Starlight and Time

[dad1]

Does science know what time, specifically time in the distant universe is? If you claim it does, then be prepared to support that claim.

If science does not know that time exists out there in a way we know it here, then one implication is that no distances are knowable to distant stars.

Why? Because distances depend on the uniform existence of time. If time (in this example 4 billion light years from earth) did not exist the same as time near earth, then what might take a billion years (of time as we know it here) for light to travel a certain distance in space might, for all we know, take minutes weeks or seconds of time as it exists out THERE!

So what methods does science have to measure time there? I am not aware of any. Movements observed at a great distance and observed from OUR time and space would not qualify. Such observations would only tell us how much time as seen here it would take if time were the same there.

How this relates to religion is that a six day creation thousands of years ago cannot be questioned using cosmology if it really did not take light that reaches us on earth and area a lot of time to get here.

[DrNoGods]

[Replying to Inquirer in post #168]

it's not my fault you believe in the flawed unsound model of reality that you've chosen to believe.

Flawed and unsound? But believing an imaginary god being that can't be shown to exist plays a role is rational. That is certainly not the reality I believe in.

Yes, that's exactly what I said. If you disagree, if you care to defend your view, if you think reasons exist for a reason or that determinism arose from non-determinism then please, go ahead and "explain" this, I'm truly interested, I will listen.

A prior thread went on for days on this very issue ... no need rehashing it all again here. Go back and read those posts if you need a refresher ... you made most of them there.

You mean observations like the law of biogenesis? isn't that a good example of you ignoring the very same things?

Biogenesis is not a "law."

Claiming that things just appeared uncaused, claims that the presence of a deterministic universe is not itself the result of determinism is not science, it's not and never has been science that I am disagreeing with, do not elevate these unscientific beliefs you hold so dear, to the status of science.

No one knows how the universe came into existence (you included), and science does not claim to know either. I never claimed otherwise, so the above comment that I somehow did make that claim is just putting words into my mouth that I didn't type (more word games).

You and some others here routinely ridicule God as an explanation, blissfully unaware of the sheer absurdity and self contradictory alternative that this leaves you with, you need to understand that that alternative is far from any definition of "science" I've ever seen.

Then you have a very distorted understanding of what science actually is. It does not involve invoking explanations of anything using imaginary gods or other supernatural entities. If a god being was ever shown to exist then science no doubt could and would take that into consideration. But until then, it is pointless and nonscience to use gods as explanations for anything. It isn't that science adherents ridicule gods as explanations, as much as not seeing a good reason to attribute anything to them without evidence that they actually exist. There is nothing absurd or self contradictory about that simple concept ... just the opposite.

[Inquirer]

Biogenesis is not a "law."

You are quite wrong Dr. It is a law, it is an empirically established law, all laws in science are empirically established by repeated observations of it and no observations of it being violated. It is as much a law for example as Hubble's law.

If you object to the law of biogenesis being so described then I'm afraid you must object to all scientific laws, that is if consistency means anything to you...

[Jose Fly]

Reposting/bumping.....

As Inquirer expressed earlier in this thread, when faced with conflicting interpretations we determine which is valid/accurate by applying scientific testing. That seems very sensible, so let's put it to use.

With the question of the origins of humans (H. sapiens), we have the creationist interpretation of humans arising separately from primates and the evolutionary interpretation of humans arising via common ancestry with other primates. This provides an excellent example to put the "scientific testing" approach to use.

In a 2016 paper, a team of scientists describe the results of a series of tests they conducted addressing this very question....

https://www.readcube.com/articles/10.1101/036327

While there is no doubt among evolutionary biologists that all living species, or merely all living species within a particular group (e.g., animals), share descent from a common ancestor, formal statistical methods for evaluating common ancestry from aligned DNA sequence data have received criticism. One primary criticism is that prior methods take sequence similarity as evidence for common ancestry while ignoring other potential biological causes of similarity, such as functional constraints. We present a new statistical framework to test separate ancestry versus common ancestry that avoids this pitfall. We illustrate the efficacy of our approach using a recently published large molecular alignment to examine common ancestry of all primates (including humans).

We find overwhelming evidence against separate ancestry and in favor of common ancestry for orders and families of primates. We also find overwhelming evidence that humans share a common ancestor with other primate species.

The novel statistical methods presented here provide formal means to test separate ancestry versus common ancestry from aligned DNA sequence data while accounting for functional constraints that limit nucleotide base usage on a site-by-site basis.

Thus, according to the process for identifying the valid/accurate interpretation that we agreed to in this thread, we have our answer. Humans arose via common ancestry with other primates and did not arise separately.

Now comes the fun part. Will creationists accept the results of the process they advocated? Or will they find excuses to reject it because human/primate common ancestry is a conclusion that they will never accept under any circumstances?

[DrNoGods]

[Replying to Inquirer in post #172]

It is a law...

No it isn't. Biogenesis simply invalidates the idea of spontaneous generation. It says nothing about how life may have formed from nonliving molecules in the distant past, or over millions of years. But creationists love to claim it is a "law" ... especially when arguing against evolution or abiogenesis.

[Jose Fly]

Do you believe that some interpretations are closer to the actual reality than others? If so, how do you tell?

You really don't know? by scientifically testing theoretical expectations against observations.

I've given you an opportunity to apply that to the different interpretations of the data relating to human origins. Any response?

[EarthScienceguy]

[Replying to Jose Fly in post #173]

While there is no doubt among evolutionary biologists that all living species, or merely all living species within a particular group (e.g., animals), share descent from a common ancestor, formal statistical methods for evaluating common ancestry from aligned DNA sequence data have received criticism. One primary criticism is that prior methods take sequence similarity as evidence for common ancestry while ignoring other potential biological causes of similarity, such as functional constraints. We present a new statistical framework to test separate ancestry versus common ancestry that avoids this pitfall. We illustrate the efficacy of our approach using a recently published large molecular alignment to examine common ancestry of all primates (including humans).

We find overwhelming evidence against separate ancestry and in favor of common ancestry for orders and families of primates. We also find overwhelming evidence that humans share a common ancestor with other primate species.

The novel statistical methods presented here provide formal means to test separate ancestry versus common ancestry from aligned DNA sequence data while accounting for functional constraints that limit nucleotide base usage on a site-by-site basis.

Ok, let's make this really simple for you all. There really has only been one observable study on the veracity of evolution. Richard Lenski's e'coli experiment at Michigan State. Last time I checked he was at 70,000 generations which have been generated in around 30 years. In that time 12 mutations have been observed. I am going to count all twelve of those mutations as adding information to the genome but a very good case can be made that it is actually subtracting information from the genome. So 12 mutations in 30 years equate to .4 mutations per year. It is usually assumed that life began as a single cell. The number of nucleotides in a single cellular organism is usually around somewhere around 1E6 humans have 3.5E9 nucleotides. So to go from a one-celled organism to the human genome would take right around 9 billion years does anyone else see a problem with this? That is if every species that is mutated can be produced 2333 generations in one year which I think we all know is not the case. So I believe evolution has a problem here with observational science.

Now, what if we take into account a species' generational time? The human genome has 3.5E9 nucleotides, it is commonly accepted that apes, or what every evolutionist wants to call them are man's closest relative and that there is only a difference of 1% in the genetic material. So how long would this take using observational science? 12 mutations in 70,000 generations is 0.0001714 mutations per generation. A 1% difference change would mean that 3.5E7 nucleotides would have to be changed. That means that it would take 2E11 generations if each generation is 20 years that means it would take 4 trillion years.

The problem is actually worse because bacteria are much more prone to genetic change than more complex species.

The math says that evolution is not possible.

[Jose Fly]

There really has only been one observable study on the veracity of evolution. Richard Lenski's e'coli experiment at Michigan State.

That's not only not true, it's a completely bizarre claim (especially given our previous exchanges at ToL). I mean, Dobzhansky was demonstrating speciation in the lab back in the 1930's for Pete's sake!

Last time I checked he was at 70,000 generations which have been generated in around 30 years. In that time 12 mutations have been observed.

Huh? Citation please.

I am going to count all twelve of those mutations as adding information to the genome but a very good case can be made that it is actually subtracting information from the genome.

Oh boy, here we go again....

How are you defining and measuring "genetic information"?

And please, please just answer the question this time, either with a "I don't know" or a definition and quantifiable metric. No more of the stereotypical creationist dodging until you eventually claim to have already answered.

So 12 mutations in 30 years equate to .4 mutations per year. It is usually assumed that life began as a single cell. The number of nucleotides in a single cellular organism is usually around somewhere around 1E6 humans have 3.5E9 nucleotides. So to go from a one-celled organism to the human genome would take right around 9 billion years does anyone else see a problem with this? That is if every species that is mutated can be produced 2333 generations in one year which I think we all know is not the case. So I believe evolution has a problem here with observational science.

No, the problem here is with your lack of understanding, not with the science. For example, each human is born with 100-200 mutations that were not present in either parent.

The math says that evolution is not possible.

Your math is not only wrong, it's incredibly and laughably wrong.

[DrNoGods]

[Replying to EarthScienceguy in post #176]

Ok, let's make this really simple for you all. There really has only been one observable study on the veracity of evolution. Richard Lenski's e'coli experiment at Michigan State. Last time I checked he was at 70,000 generations which have been generated in around 30 years. In that time 12 mutations have been observed.

Are you talking about this Lenski?

https://news.harvard.edu/gazette/story/ ... real-time/

Are you confusing the 12 lines of bacteria he worked with with 12 mutations? Your story is sure different from the article above!

The math says that evolution is not possible.

Since evolution is observed directly and therefore possible (eg. coronavirus mutations for just one of zillions of examples), your math clearly must be wrong.

Explain this:

[EarthScienceguy]

[Replying to DrNoGods in post #178]

Are you confusing the 12 lines of bacteria he worked with with 12 mutations? Your story is sure different from the article above!

I do not think so. I may have been mistaken about there being 12 when there was only 11.

First is the pykF gene. This gene encodes one of two pyruvate kinase enzymes that catalyzes the transfer of a phosphate group from phosphoenolpyruvate (PEP) to adenosine diphosphate (ADP) yielding a molecule of adenosine triphosphate (ATP). PEP is also used to help drive the uptake of glucose, a limited energy source in the experiment. The researches noted an insertion in this genetic region that they hypothesized to have inactivated this gene leading to a greater amount of PEP available to drive glucose uptake.9,16

Second was an insertion mutation in the regulatory region of the pbpA-rodA operon. This operon (which is a cluster of genes under the control of a similar regulatory unit) encodes two important proteins involved with cell wall synthesis. As all 12 E. coli populations evolved larger cell volumes, the authors hypothesized that altered cell wall synthesis or timing of synthesis may have been beneficial.9,16 The exact mechanism of this mutation regarding a gain or loss of novel information is unknown.

A single nucleotide polymorphism (SNP) mutation was found in the mutS gene. This SNP produced a premature stop codon and truncated the MutS protein leading to a defect in DNA repair. This particular mutation was of importance because it greatly increases the number of mutations a bacterial population will accumulate over time.21,27

The hokB-sokB gene locus in E. coli is a toxin-antitoxin system. When found in bacterial chromosomes, these systems are commonly involved in responding to stresses and bringing about programmed cell death. The authors hypothesized that the observed insertion mutation would have knocked out this gene, and a disruption of hokB/sokB would likely be beneficial in the experimental environment.9,16

The researchers observed that all 12 populations of E. coli lost the ability to catabolize D-ribose, an energy source that was not available in this experimental environment. Furthermore, this loss of function was remarkably quick—within 2,000 generations all populations had lost the ability. It was noted that this loss was caused by deletion mutations in the rbs operon.11,15 Interestingly, ribose is one of the energy sources that commensal E. coli use in the intestine.

DNA coiling is an important factor in gene regulation. and a mutation was found in the topA gene that encodes an enzyme that relaxes DNA coils. Along with this, a mutation was found in the genetic region upstream of the fis gene. The product of fis reduces activity of DNA gyrase which itself increases DNA supercoiling. A loss or decrease of function in the protein products of both the topA and fis genes would contribute to the observed increase in DNA supercoiling.14,15

The researchers found a small insertion mutation upstream of glmUS, an operon involved in cell wall biosynthesis. It was hypothesized that this mutation inhibited normal binding of a transcriptional activator to this region thereby reducing glmUS expression.23

The nadR gene encodes a bi-functional protein involved in aspects of nicotinamide adenine dinucleotide (NAD) metabolism. Specifically, this protein represses several genes involved in NAD synthesis so a disruption of this gene and its corresponding protein, especially the repressor function of the protein, would result in more NAD. Dr. Lenski and colleagues observed an insertion mutation into the nadR gene and hypothesized that an increased intracellular concentration of NAD may be beneficial in this environment.9,16 This increase in NAD would be due to a loss of function in the repressor component of the protein.

Dr. Lenski and colleagues noted a mutation in spoT, the product of which is involved in the stringent response through a cell signaling molecule (ppGpp). The precise physiological basis for this advantage is unknown; however no two mutations were identical among bacterial populations that evolved a mutation in this gene.12,15 This finding suggests that any fitness benefits from these mutations were due to a disruption of function.

Interestingly, many bacterial populations evolved resistance to a certain virus even though they were not exposed to that virus throughout the experiment. The protein that the bacteria use to transport and metabolize maltose, an energy source that was not present in their experimental environment, is the same protein that the virus targets to infect the bacteria. Since there is no maltose in the growth media, downregulating this unused metabolic pathway would be beneficial for the bacteria and just so happens to confer viral resistance as well. Genetically this change resulted from a mutation in the malT gene, the regulator of maltose metabolism through positive regulation of the LamB surface protein. Mutation in malT likely rendered its protein product nonfunctional thereby eliminating expression of LamB.24

Perhaps the most famous of all observations in Dr. Lenski’s long-term evolution experiment was when an E. coli population began to utilize a new energy source (citrate) that they normally could not use under aerobic conditions. It is important to note that E. coli already have the ability to transport and metabolize citrate, but the bacteria typically cannot do so in oxic conditions as it does not produce an appropriate transporter in this type of environment (among other required factors). The genetic changes that underlie this particular adaptation are complex, but a key event involved the replication of a genomic region that regulates a citrate transporter. This amplification captured a previously existing and aerobically expressed promoter (the promoter for rnk) which could then direct transcription of the citrate transporter (citT). Repeated tandem amplifications refined this function.27

https://answersingenesis.org/genetics/m ... -creation/
https://www.ncbi.nlm.nih.gov/pmc/articl ... 014799.pdf

Now concerning your video. It does not give the type of mutation that happen or whether there was just one on several. Your event is not representing natural growth but an extinction event. Next time they can try bleach and see if any survive.

[DrNoGods]

[Replying to EarthScienceguy in post #179]

I do not think so. I may have been mistaken about there being 12 when there was only 11.

I didn't read the entire 2000 paper (not the AIG propoganda, but the actual science paper), but it appears they only investigated certain IS mutations that went to fixation, with the goal of tracing them back to the genetic loci. They traced 9 of these (Table 1 shows 11, but two were from a different study), but I didn't see any comments that these specific mutations were the ONLY mutations that were observed ... just the ones studied in detail for this particular paper.

Now concerning your video. It does not give the type of mutation that happen or whether there was just one on several. Your event is not representing natural growth but an extinction event. Next time they can try bleach and see if any survive.

But you had claimed that "the math" shows that evolution doesn't happen. The short video doesn't have to get into the type of mutation or how many there were ... its point was to show that mutations do happen and the bacteria evolved to survive the successive barriers they faced. If there is math that shows this can't happen, it clearly must be wrong.