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Δεν υπήρχαν φίλε μου allzzaro, ή τουλάχιστον η επιστήμη, ΔΕΝ ΕΧΕΙ ΚΑΜΙΑ ΕΞΗΓΗΣΗ....

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Δεν έχω ήχο εδώ που είμαι idustrialangel για να δώ το βίντεο.
Θα το δώ ομως.

Η μάνα μου έχει πεθάνει και ήταν άνθρωπος όχι θεωρία. Οπότε άσε τα αστεία γιατί μπορεί να εκτροχιαστώ

Σου ζήτησα να φέρεις την παράγραφο όπου αναφέρεται ο Δαρβίνος σε "ζωντανά απολιθώματα". Γιατί δεν την φέρνεις; Αφού βρήκες τη φράση εκεί (υποτίθεται)

Βαρέθηκα τα δημαγωγικά κόλπα παραπληροφόρησης που κάνεις. Πραγματικά βαρέθηκα.

All fresh-water basins, taken together, make a small area compared with that of the sea or of the land; and, consequently, the competition between fresh-water productions will have been less severe than elsewhere; new forms will have been more slowly formed, and old forms more slowly exterminated. And it is in fresh water that we find seven genera of Ganoid fishes, remnants of a once preponderant order: and in fresh water we find some of the most anomalous forms now known in the world, as the Ornithorhynchus and Lepidosiren, which, like fossils, connect to a certain extent orders now widely separated in the natural scale. These anomalous forms may almost be called living fossils; they have endured to the present day, from having inhabited a confined area, and from having thus been exposed to less severe competition.

Προέλευση των ειδών σελίδα 49

Κατάλαβες τρέχα γιατί είσαι ο μεγαλύτερος ψεύτης όλων των εποχών;

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εν υπήρχαν φίλε μου allzzaro, ή τουλάχιστον η επιστήμη, ΔΕΝ ΕΧΕΙ ΚΑΜΙΑ ΕΞΗΓΗΣΗ....
Αγορι μου Βιομηχανικέ, εσύ δίνεις ρεσιτάλ, αποπροσανατολισμού...
Καλά, ..μαμά σου ήταν η θεωρία του Δαρβίνου;....

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Ρε γείτονα το άτομο δεν έχει γνώσεις. Πληροφορίες έχει, ασυνάρτητες και σκόρπιες που τις πετάει όπως λάχει. Νομίζει ότι διαψεύδοντας την εξέλιξη, θα φυτρώσει αυτόματα μια θεωρία "θεϊκής παρέμβασης που θα βγάλει νόημα. Δεν έχει παρουσιάσει ποτέ ολοκληρωμένα μια δικιά του κοσμογονία γιατί τότε θα αποκαλυφθεί ότι η θεωρία που πολεμάει είναι 1000000000 φορές πληρέστερη από αυτή που νομίζει ότι είναι σωστή

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Κάνε μια προσπάθεια και εξήγησε μου, αφού τα είδη αυτά που λές δεν προέρχονται απο την εξέλιξη πως βρέθηκαν? Υπήρχαν πάντα?

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Μια προφανής τρύπα της όποιας δημιουργιστικής θεωρίας είναι αυτή.

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- Η γεωλογία, οπωσδήποτε, δεν αποκαλύπτει καμία τέτοια βαθμιαία οργανική αλυσίδα και αυτή, πιθανώς, είναι η προφανέστερη και σημαντικότερη αντίρρηση, που μπορεί να προβληθεί ενάντια στη θεωρία μου.»

Αυτά τα λεει ο Δαρβίνος, φίλε μου, όχι εγώ...Διαβάζεις ότι λέει ο ίδος, ότι δεν αποδεικνύεται η εξέλιξη του;Ποιόν άλλο θέλεις να το πει;...

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Και αυτό το οποίο ειλικρινώς κατέθεσε ο Δαρβίνος , αποτελεί απόδειξη ότι δεν υφίσταται η θεωρία του???

Απο που προκύπτει αυτό Βαγγέλη???

Αυτό καταλαβαίνεις εσύ???

Μείνε μέσα στο παιχνίδι...

Ο τρέχα λοιπόν παραπληροφορεί ΕΛΕΕΙΝΑ

Η ακριβής ρήση του Δαρβίνου είναι:

I have attempted to show that the geological record is extremely imperfect; that only a small portion of the globe has been geologically explored with care; that only certain classes of organic beings have been largely preserved in a fossil state; that the number both of specimens and of species, preserved in our museums, is absolutely as nothing compared with the incalculable number of generations which must have passed away even during a single formation; that, owing to subsidence being necessary for the accumulation of fossiliferous deposits thick enough to resist future degradation, enormous intervals of time have elapsed between the successive formations; that there has probably been more extinction during the periods of subsidence, and more variation during the periods of elevation, and during the latter the record will have been least perfectly kept; that each single formation has not been continuously deposited; that the duration of each formation is, perhaps, short compared with the average duration of specific forms; that migration has played an important part in the first appearance of new forms in any one area and formation; that widely ranging species are those which have varied most, and have oftenest given rise to new species; and that varieties have at first often been local. All these causes taken conjointly, must have tended to make the geological record extremely imperfect, and will to a large extent explain why we do not find interminable varieties, connecting together all the extinct and existing forms of life by the finest graduated steps.

He who rejects these views on the nature of the geological record, will rightly reject my whole theory. For he may ask in vain where are the numberless transitional links which must formerly have connected the closely allied or representative species, found in the several stages of the same great formation. He may disbelieve in the enormous intervals of time which have elapsed between our consecutive formations; he may overlook how important a part migration must have played, when the formations of any one great region alone, as that of Europe, are considered; he may urge the apparent, but often falsely apparent, sudden coming in of whole groups of species. He may ask where are the remains of those infinitely numerous organisms which must have existed long before the first bed of the Silurian system was deposited: I can answer this latter question only hypothetically, by saying that as far as we can see, where our oceans now extend they have for an enormous period extended, and where our oscillating continents now stand they have stood ever since the Silurian epoch; but that long before that period, the world may have presented a wholly different aspect; and that the older continents, formed of formations older than any known to us, may now all be in a metamorphosed condition, or may lie buried under the ocean.

εξέλιξη των ειδών κεφάλαιο 10 προς το τέλος...

Για τις αλλάγες που και καλά δεν είδε

"This extraordinary abundance of some fossils illustrates something important about the history of life. Evolution is a theory about change through time -- "descent with modification," in Darwin's words. Yet when fossils are most abundant during substantial stretches of time, well-represented species are usually stable throughout their temporal range or alter so little and in such superficial ways (usually in size alone) that an extrapolation of observed change into longer periods of geological time could not possibly yield the extensive modifications that mark general pathways of evolution in larger groups. Most of the time, when the evidence is best, nothing much happens to most species.

Niles Eldredge and I have tried to resolve this paradox with our theory of punctuated equilibrium. We hold that most evolution is concentrated in events of speciation, the separation and splitting off of an isolated population from a persisting ancestral stock. These events of splitting are glacially slow when measured on the scale of a human life -- usually thousands of years. But slow in our terms can be instantaneous in geological perspective. A thousand years is one-tenth of one percent of a million years, and a million years is a good deal less than average for the duration of most fossil species. Thus, if species tend to arise in a few thousand years and then persist unchanged for more than a million, we will rarely find evidence for their momentary origin, and our fossil record will tap only the long periods of prosperity and stability. Since fossil deposits of overwhelming abundance record such periods of success for widespread species living in stasis, we can resolve the apparent paradox that when fossils are most common, evolution is most rarely observed."

Μόνο το γεγονός ότι ο τρέχα διαστρέβλωσε 2 ρήσεις σε ένα πόστα τα λέει όλα

[7]. Το μαστίγιο είναι μια περιστροφική προπέλα, την οποία κάποια βακτηρίδια χρησιμοποιούν για τη μετακίνηση τους εντός υγρών. Αποτελείται από τα εξής (κύρια) στοιχεία: Το καθ΄αυτό μαστίγιο που περιστρέφεται εντός του νερού, έναν μοριακό κινητήρα που περιστρέφει το μαστίγιο, έναν αρθρωτό σύνδεσμο που συνδέει το μαστίγιο με τον κινητήρα και έναν στάτορα που κρατάει τον κινητήρα στη θέση του. Αν αφαιρέσουμε ένα οποιοδήποτε από τα ανωτέρω στοιχεία, ο μηχανισμός παύει εντελώς να λειτουργεί. Ένας μηχανισμός που εμφανίζει μη ελαττώσιμη πολυπλοκότητα είναι αδύνατο να εξελιχθεί σταδιακά με δαρβινικό τρόπο (τυχαίες μεταλλάξεις - φυσική επιλογή). Πράγματι, οποιοδήποτε ενδιάμεσο στάδιο της εξέλιξης του μηχανισμού, ακόμα και αν προκύψει από τυχαίες μεταλλάξεις, δεν μπορεί να επιλεγεί από τη φυσική επιλογή, επειδή δεν έχει καμία λειτουργικότητα. Δηλαδή, στη συγκεκριμένη περίπτωση, το 50% του μαστιγίου δε βελτιώνει ούτε στο ελάχιστο την ικανότητα του βακτηριδίου να κολυμπάει και, επομένως, το μαστίγιο δεν μπορεί να εξελιχθεί σταδιακά, αλλά πρέπει να προκύψει σαν ολότητα από τις τυχαίες μεταλλάξεις (κάτι που είναι αστρονομικά απίθανο να συμβεί). Ένα άλλο παράδειγμα είναι ο μηχανισμός με τον οποίο το αίμα πήζει στις πληγές, αποτρέποντας τον θάνατο των οργανισμών από ακατάσχετη αιμορραγία. Ο μηχανισμός βασίζεται σε μια αλυσίδα σαράντα τεσσάρων διαδοχικών αλληλεπιδράσεων μεταξύ πρωτεινών

H μυθολογία των ψευδεπιστημόνων,περί αμείωτης πολυπλοκότητας
http://www.newscientist.com/article/dn13663-evolution-myths-the-bacterial-flagellum-is-irreducibly-complex.html

Actually, flagella vary widely from one species to another, and some of the components can perform useful functions by themselves. They are anything but irreducibly complex

It is a highly complex molecular machine. Protruding from many bacteria are long spiral propellers attached to motors that drive their rotation. The only way the flagellum could have arisen, some claim, is by design.

Each flagellum is made of around 40 different protein components. The proponents of an offshoot of creationism known as intelligent design argue that a flagellum is useless without every single one of these components, so such a structure could not have emerged gradually via mutation and selection. It must have been created instead.

In reality, the term "the bacterial flagellum" is misleading. While much remains to be discovered, we now know there are thousands of different flagella in bacteria, which vary considerably in form and even function.

Different strokes

The best studied flagellum, of the E. coli bacterium, contains around 40 different kinds of proteins. Only 23 of these proteins, however, are common to all the other bacterial flagella studied so far. Either a "designer" created thousands of variants on the flagellum or, contrary to creationist claims, it is possible to make considerable changes to the machinery without mucking it up.

What's more, of these 23 proteins, it turns out that just two are unique to flagella. The others all closely resemble proteins that carry out other functions in the cell. This means that the vast majority of the components needed to make a flagellum might already have been present in bacteria before this structure appeared.

It has also been shown that some of the components that make up a typical flagellum - the motor, the machinery for extruding the "propeller" and a primitive directional control system - can perform other useful functions in the cell, such as exporting proteins.

Changing zooms

It has been proposed that the flagellum originated from a protein export system. Over time, this system might have been adapted to attach a bacterium to a surface by extruding an adhesive filament. An ion-powered pump for expelling substances from the cell might then have mutated to form the basis of a rotary motor. Rotating any asymmetrical filament would propel a cell and give it a huge advantage over non-motile bacteria even before more spiral filaments evolved.

Finally, in some bacteria flagella became linked to an existing system for directing movement in response to the environment. In E. coli, it works by changing flagella rotation from anticlockwise to clockwise and back again, causing a cell to tumble and then head off in a new direction.

Without a time machine it may never be possible to prove that this is how the flagellum evolved. However, what has been discovered so far - that flagella vary greatly and that at least some of the components and proteins of which they are made can carry out other useful functions in the cells - show that they are not "irreducibly complex".

More generally, the fact that today's biologists cannot provide a definitive account of how every single structure or organism evolved proves nothing about design versus evolution. Biology is still in its infancy, and even when our understanding of life and its history is far more complete, our ability to reconstruct what happened billions of years ago will still be limited.

Think of a stone archway: hundreds of years after the event, how do you prove how it was built? It might not be possible to prove that the builders used wooden scaffolding to support the arch when it was built, but this does not mean they levitated the stone blocks into place. In such cases Orgel's Second Rule should be kept in mind: "Evolution is cleverer than you are."

Αυτή είναι η απάντηση της επιστήμης στα μυθεύματα του Behe

Αμείωτα περίπλοκη η πήξη του αίματος...RRRight...! όπως θα έλεγε και ο Dr Evil

http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html
http://www.talkorigins.org/indexcc/CB/CB200_2.html

The blood clotting systems appears to be put together by using whatever long polymeric bridges are handy. There are many examples of complicated systems made from components that have useful but completely different roles in different components. There is also evidence that the genes for blood clotting (indeed, the whole genome) duplicated twice in the course of its evolution (Davidson et al. 2003). The duplication of parts and co-opting of parts with different functions gets around the "challenge" of irreducible complexity evolving gradually.

Blood clotting is not irreducibly complex. Some animals -- dolphins, for example -- get along fine without the Hagemann factor (Robinson et al. 1969), a component of the human blood clotting system which Behe includes in its "irreducible" complexity (Behe 1996, 84). Doolittle and Feng (1987) predicted that "lower" vertebrates would lack the "contact pathway" of blood clotting. Work on the genomes of the puffer fish and zebrafish have confirmed this (Yong and Doolittle 2003).

Irreducible complexity is not an obstacle to evolution and doesn't imply design.

Imitating Rube

Does the human clotting system lend itself to the same kind of analysis? At its core, the actual mechanism of clotting is remarkably simple. A fibrous, soluble protein called fibrinogen ("clot-maker") comprises about 3% of the protein in blood plasma. Fibrinogen has a sticky portion near the center of the molecule, but the sticky region is covered by little amino acid chains with negative charges. Because like charges repel, these chains keep fibrinogen molecules apart.

When a clot forms, a protease (protein-cutting) enzyme clips off the charged chains. This exposes the sticky parts of the molecule, and suddenly, fibrinogens (which are now called fibrins) start to stick together, beginning the formation of a clot.

The protease that cuts off the charged chains is called thrombin. So, just like the lobster clotting system, the heart of the reaction involves just two molecules: fibrinogen and thrombin. But, unlike the lobster, there's a lot more to this machine. It turns out that thrombin itself exists in an inactive form called prothrombin. So it, just like fibrinogen, has to be activated before it can start the clotting process. What activates prothrombin? Here's where life gets really interesting. Prothrombin, a protease itself, is activated by another protease called Factor X which clips of part of the inactive protein to produce active, clot-forming thrombin. OK, so what activates Factor X? Believe it or not, there are still more proteases, two of them, actually, called Factor VII and Factor IX, that can switch on Factor X. What switches them on? Here's where a good teacher goes the the blackboard, and so will I:

Now, "beauty" is a word that most people wouldn't think to put in the same sentence with "biochemistry," but the biochemistry of this pathway is beautiful indeed. Start at the bottom, with the conversion of soluble fibrinogen into clot-forming fibrin. As you look up, you can trace this process to one of two different external stimuli, both of which make good sense. At the upper left, the pathway can be started with damage to a cell surface, something that happens whenever blood is exposed to the air or a foreign object at the surface of a wound. At the upper right, tissue factor, a soluble protein found in most tissues but not in the bloodstream, activates the pathway. This is where clotting starts from an internal hemorrage, a broken vessel within the tissues of the body. So, both of these ultimate stimuli lead to the same set of clot-forming proteins (Factor X, thrombin, and fibrin), but neither does it directly. Instead, each activates a "cascade" of intermediate factors, nearly all of them proteases, which eventually activate clot formation.

It sure does look pretty, but why a cascade? Why couldn't we have a simpler pathway, like the lobster, where something like tissue factor activated clotting directly? Well, we could, but a complex pathway, even if it drives biochemistry students to distraction, has advantages of its own. For one thing, the multiple steps of the cascade amplify the signal from that first stimulus. If a single active molecule of Factor XII could activate, say, 20 or 30 molecules of Factor XI, then each level of the cascade would multiply the effects of a starting signal. Put 5 or 6 steps in the cascade, and you've amplified a biochemical signal more than a million times. Clotting with fewer steps would still work, but it would take longer to produce a substantial clot, and would be much less responsive to smaller injuries.

Michael Behe is in awe of the the intricate complexity of this system, and so am I. And he is also correct in pointing out that if we take away part of this system, we're in trouble. Hemophiliacs, for example, are unable to synthesize the active form of Factor VIII. This means that they are unable to complete the final step of one of the pathways, and that's why hemophilia is sometimes known as the bleeder's disease. Defects or deficiencies in any of the other factors are equally serious. No doubt about it - clotting is an essential function and it's not something to be messed with. But does this also mean that it could not have evolved? Not at all. The key to understanding the evolution of this intricate system, as Russell Doolittle has pointed out, is the fact that the clotting factors share an exquisite and revealing similarity.

Building the Machine

To paraphrase Darwin, the notion that evolution could have produced a system as intricate as the blood clotting cascade seems, we might freely confess, "absurd in the highest possible degree." This is especially true if you believe, as Behe seems to, that clotting is not possible until the entire cascade of factors is assembled.

But we already know that evolution doesn't start from scratch, and it doesn't need fully-assembled systems to work. Remember the lobster system as an example. Blood clotting evolved there from two pre-existing proteins, normally found in separate compartments of the body, that had a fortuituous interaction when damage to a blood vessel brought them together. Once that interaction was established, natural selection did the rest.

Could something like this have happened here?

Remember, we're not starting from nothing. We're starting about 600 million years ago in a small pre-vertebrate. with a low-volume low-pressure circulatory system. Just like any small inverterbate with a circulatory system, our ancestral organism would have had a full compliment of sticky white cells to help plug leaks. In addition, that ancestral system would have had something else. Most of the time, hemorrage starts with cell injury, meaning that cells are broken in the vicinity of a wound and their contents are dumped out. That means, among other things, that all of a cell's internal signalling molecules are suddenly spilled out into the damaged vascular system. Included among the contents are a whole slew of internal signalling molecules, including prominent ones like cyclic adenosine monophosphate (abbreviated: cAMP), all dumped into the tissue surrounding a wound.

Why would a sudden gusher of cAMP in a wound be significant? Well, it turns out that vertebrates use cAMP as a signalling molecule to control the contractions of smooth muscle cells, the very sort of muscle cells that surround blood vessels. Therefore, the release of internal cAMP from broken cells would automatically cause smooth muscles around a broken vessel to contract, limiting blood flow and making it more likely that the blood's own sticky white cells would be able to plug the leak. That means that we already have some ability to limit damage and plug leaks in a primitive, low-pressure system. Not a bad place to begin.

Our next step is to consider the nature of blood itself. For reasons relating to osmotic pressure, the tendency of water to move across cell membranes, blood plasma is a viscous, protein-laden solution. And it's also important to note that the extracellular environment of ordinary tissue is very different from blood. These spaces are laden with protein signals, insoluble matrix molecules, and extracellular proteases that cut and trim these molecules to their final shapes and sizes. In fact, such proteases constitute one of the major forms of extracellular signalling. So the tissues of our ancestral vertebrate would be laden with protein-cutting enzymes for reasons completely unrelated to clotting.

Keeping all of this in mind, what would happen when a blood vessel broke in such an organism?

Well, protein-rich plasma flows into an unfamiliar environment, and sticky white cells quickly "glom" up against the fibers of the extracellular matrix. Tissue proteases, quite accidentally, are now exposed to a new range of proteins, and they cut many of them to pieces. The solubility of these new fragments vary. Some are more soluble than the plasma proteins from which they were trimmed, but many are much less soluble. The result is that clumps of newly-insoluble protein fragments begin to assumulate at the tissue-plasma interface, helping to seal the break and forming a very primitive clot. (Could one object that this is too primitive and too nonspecific to work? That it wouldn't be sufficient to seal breaks? Well, it turns out that you can't make this objection for the very simple reason that this is pretty much the clotting mechanism used today by a large number of invertebrates. Works for them, and therefore there is no reason why it wouldn't have worked for the ancestors of today vertebrates, either!)

Now we get down to business. A mutation duplicates an existing gene for a serine protease, a digestive enzyme produced in the pancreas. Gene duplications happen all the time, and they are generally of such little importance that they are known as "neutral" mutations, having no effect on an organism's fittness. However, the original gene had a control region that switched it on only in the pancreas. During the duplication, the control region of the duplicate is damaged so that the new gene is switched on in both the pancreas and the liver. As a result, the inactive form of the enzyme, a zymogen, is relesased into the bloodstream.

This causes no problem for the organism - most pancreatic proteases are inactive until a small piece near their active sites can be cut away by another protease. However, when damage to a blood vessel allows plasma to seep into tissue, suddenly our previously inactive plasma serine protease is activated by tissue proteases, increasing the overall protein-cutting activity at the site of the hemorrage. Blood clotting is enhanced, so our duplicate gene (with the mistargeted protein) is now favored by natural selection.

That plasma protease gene is now subject to the same witches' brew of copying errors, rearrangements, and genetic reshuffling that affect the genes for every other cellular protein. Over time, bits and pieces of other genes are accidentally spliced into the plasma protease sequence. Because the selective value of the plasma protease is pretty low (it doesn't help clotting all that much), most of these changes make very little difference. But one day, through a well-understood process called "exon shuffling," a DNA sequence known as an "EGF domain" is spliced into one end of the protease gene. EGF stands for epidermal growth factor, a small protein used by cells throughout the body to signal other cells. EGF is so common that just about every tissue cell has "receptors" for it. These receptors are cell surface proteins shaped in such a way that they bind EGF tightly.

The fortuitious combination of a EGF sequence with the plasma protease changes everything.

In a flash, the tissue surrouding a broken blood vessel is now teeming with receptors that bind to the new EGF sequence on our serum protease. As a result, high concentrations of the circulating protease bind directly to the surfaces of cells near a wound. The proteases are activated in the same way, but now their proteolytic activities are highly localized. The production of a clot of insoluble protein fragments is now faster and more specific than ever. Organisms with the new EGF-protease can clot their blood much more quickly than before, and therefore are favored by natural selection. To emphasize its role in the clotting process, that cell surface protein with the EGF receptor is called Tissue Factor.

What happens next? Well, remember the case of the lobster in which a duplicate of a circulating protein (vitellogenin) became specialized to produce a clot-forming protein (lobster fibrinogen)? Once we have a situation in which every hemorrage activates a protease bound to tissue receptors, a gene duplicate of one of the major plasma proteins would then be under strong selective pressure to increase its ability to interact with the bound protease. Fibrinogen, the soluble protein that now is now the primary target of proteolysis in the clotting cascade, clearly arose in this way. Natural selection would favor each and every mutation or rearrangement that increased the sensitivity of fibrinogen to the plasma protease, dramatically enhancing the ability of the new protease to form specific clots of insoluble protein.

There is no doubt that these three steps, each one supported by classic Darwinian mechanisms, would have been sufficient to fashion a rudimentary clotting system. This would leave us with system in which circulating plasma contains both an inactive serine protease and its fibrinogen target. The protease would activated by contact with tissue factor, and the active protease, in turn, would cleave sensitive sites in fibrinogen to form a clot. This system wouldn't be nearly as quick, as responsive, or as sensitive as the current system of vertebrate clotting, but it would work a little better than the system that preceeded it, and that's all that evolution requires.

Adding Complexity

Could evolution take this rudimentary system and produce a multilayered cascade of factors? Just watch. Most serine proteases, including trypsin and thrombin, are auto-catalytic. That means that some extent they can activate themselves, in many cases by cleaving a few amino acids to switch on their active sites. So, we could diagram the actual functions of our ancestral plasma protease (which we'll call protease A) like this:

As we have seen, the inactive form of the protease (A) is changed into the active form (A*) when two things happen: it is bound to tissue factor (TF) and it is activated by tissue proteases, including our protease itself (that's the autocatalytic part). This means - and this is important - that our protease is actually involved in cutting two things: Fibrinogen, and also itself, converting A's inactive precursor protein into A*.

Now, let's suppose that a gene duplication occurs in the gene for our protease, producing a new (B) version of the gene:

At first, just like most gene duplications, this is no big deal. Proteins A and B are identical. Each can bind to TF, each can cleave fibrinogen into fibrin, and each can activate itself or its sister serum protease. So nothing has really changed - we've just got two copies of the same gene. But now let's suppose that a mutation in the active site of B changes its behavior, making it a little less likely to cut fibrinogen and a little more likely to activate protease A. In essence, this would change the relationship between these previously duplicate genes to something like this:

Suddenly, the ability of A to bind to TF becomes much less important. If B can saturate all of the available TF-binding sites itself (by virtue of its EGF domain), then the TF-mediated activation of B, combined with B's affinity for A, will result in a rapid activation of A, producing plenty of activated A to convert fibrinogen into clottable fibrin. Sounds good. But why would natural selection favor a mutation like this in B's active site? Simple: it would increase the efficiency of the clotting process by producing a 2-level cascade. Look closely, and you'll see that our 1-step clotting system required a direct interaction with TF to activate each protease. The new 2-step system allows each TF to activate a protease B, each of which in turn can activate scores or hundreds of A's. With so many more active proteases in the neighborhood of the injury, clotting can now occur more quickly, increasing the chances of surviving a hemorrage. Exactly the sort of stuff that natural selection favors.

Step back for a second and think about what we've just seen. A simple gene duplication sets the stage for the selection of active site mutations that would dramatically improve the clotting process. Gene duplications are neutral mutations, the sort that occur all the time and therefore, given enough time, are highly probable. Once the duplication has taken place, any mutation in the active site that shifts the preferences of the active site in the direction I have mentioned will be strongly favored. And that means that a true 2-step system will evolve very quickly.

Two additional points have to be mentioned. The first one is obvious. If gene duplication and subsequent mutation of the duplicate protease can change a 1-step system into a 2-step one, they could certainly change a 2-step system into a 3-step one. This means that increases in biochemical complexity are not only accomodated by evolutionary theory, they are actually predicted by it. The second point is a little more subtle. Early stages in the evolution of a clot forming-system are bound not to work very well. But as the system starts to work better, as it increases in complexity and efficiency, it begins to present a danger to the organism. That danger, simply put, is that clotting might get out of hand. As the clot-forming cascade evolves larger and larger, there is a chance that a small stimulus will start a reaction that might cause all of an organism's blood to clot, or at least enough of it to cause serious problems. Does evolution have an answer to that, too?

Well, it turns out that it does. First, keep in mind that a primitive clotting system, adequate for an animal with low blood pressure and minimal blood flow, doesn't have the clotting capacity to present this kind of a threat. But just as soon as the occasional clot becomes large enough to present health risks, natural selection would favor the evolution of systems to keep clot formation in check. And where would these systems come from? From pre-existing proteins, of course, duplicated and modified. The tissues of the body produce a protein known as a1-antitrypsin which binds to the active site of serine proteases found in tissues and keeps them in check. So, just as soon as clotting systems became strong enough, gene duplication would have presented natural selection with a working protease inhibitor that could then evolve into antithrombin, a similar inhibitor that today blocks the action of the primary fibrinogen-cleaving protease, thrombin.

In similar fashion, plasminogen, the precursor to a powerful clot-dissolving protein now found in plasma, would have been generated from duplicates of existing protease genes, just as soon as it became advantageous to develop clot-dissolving capability.

In short, the key to understanding the evolution of blood clotting is to appreciate that the current system did not evolve all at once. Like all biochemical systems, it evolved from genes and proteins that originally served different purposes. The powerful opportunistic pressures of natural selection progressively recruited one gene duplication after another, gradually fashioning a system in which high efficiences of controlled blood clotting made the modern vertebrate circulatory system possible.

Mining the Biochemical Past

Can we know for sure that this is how blood clotting (or any other biochemical system) evolved? The strict answer, of course, is we cannot. The best we can hope from our vertebrate ancestors are fossils that preserve bits and pieces of their form and structure, and it might seem that their biochemistry would be lost forever. But that's not quite true. Today's organisms are the descendents of that biological (and biochemical) past, and they provide a perfect opportunity to test these ideas.

Even a general scheme, like the one I've just presented, leads to a number of very specific predictions, each of which can be tested. First, the scheme itself is based on the use of well-known biochemical clues. For example, most of the enzymes involved in clotting are serine proteases, protein-cutting enzymes so-named because of the presence of a highly reactive serine in their active sites, the business ends of the protein. Now, what organ produces lots of serine proteases? The pancreas, of course, which releases serine proteases to help digest food. The pancreas, as it turns out, shares a common embryonic origin with another organ: the liver. And, not surprisingly, all of the clotting proteases are made in the liver. So, to "get" a masked protease into the serum all we'd need is a gene duplication that is turned on in the pancreas' "sister" organ. Simple, reasonable, and supported by the evidence.

Next, if the clotting cascade really evolved the way I have suggested, the the clotting enzymes would have to be near-duplicates of a pancreatic enzyme and of each other. As it turns out, they are. Not only is thrombin homologous to trypsin, a pancreatic serine protease, but the 5 clotting proteases (prothrombin and Factors X, IX, XI, and VII) share extensive homology as well. This is consistent, of course, with the notion that they were formed by gene duplication, just as suggested. But there is more to it than that. We could take one organism, humans for example, and construct a branching "tree" based on the relative degrees of similarity and difference between each of the five clotting proteases. Now, if the gene duplications that produced the clotting cascade occurred long ago in an ancestral vertebrate, we should be able to take any other vertebrate and construct a similar tree in which the relationships between the five clotting proteases match the relationships between the human proteases. This is a powerful test for our little scheme because it requires that sequences still undiscovered should match a particular pattern. And, as anyone knows who has followed the work in Doolittle's lab over the years, it is also a test that evolution passes in one organism after another.

There are many other tests and predictions that can be imposed on the scheme as well, but one of the boldest was made by Doolittle himself more than a decade ago. If the modern fibrinogen gene really was recruited from a duplicated ancestral gene, one that had nothing to do with blood clotting, then we ought to be able to find a fibrinogen-like gene in an animal that does not possess the vertebrate clotting pathway. In other words, we ought to be able to find a non-clotting fibrinogen protein in an invertebrate. That's a mighty bold prediction, because if it could not be found, it would cast Doolittle's whole evolutionary scheme into doubt.

Not to worry. In 1990, Xun Yu and Doolittle won their own bet, finding a fibrinogen-like sequence in the sea cucumber, an echinoderm. The vertebrate fibrinogen gene, just like genes for the other proteins of the clotting sequence, was formed by the duplication and modification of pre-existing genes.

Now, it would not be fair, just because we have presented a realistic evolutionary scheme, supported by gene sequences from modern organisms, to suggest that we now know exactly how the clotting system has evolved. That would be making far too much of our limited ability to reconstruct the details of the past. But nonetheless, there is little doubt that we do know enough to develop a plausible and scientifically valid scenario for how it might have evolved. And that scenario makes specific predictions that can be tested and verified against the evidence.

References:

Doolittle, R. F., (1993) "The evolution of vertebrate blood coagulation: A case of yin and yang," Thrombosis and Haemostasis 70: 24-28.

Doolittle, R. F., and Feng, D. F., (1987) "Reconstructing the evolution of vertebrate blood coagulation from a consideration of the amino acid sequences of clotting proteins," Cold Spring Harbor Symposia on Quantitative Biology 52: 869-874.

Doolittle, R. F., and Riley, M. (1990) "The amino-acid sequence of lobster fibriongen reveals common ancestry with vitellogenin." Biochemical and Biophysical Research Communications. 167: 16-19.

Απο το να αντιγράφεις σεντόνια , δώσε μας απευθείας την πηγή της ΚΟΤΣΑΝΑΣ για να ξέρουμε και απο που προέρχονται :

http://www.zoiforos.gr/index.php?option=com_content&task=view&id=1736&Itemid=164

Εγω απλά θα τονίσω οτι αν η επίσημη εκκλησία υιοθετεί , αυτά που αναφέρει η ιστοσελίδα αυτή , τοτε πρόκειται για ευθεία ΕΞΑΠΑΤΗΣΗ των αφελών πιστών .

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Ένας από τους σπουδαιότερους εξελικτές παλαιοντολόγους της εποχής μας, ο Stephen J. Gould μιλώντας για τα απολιθώματα, λέει: «Η ιστορία των περισσότερων απολιθωμένων ειδών περιλαμβάνει δύο στοιχεία ιδιαίτερα ασύμβατα με τη βαθμιαία εξέλιξη:
.....

Βιομηχανικούλη, μπαγασάκο, αν διαβάσεις το κείμενο, που παραθέτω, μπορεί να δεις το ..,φώς....Να καταλάβεις ποσο δύσκολο είναι η κατανόηση της ύπαρξης ή όχι της θεωρίας του Δαρβίνου...

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Οσο για τα περι στάσης και ξαφνικής εμφάνισης που γράφει ο
Gould είναι αποτελεσμα ΕΣΚΕΜΜΕΝΗΣ ΔΙΑΣΤΡΕΒΛΩΣΗΣ του κειμένου του .

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Edited by - IndustrialAngel on 20/06/2010 12:52:07

Λένε οι μέγιστοι παπάδες επιστήμονες

http://evolution.berkeley.edu/evosite/evo101/VIIB1cCambrian.shtml

Ας δούμε τι λέει ένα πανεπιστημιο

Around 530 million years ago, a wide variety of animals burst onto the evolutionary scene in an event known as the Cambrian explosion. In perhaps as few as 10 million years, marine animals evolved most of the basic body forms that we observe in modern groups. Among the organisms preserved in fossils from this time are relatives of crustaceans and starfish, sponges, mollusks, worms, chordates, and algae, exemplified by these taxa from the Burgess Shale.

An “explosion”?
The term “explosion” may be a bit of a misnomer. Cambrian life did not evolve in the blink of an eye. The Cambrian was preceded by many millions of years of evolution, and many of the animal phyla actually diverged during the Precambrian.
The animals of the Cambrian did not appear out of thin air. Animal fossils from before the Cambrian have been found. Roughly 575 million years ago, a strange group of animals known as Ediacarans lived in the oceans. Although, we don’t know much about the Ediacarans, the group may have included ancestors of the lineages that we identify from the Cambrian explosion.

Επίσης

http://www.pbs.org/wgbh/evolution/library/03/4/l_034_02.html

The Cambrian Explosion:

For most of the nearly 4 billion years that life has existed on Earth, evolution produced little beyond bacteria, plankton, and multi-celled algae. But beginning about 600 million years ago in the Precambrian, the fossil record speaks of more rapid change. First, there was the rise and fall of mysterious creatures of the Ediacaran fauna, named for the fossil site in Australia where they were first discovered. Some of these animals may have belonged to groups that survive today, but others don't seem at all related to animals we know.

Then, between about 570 and 530 million years ago, another burst of diversification occurred, with the eventual appearance of the lineages of almost all animals living today. This stunning and unique evolutionary flowering is termed the "Cambrian explosion," taking the name of the geological age in whose early part it occurred. But it was not as rapid as an explosion: the changes seems to have happened in a range of about 30 million years, and some stages took 5 to 10 million years.

It's important to remember that what we call "the fossil record" is only the available fossil record. In order to be available to us, the remains of ancient plants and animals have to be preserved first, and this means that they need to have fossilizable parts and to be buried in an environment that will not destroy them.

It has long been suspected that the sparseness of the pre-Cambrian fossil record reflects these two problems. First, organisms may not have sequestered and secreted much in the way of fossilizable hard parts; and second, the environments in which they lived may have characteristically dissolved those hard parts after death and recycled them. An exception was the mysterious "small shelly fauna" -- minute shelled animals that are hard to categorize -- that left abundant fossils in the early Cambrian. Recently, minute fossil embryos dating to 570 million years ago have also been discovered. Even organisms that hadn't evolved hard parts, and thus didn't leave fossils of their bodies, left fossils of the trails they made as they moved through the Precambrian mud. Life was flourishing long before the Cambrian "explosion".

Σημείωση δικιά μου: Η ζωή υπήρχε και εξελισσόταν πιο πριν από την έκρηξη της Καμβρίου και άφησε ίχνη για να τα βρούμε σήμερα ΑΛΛΑ δεν είχαν σκελετό τα ζώα πιο πριν οπότε τα απολιθώματα είναι πιο αραιά

The best record of the Cambrian diversification is the Burgess Shale in British Columbia. Laid down in the middle-Cambrian, when the "explosion" had already been underway for several million years, this formation contains the first appearance in the fossil record of brachiopods, with clamlike shells, as well as trilobites, mollusks, echinoderms, and many odd animals that probably belong to extinct lineages. They include Opabinia, with five eyes and a nose like a fire hose, and Wiwaxia, an armored slug with two rows of upright scales.

The question of how so many immense changes occurred in such a short time is one that stirs scientists. Why did many fundamentally different body plans evolve so early and in such profusion? Some point to the increase in oxygen that began around 700 million years ago, providing fuel for movement and the evolution of more complex body structures. Others propose that an extinction of life just before the Cambrian opened up ecological roles, or "adaptive space," that the new forms exploited. External, ecological factors like these were undoubtedly important in creating the opportunity for the Cambrian explosion to occur.

(Σημείωση δικιά μου: ένα περιβάλλον που αλλάζει έντονα αναγκάζει τους οργανισμούς να εξελιχθούν)

Internal, genetic factors were also crucial. Recent research suggests that the period prior to the Cambrian explosion saw the gradual evolution of a "genetic tool kit" of genes that govern developmental processes. Once assembled, this genetic tool kit enabled an unprecedented period of evolutionary experimentation -- and competition. Many forms seen in the fossil record of the Cambrian disappeared without trace. Once the body plans that proved most successful came to dominate the biosphere, evolution never had such a free hand again, and evolutionary change was limited to relatively minor tinkering with the body plans that already existed.

Interpretations of this critical period are subject of lively debate among scientists like Stephen Jay Gould of Harvard University and Simon Conway Morris of Cambridge University. Gould emphasizes the role of chance. He argues that if one could "rerun the tape" of that evolutionary event, a completely different path might have developed and would likely not have included a humanlike creature. Morris, on the other hand, contends that the environment of our planet would have created selection pressures that would likely have produced similar forms of life to those around us -- including humans.

Αυτή είναι η γνώση σου για το πείραμα του Λένσκυ, πανίβλακα; Έχω ανεβάσει το λινκ της εργασίας του. Διάβασε το και ξεστραβώσου. ΟΛΑ λάθος τα γράφει... Στην εξέλιξη δεν έχει σημασία ο αριθμός των ατόμων όσο ο αριθμός των γενεών. Ξύπνα γκασμά... Το ότι είμαστε σήμερα 6 δις δε σημαίνει ότι θα έχουμε 6 δις μεταλλάξεις....

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Ξύπνα γκασμά... Το ότι είμαστε σήμερα 6 δις δε σημαίνει ότι θα έχουμε 6 δις μεταλλάξεις....

Edited by - IndustrialAngel on 20/06/2010 13:28:48

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Ισχυρίζεσαι ότι σε βρίζει γι'αυτό και μιλάς αντίστοιχα...εδώ όμως και τόσα μηνύματα δεν σου έχει απαντήσει και παρ'ολ'αυτά συνεχίζεις προκλητικά να τον βρίζεις...

Μήπως Γιώργο κάτι συμβαίνει με σένα και το οποίο δεν έχει να κάνει με τον Βαγγέλη..???

Σε καθε περίπτωση είναι δικαιωμά του να πιστεύει ότι θέλει...εσύ γιατί θέλεις "σώνει και καλά" να τον πείσεις???

Αναρρωτιέμαι...

Όσο για την απάντησή μου περί συνθέσεως και δημιουργίας εκ του μηδενός..δεν απάντησες τίποτα...

Μείνε μέσα στο παιχνίδι...

Θα πω για πολλοστή φορά. Ο σεβασμός κερδίζεται. Κερδίζεται με την αξιοπρέπεια, την ειλικρίνεια, το σεβασμό που δείχνεις για τους άλλους. Δεν κερδίζεται με την υπεροψία, την αδιαλλαξία και το ψεύδος. Δεν κερδίζεται με την κατάργηση των κανόνων του διαλόγου. Όταν ο άλλος δε σέβεται, δε μιλάει ειλικρινά αντιμετωπίζεται αναλόγως.

Γιατί δε διαβάζεις το πείραμα του Λένσκι να δεις τι λέει ο ίδιος και τι έχουν μεταφέρει στο σάιτ που αντιγράφει και υιοθετεί ο τρέχα; Τι γνώμη έχεις για αυτό; Είναι ΚΑΤΑΦΟΡΗ παραπληροφόρηση ή όχι; Αν ναι, τότε εγώ πιστεύω ότι έχει συμφέρον και σκοπούς να παραπληροφορεί ο τρέχα. Και αυτό με οδηγεί στη σκέψη ότι χρησιμοποιεί το φόρουμ ως πηγή προπαγάνδας για τα πιστεύω του. Και αυτό με εξοργίζει...

Καλώς ή κακώς, επιτρέπεται σε όλους να μιλάνε στη δημοκρατία. Για εμένα είναι καλώς να ομιλούμε όλοι, για τον τρέχα είναι κακώς, δεν τον συμφέρουν οι απόψεις μου. Όμως η ελευθερία λόγου γίνεται ασυδοσία και για αυτό κρίνουμε απόψεις και άτομα.

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Εαρινέ, όταν φέρνεις ένα κείμενο σημαίνει ότι το υιοθετείς. Ο καθένας κρίνεται από την ποιότητα των ισχυρισμών του και των αποδείξεων που έχει για αυτούς. Όταν φέρνεις ένα κείμενο γεμάτο πλάνες και ψεύδη και λες στους άλλους υπεροπτικά ότι εσύ είσαι ο πληροφορημένος το λιγότερο που μπορείς να ακούσεις είναι ότι είσαι ένας βλάκας και μισός.

Θα πω για πολλοστή φορά. Ο σεβασμός κερδίζεται. Κερδίζεται με την αξιοπρέπεια, την ειλικρίνεια, το σεβασμό που δείχνεις για τους άλλους. Δεν κερδίζεται με την υπεροψία, την αδιαλλαξία και το ψεύδος. Δεν κερδίζεται με την κατάργηση των κανόνων του διαλόγου. Όταν ο άλλος δε σέβεται, δε μιλάει ειλικρινά αντιμετωπίζεται αναλόγως.

Γιατί δε διαβάζεις το πείραμα του Λένσκι να δεις τι λέει ο ίδιος και τι έχουν μεταφέρει στο σάιτ που αντιγράφει και υιοθετεί ο τρέχα; Τι γνώμη έχεις για αυτό; Είναι ΚΑΤΑΦΟΡΗ παραπληροφόρηση ή όχι; Αν ναι, τότε εγώ πιστεύω ότι έχει συμφέρον και σκοπούς να παραπληροφορεί ο τρέχα. Και αυτό με οδηγεί στη σκέψη ότι χρησιμοποιεί το φόρουμ ως πηγή προπαγάνδας για τα πιστεύω του. Και αυτό με εξοργίζει...

Καλώς ή κακώς, επιτρέπεται σε όλους να μιλάνε στη δημοκρατία. Για εμένα είναι καλώς να ομιλούμε όλοι, για τον τρέχα είναι κακώς, δεν τον συμφέρουν οι απόψεις μου. Όμως η ελευθερία λόγου γίνεται ασυδοσία και για αυτό κρίνουμε απόψεις και άτομα.

Edited by - IndustrialAngel on 20/06/2010 17:09:23

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Τον Βαγγέλη "θέλεις" να πείσεις ή τους υπολοίπους συνδικτυους σου και όχι μόνον...???

Εσύ εστιάζεις όλη την προσοχή και την ενέργειά σου , σε ένα και μόνο πρόσωπο...και αυτό μπορώ να πώ ότι σε περιορίζει και σε θέτει σε εγκλωβισμό..!

Κοίτα γύρω σου..μην κοιτάς το δένδρο..κοίτα το δάσος , το χάνεις φίλε μου και είναι κρίμα...!

Μείνε μέσα στο παιχνίδι...

Παρεπιπτόντως βλέπεις πώς εκφράζεται ο πολιτισμένος. Επίσης προτείνω να ασχοληθείς με τα επιχειρήματα και των δύο πλευρών ώστε να λάβεις θέση.

Βρίσε τρέχα και σκούπισε τα δάκρυα και τους αφρούς που βγάζεις. Συνετρίβησαν οι θέσεις σου εφημεριδοπώλη.Η πληροφορία που μας παραθέτεις ΜΠΑΖΕΙ από όλες τις μπάντες, αμερόληπτε δημοσιογράφε της δεκάρας.

15 επιστήμονες γράψανε ένα ανυπόγραφο κείμενο; ΘΑΥΜΑ ΘΑΥΜΑ. Μήπως θα μας πεις ότι ο Μπέχε ξέρει ελληνικά; Καλά είναι δυνατόν να είσαι τόσο βλάκας, τόσο πορωμένος με τη θρησκεία, που να μη βλέπεις ότι σε δουλεύουν ΚΑΝΟΝΙΚΑ; Η' μήπως πληρώνεσαι για να τα λες αυτά; Το κείμενο αυτό είναι ένα μάζεμα από κομμάτια βιβλίων τα οποία δεν είναι επιστημονικά και έχουν διαψευστεί 8000 φορές σε διάφορες περιστάσεις. Το μάζεμα αυτό το έκανε κάποιος Κορναράκης όχι 15 επιστήμονες... Αυτή είναι η πηγή σου βλάκα. Μια μπουρμπουλήθρα...

Έχω πει 8000 φορές. Γιατί να μη φέρνουμε ΠΡΩΤΟΤΥΠΟ κείμενο όταν αναφερόμαστε σε ρήσεις;

Edited by - IndustrialAngel on 20/06/2010 18:39:50

Αυθεντική πηγή είναι οι εξής μεγάλοι επιστήμονες

http://vatopaidi.wordpress.com/2009/09/04/darwin1/#more-14929

ΟΙ...Βατοπεδινοί...

Δε λέω... οικονομικά ξέρουν...Ξέρουν ΚΑΙ βιολογία;

http://news.nationalgeographic.com/news/2005/04/0427_050427_intelligent_design.html

Η απάντηση των επιστημόνων είναι ένα ΒΡΟΝΤΕΡΟ ΟΧΙ

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