BilliardsBall
Veteran Member
Wait, where did the additional 1000 come from again?
Are you now saying that modern primate hemostasis requires 1030 proteins?
Good question - I have no idea what you mean and I also think that you don't either, and are just adding extraneous criteria to avoid admitting that you earlier claim was nonsense.
Again, what does that mean?
There are NO other body systems that "recognize bleeding, enforce clotting, send white cells to the site, etc.", but I am getting a kick out of your crazy anthropmomorphizing and pretty obvious shallow understanding of how hemostasis works. See below.
No idea what you mean.
You can calculate the odds on anything, but like any calculation, if what you stick into the calculation is garbage, what you get out will also be garbage.
From your previous and this post, I can see that 1. you don't understand hemostasis, not to mention the fact that there is more than 1 way to stop blood loss, and 2. you seem to think that you can bolster your case by just throwing more and more variables into the mix, hoping that they will stick and/or make others 'back down' in awe at your amazing stats ability.
HEMOSTASIS
As a biologist, this question of yours:
"Can you name 10 other body systems to recognize bleeding, enforce clotting, send white cells to the site, etc.?"
told me a great deal about how much you actually know about this topic.
Hemostasis does NONE of those things.
General flow of events ending with clotting:
1. Trauma to tissue including blood vessel
2. Damaged blood vessel and tissues release various compounds due to damage (note that these compounds are similar, but not identical in all vertebrates)
3. Damage to vessel endothelium creates 'rough' surface; blood components now exposed to collagen and other extravascular proteins ('foreign' materials, in effect); larger blood vessels experience muscular spasm
4. Platelets bind to 'rough' damaged endothelium, release clotting factors
5. Clotting factors (not the same in all vertebrates) initiate cascade of reactions that results in cleavage of fibrinogen, which then reforms as a fibrin network, 'catching' RBCs
6. clotting factors, material released from damaged tissues, and some clotting cascade intermediates act as chemo-attractants for some WBCs
There is not 'recognition' of bleeding; no 'enforcement' of clotting; no act of sending white cells, etc. It is all in effect a series of simple stimulus-response cycles governed by chemical interactions.
I get your line of reasoning, it is pretty common - you are looking at a current extant complex system, rejecting/ignoring/not understanding its lengthy 'history' to get where it is today, and 'wondering' how it all could have come together by 'random change' (and toss in any additional creationist tropes as needed).
As a crude analogy, it would be like someone visiting NYC, being amazed at how many systems have to be operating to keep so large and vibrant a city going - sewage disposal and treatment, water supply, electrical grid, communications lines, safety systems, mass transit, etc., and declaring that since all of these systems have to be in place and up and running for the city to function, that they must have been implemented all at once at the same time, thus only aliens could have built NYC - all the while ignoring/forgetting that NYC has several hundred years of history during which it grew and those complex systems were implemented as technology allowed and constantly upgraded or replaced as needed to get to where NYC is today.
For further info, I suggest you read up on hemostasis -
Evolution of Primary Hemostasis in Early Vertebrates
REVIEW ARTICLE
450 million years of hemostasis
https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1538-7836.2003.00334.x
"...Biochemical evidence, molecular cloning data and comparative sequence analysis support the existence of all components of this network in all jawed vertebrates, and strongly suggest that it evolved
before the divergence of teleosts over 430 million years ago.
Phylogenetic analysis of the amino acid sequences of the Gla–EGF1–EGF2–SP domain serine proteases (FVII, FIX, FX, PC) and the A domain-containing cofactors (FV and FVIII) strongly supports the evolution of the blood coagulation network through
two rounds of gene duplication, and supports the hypothesis that vertebrate evolution benefited from two global genome duplications. The jawless vertebrates (hagfish and lamprey) that diverged over 450 million years ago have a blood coagulation
network involving TF, PT and fibrinogen..."
And to revisit this claim:
I note that you did not, in fact, do any odds calculating, even with your apparently fabricated new numbers.
Kindly read my posts carefully before replying.
When challenged re: 30 proteins being less than unique, I suggested as a conservative allowance (to make the odds INCREASE for evolution) that 1,000 hypothetical proteins, any 30 of which will work. The odds are still quite high, even though I've gone ahead via natural selection and etc. to increase them by billions.
The odds are also astronomical of simultaneity regarding the evolution of the six factors you cited (note my remarks added to the below):
1. Trauma to tissue including blood vessel (to some of a population)
2. Damaged blood vessel and tissues release various compounds due to damage (note that these compounds are similar, but not identical in all vertebrates) (compound release factors evolve)
3. Damage to vessel endothelium creates 'rough' surface; blood components now exposed to collagen and other extravascular proteins ('foreign' materials, in effect); larger blood vessels experience muscular spasm (spasm response evolves or has already evolved)
4. Platelets bind to 'rough' damaged endothelium, release clotting factors (platelets "release clotting factors" evolve)
5. Clotting factors (not the same in all vertebrates) initiate cascade of reactions that results in cleavage of fibrinogen, which then reforms as a fibrin network, 'catching' RBCs (fibrinogen in organic life evolves)
6. clotting factors, material released from damaged tissues, and some clotting cascade intermediates act as chemo-attractants for some WBCs (WBCs naturally selected to bind, cascade intermediates evolve)
The just-so story is vastly, exponentially enlarging, given the fact that the mutations in DNA needed to build a complicated new part (or up to 6 parts in the above, not including cellular motor parts to drive them except platelets as you wrote) quietly accumulate in duplicate genes, because by themselves each of the necessary mutations is neutral, neither beneficial nor harmful. Then, thousands to millions of years later, all are in place, while the species that needed clotting survives when it bleeds from natural causes or prey attack.
The new part starts working, (clotting) natural selection chooses it, and the improved creature is off to the races.
Since this is a religiousforum, I feel it's okay to mention, respectfully, you have a spiritual block in place that makes you believe evolution is magic, all-powerful.