrations in the cytoplasm. In paramecium there are organelles which seem to store calcium ions, releasing it in harmony with the wave (see Lauren and Fleury (1995).
It is not surprising that membrane proteins controlling calcium ion permeability are involved in cell waves and there are analogies with the membrane waves involved in the transmission of nerve impulses. These are very fast waves and involve control of sodium ion permeability. Sodium channel proteins seem largely confined to nerve cells and in nerves they and calcium channels sometimes play sympathetic roles. Calcium channels are much more widely distributed and seem to have an earlier evolutionary origin. The sodium channel of nerve cells, and its wave generating activity, probably evolved from the earlier calcium channels.
Research into calcium waves is an active field with a widely known literature, a recent review was Jaffe (1994) and a collection of review articles make up the book edited by Bock and Ackrill (1995). Calcium waves have found their way into the pages of Nature and even onto its front cover (5 October 1995). Calcium concentration and waves are controlling factors in muscle contraction. Calcium concentration is also thought to regulate the action of the cytoskeletal proteins of ameoboid cells. Since the calcium concentration has wave properties, it is likely the cytoskeleton will contract in waves. There are at least three different classes of calcium waves in cells, the slowest class, has a velocity the same order as particles on a cell surfac and Jaffe described them as "contractile waves." In muscle, calcium ion concentration is well known to be maintained through a link to calcium permeability through membrane (in that case the membrane is known as the sarcoplasmic reticulum). Muscle is also well known to contract in wave type patterns, for example cardiac muscle.
Jaffe says, of the calcium waves that are his chief interest, "their velocity and hence mechanism has been remarkably conserved among all or almost all eukaryotic cells." (Italics added.) It is a fact that various classes of calcium waves exist, both on cell surfaces and also within cells. Such waves are widespread on eukaryotic cells. It is likely that these waves will be linked to cytoskeletal contraction and the resulting cytoskeletal waves will be similarly widespread.
Membrane permeability to calcium determines the nature of calcium waves. The control of that permeability can be disrupted, by greatly increasing the permeability of the whole membrane, using drugs called calcium ionophores. The most widely used such agent being called (rather catchily) A23187 and its use should disrupt calcium waves. One of the effects A23187 has on cells is to prevent capping - a result consistent with the notion that the waves involved with capping have calcium waves associated with them.
the centripetally moving waves ... seem to be correlated with the systematic transport of surface particles. (Kucik, Elson & Sheetz (1990))This section describes the behaviour of single particles from one of the publications from Sheetz's laboratory, Kucik et al. (1990). Prof. Sheetz is an advocate of the cytoskeletal flow model and, in correspondence, states that he is unable to see waves on cells. It is simplest to quote his own words from page 1620,
The lack of systematic drift of the diffusing particles in the frame of reference of the cell was particularly striking in the light of the dramatic centripetal cytoplasmic waves visible within the lamellipodium. We observed centripetal transport of some surface bound particles in concert with these waves on all parts of the lamellipodium, particularly with large (0.3 æm) latex beads and with large aggregates of gold particles but only rarely with individual gold particles. This centripetal transport was easily distinguished from diffusion by the steady rearward migration and relative lack of Brownian motion as compared to diffusing particles in the same region of the lamella ..... The diffusing particles (that is, those not moving in a directed fashion) were not influenced by the underlying cytoplasmic waves even in the lateral regions of the cell, where the motion of the waves is at right angles to the direction of cell migration.The whole text of the italicised phrase was added. They remark later, on page 1621, that
the centripetally moving waves ... seem to be correlated with the systematic transport of surface particles.In other words these authors have observed and recorded "dramatic" cell waves in their subject cells. They see particles moving "in concert" with those waves. Large particles move readily in concert with the waves while small particles do not move with the waves nearly so readily. These waves are correlated with the transport of surface particles. It seems very likely that the movement of these particles is wave driven. The observations described in this paragraph seem close to being a direct observational demonstration of the correctness of the wave model. In science, which does not allow the concept of proof, they seem as close to a "proof" of the wave model as could easily be imagined.
Those who reject the wave model should do so while being aware of such observations and should reject it on record, explaining how their own ideas better explain the data. It is hard to see on what basis, other than wave driving, that particles would be expected move "in concert with" waves.
However, the paper from which this quote is taken, did not mention the wave model or the possibility of surf-riding at all. At about the same time, the same group published in Nature, papers claiming to establish the correctness of the cytoskeletal model, by elimination of the flow model. In the Nature papers, whose primary topic was possible mechanisms of capping and particle movement, the authors did not mention the waves they could see. The observation that particles travel in concert with those waves was omitted. The papers did not discuss the wave model at all and the reasoning used to eliminate is not on record. In a letter to this author (section 8.7), the senior author on these papers, Prof. Sheetz, states that he is unable to observe waves at all, merely "other undulations."
The wave model makes a prediction not made by any other description of particle movement. In the case of particles subject to wave driving, one would expect to observe intermittent or saltatory motions. In some cases even reversals of direction and backwards travel from the overall direction of motion might be seen.
Once a large particle is fully entrained, it should move steadily at the same speed as the wave itself. On the other hand, small particles would be unaffected by the wave as successive peaks and troughs passed it by. Thus the behaviour of very large and very small particles would be relatively simple. The behaviour of intermediate sized particles is likely to be more complex. Because they are not fully entrained on the wave motion, the waves will occasionally pass under them.
Two things can then happen, the first, and simplest, is that a particle can remain stationary until the next wave comes along. This would give rise to a saltatory motion being observed, with the particle moving for a period, then stopping etc. How long the particle remained still after a wave passed would depend on the nature of the wave train. If waves were frequent the particle would soon be picked up by the next wave. If waves were infrequent, the particle would remain stationary until the next wave. The second thing that can happen is that particles might be seen occasionally to reverse direction. As a wave passes under the particle it will spend a short time on the back of the wave. At that point, falling downhill, so to speak, will reverse its direction from its principle motion. Such reversals would be expected to be very short lived.
The prediction of such behaviours is unique to the wave model, it would certainly not be expected on the basis of any flow model. The cytoskeletal model actually makes hardly any predictions but even so transient reversals of motion do not arise obviously from any of its incarnations. It is therefore very striking that such behaviour is indeed reported.
Standard textbooks often use the word saltatory to describe the motions of intracellular organelles, they move for a little while, then stop, then move again. In studies of cell surface particles there are indeed examples of stop start and even occasional reverse motions. Fig. 7.4 shows an example taken from Sheetz's team (Kucik et al. (1989)). The particle moves backward several times, on one occasion for three consecutive time intervals. Such behaviour seems strongly supportive of the wave model.
Amoeboid cells normally derive from eukaryotic organisms which are diploid, they have two copies of each gene. Diploidy makes genetic studies difficult and to avoid this, scientists have turned to a group of organisms known as slime moulds with the convenient property of being haploid, just one copy of each gene. Haploidy makes it possible to produce mutants deficient in a single protein. By comparing the characteristics of the mutant organism with those of the wild type, inferences can be drawn about the biological role played by that protein. Slime moulds produce, at one stage in their life cycle, amoeboid cells that look and behave much like eukaryotic amoeboid cells. Mutants deficient in their cytoskeletal proteins have been made to help analyse the role played by different cytoskeletal proteins in amoeboid motion.
Prof. Sheetz maintains that some results obtained from these mutants disprove the wave model. However, he has been unwilling to cite the actual papers or otherwise document his view. No worker seems to have voiced this position on the scientific record. It is hard to reply to a vague claim but this section is, in part, a rebuttal of it. Actually, the genetic evidence seems, if anything, supportive of the wave model. A succinct review of the results, though not the claim about capping, is in Bray (1992).
The issue lies in the behaviour of mutants deficient in myosin II, a protein found in the cytoskeleton and also muscle, where it is essential for contractile activity. The view is that any activity requiring contraction will not occur, or be very heavily impaired, in cells lacking this protein. Mutant cells lacking myosin II do not die but are very heavily impaired and have motility reduced to 10-20% of wild type. The mutant cells do not cap at all whereas the wild type cells cap normally.
The argument put by Prof. Sheetz seems to go thus - myosin II is a contractile protein. Removing it from the cell produces an organism still able to move, therefore contractility is not important for cell motility and since motility is linked to capping, cytoskeletal contractions cannot be important for capping. Contractility would be important for producing the shape changes in peristaltic waves of the type proposed as likely by the wave model; therefore, waves are not important for movement or capping.
This reasoning is hard to follow, though it might be easier if it were given more clearly. The results seem to suggest the opposite conclusion, that contractility of the cytoskeleton is important for motility. After all the motility of such cells is very heavily impaired. It is far less than half that of a normal cell (Wessels et al. (1988)), Pasternak et al. (1989). Myosin II is not the only myosin in the cell, there is a related protein, myosin I, which is not normally involved in muscle contraction but Bray, discussing these results, suggests that myosin I can to some extent substitute for myosin II. It is also possible that there are other mechanisms of motility besides contractility. If this latter is true, it still seems that cytoskeletal contractility is needed for the greater part of cell motility.
The critical observation for this discussion is that these cells do not undergo capping. It seems to follow that contractility and waves are important for capping and that capping is linked to the dominant mechanism of motility. Any type of travelling wave should generate surf-riding, so, contractility is not technically essential for the success of the wave model. Therefore, to be exact, even if this argument were valid it would not fully rebut the wave model. However, the author can at least agree that contractile waves are the type of waves most likely to drive capping and that the removal of myosin II from the cell would indeed be expected to severely impair their production. On that basis, it is therefore supportive of the wave model, and of the role of contractile waves in capping, that cells carrying such mutations no longer display this behaviour.
In principle a more direct observation of waves on the surface of these cells would offer valuable data but unfortunately there are no reports of waves on the surface of dictyostelium amoebae. Correspondingly, there are no reports about whether or not the deletion of the myosin II does indeed impair such surface waves. There are many other proteins thought to be associated with the cytoskeleton and therefore postulated to be important to motility. Mutants lacking many of these proteins have been made and are generally unimpaired in motility (and, presumably, in capping) - a set of observations seemingly in conflict with most established notions about cytoskeletal function.
Letters were written to workers in slime mould genetics, asking about papers reporting data that might contradict the wave model. One expert clarified my understanding of these cells and gave the opinion that the genetic results do not refute the wave model (the others did not reply).
Taken together these facts suggest that myosin II associated contractility is the main cytoskeletal activity leading both to motility and capping. This is entirely consistent with the wave model, indeed it seems supportive of it, an inference diametrically contrary to the undocumented conclusion seemingly drawn by some leaders in the field.
There has been little criticism of the wave model on record, it is normally ignored. Harris (1972) rejected an early version of the wave model (Ambrose (1961) arguing that, if particles were associated with a cell wave, they would fall off if the petri dish were tipped to one side. He was assuming that the particle is bound to the cell by its weight but this is not so, it is weak chemical forces that will be responsible for the adhesion between particles and the cell. Harris further argued that wave driving would cause particles to move in an oscillatory pattern. In fact, as my later work pointed out, this would not generally be expected. Normally, entrained particles would move at the same rate as waves but saltatory movements are common and reverse movement is rarer but reported.
Bowser & Bloodgood (1984), published a paper entitled "Evidence against Surf-riding as a General Mechanism for Surface Motility" and later a review (Blooodgood (1993)). Prof. Bloodgood kindly sent a reprint. The paper is a study of a shelled protozoan organism called a foraminifer. The organism puts out long protuberances (reticulopods) from its shell and these workers studied particle movement and the movement of "waves" along these. The "waves" are deformations of the membrane due to an underlying organelle, for example a mitochondrion, moving inside the reticulopod and in contact with a deep-lying microtubular bundle, a type of cytoskeletal structure not based on actin or myosin.
They argued (quite reasonably) that these membrane deformations should act as any other wave and transport particles with them. This was not the observation, instead adherent particles travelled in the opposite direction, toward the body of the animal. They argue, on that basis, that the wave model must be wrong, though they did acknowledge there may be wave trains they were unable to observe. As an alternative interpretation, they suggested that some direct contact with the cytoskeleton was able to move objects (the underlying organelle and the surface particle) in two directions at once. It is unclear why they felt their results made this more likely than the presence of a second wavetrain on the other, actomyosin, cytoskeleton just beneath the membrane. It does seem unfortunate that the journal in question did not invite a reply to this paper. This is not the place to respond in further detail. However, although the work is interesting in itself, it did not settle the point the authors hoped to establish, not even in foraminifer, which are hardly typically amoeboid.
Finally, one person (Grebecki (1986)), rejected the wave model on the grounds that he was unable to see waves on the surface of Amoeba Proteus, the organism he was studying. In his study he gave no indication of the minimum wavelength or amplitude of wave he might expect his equipment to detect. Of course, Nelson was unable to see ships, though they were there all the same. Searches reveal no other published criticisms of the wave model. Approaches have been made to many former colleagues and other workers, asking them to give their reasons for rejecting it. Where any reply at all is given, these "critics" of the wave model tend simply cite the lack of evidence "for" it.
It is not really correct to be seeking evidence "for" a model. However, the seriousness with which a model is considered, should reflect the strength of the prima facie case supporting it. There seems ample evidence to present such a case for the wave model. By contrast, no worthwhile prima facie case can be made for the cytoskeletal flow model or any of the other alternatives. Readers still in doubt are invited to reread the above paragraphs and the previous sections on the cytoskeletal and flow models. Where does the lack of evidence "for" really lie? Remembering that it is evidence "against" that carries the logical weight, is there a rebuttal of the evidence against the cytoskeletal models?
In any one experiment, the failure to observe waves may reflect their absence, but it is just as likely to reflect the limitations of light microscopy and a particular observational set up; not to mention the fact that an experimenter who is not looking for waves, and does not want to find them, will not be looking very hard! The observations of Couchman, Lenn & Rees (1985) are very relevant (Fig. 7.5). They observed their cellular waves only under unusual microscopic conditions and showed how they became invisible under more normal conditions. In other words, not seeing waves is no proof they are absent!
Such failures should be set against positive observations in other cases. There is clear evidence that waves are present on and in virtually all eukaryotic cells. By contrast, no positive observations of the membrane or cytoskeleton flowing justify the attention lavished on those notions. In any case, the main "criticism" of the wave model is disregard which is meaningless.
The wave model offers the big advantage of clearly relating capping and particle movement to motility, and aligning the subject with the rest of biology. It is an independently testable proposal, with no obvious negations. Unlike the alternatives it respects the evolvability criterion. When published it seemed a valuable contribution to the field and probably correct. The grounds for this belief seem to become clearer with time.
However, leading scientists do not positively reject the wave model. Instead of disagreeing with it, experts seem unanimously to believe the wave model can be disregarded! The omission of reasonable alternatives distorts and invalidates scientific debate, it is falsehood by omission. Even so, it is difficult to reply to such disregard, there is simply nothing to reply to! Remembering again, that it is evidence against a hypothesis that carries logical weight, scientists who assert such evidence exists should disclose their evidence or argument to those who may disagree. It is a matter of critical rationalism, the integrity of scientific debate and the reliability of scientific knowledge. However, in the capping field, no matter how many times the information is requested, there is simply no real reply.
The reader might like to pause for thought at this point. Opinions of the wave model can be put on a scale from one to ten. One man, like this author, might find the weight of evidence in favour of the wave model compelling and think a rational rebuttal of it would be very difficult if not impossible. (Ten out of ten.) The next man might take a middle ground and view the wave model as a good idea, worth considering alongside alternatives. (Five out of ten.) Another might perceive it as an absurdity - the evidence and arguments presented here are worthless and the model is not worth rebuttal or discussion. (None out of ten.) As a scientific model, how many marks out of ten do you, the reader, give the wave model?
In the next chapters "A Habit of Lies" will describe the debate forming this field and the stated positions and behaviour of its senior figures. They have not stated their opinion of the wave model. However, judging from their actions, it seems they give the wave model none out of ten. It does not deserve rebuttal and raises no questions needing a reply. It is so manifestly wrong, that even this conclusion needs no explanation.
Many of these scientists are major establishment figures, gatekeepers with considerable influence. Although unwilling to explain their views, they can and do put them into practice. The problems arising from this situation need to be resolved and the first step in that direction was to write to the workers concerned, asking how they had eliminated the wave model from debate. Their replies are summarised in the next chapter and a fuller, but still incomplete, archive of their letters will appear in the associated internet site.
The second response was this book. "A Habit of Lies" is, as nearly as practical, a correct record of the scientific situation and the arguments given. It is an accurate history of the field and its development from a standpoint that would otherwise go unrecorded.
This Chapter has :-
- Summarised the wave model and its assumptions.
- Set out the evidence providing a prima facie case for the wave model including the experimental facts and previous knowledge on which it is founded.
- Pointed out the criticisms offered of the wave model and given a summary response.
- Pointed out that the main response of establishment scientists to the wave model has been disregard.
- Explained that this disregard is the reason for writing "A Habit of Lies".
© Copyright John A Hewitt.
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Last Modified 21 August 2005