[_ Old Earth _] Can a whale turn into a hamster if given millions of years?

[Paidion]

Could a whale eventually turn into a hamster if given millions of years?

The whale can do better than that! It can turn into a human being!

Just open your hand, and look at the palm. You can clearly the tail of a whale. Clear proof that we have all evolved from whales.

 

[Rick W]

Interesting research, Rick.

Thanks for sharing.

This is why evolutionary biologists need to be very careful in designating drug resistant bacteria as a new species and evidence of macroevolution. This research indicates that the drug resistance was built into the species, and is in fact part of the species genome.

:yes

Not many know about this discovery and yet it's poised on bringing to mankind a weapon against disease for which there will be no defense, no "evolved" resistance. No longer will we simply be reacting to a drug's degrading effectiveness. The implications of this research are enormous. It will give a different point of view in unlocking the defense mechanisms of drug resistant strains of disease that seem to be keeping one step ahead of the medical field.
This should have been front page news worldwide hailed as one of the biggest discoveries since vaccinations. The possibilities of this research shouldn't go unpublicized and I honestly pray these people get as much funding as they need to continue research.

The video acknowledges diseases becoming resistant over the past 50 to 60 years. With this research it's hoped that the older antibiotics, now somewhat ineffective against the diseases, can regain their potency when administered with the inhibitors they are creating so the diseases cannot develop resistance against the antibiotics.

The research isn't simply for Streptococcus pneumoniae. Streptococcus pneumoniae was the first bacteria studied and certainly won't be the last. One must start somewhere and something has to be first. Now that it's known what to look for other drug-resistant diseases can be targeted such as Tuberculosis.

These diseases don't mutate. They already have a defense mechanism that modern technology is now becoming able to uncover and do something about it rather than attempting to develop new antibiotics on a continuous basis. Nowhere in the video is mutation even mentioned to explain a bacteria's ability to become drug resistant. There's no reason anymore.

 

[coelacanth]

Can animals evolve into another kind of animal if given enough time? In other words, could a dog evolve into a cat? A wolf into a peacock? A mouse into a hippopotamus?

Either Dave Slayer has never read any past responses to his questions, or he is trolling. May I invoke the "do not feed the troll" rule? This is absurdity at its finest. I'm serious. I even asked him if my last response to the donkey thing was helpful and I got nothing.

 

[coelacanth]

ooooohhhhhh, a furry whale? Cool!

I really like watching whales. Ever see that show on discovery where a group tries to save whales all the time?

Whales are distributed throughout the world’s oceans and seas, from the Equator to the polar ice, except for the landlocked Caspian and Aral seas. They are mammals, and they share the defining traits of that group: they breathe air, are warm-blooded, give live birth, suckle their young on milk, and have hair.

http://www.britannica.com/EBchecked/topic/641397/whale

 

[kenan]

Either Dave Slayer has never read any past responses to his questions, or he is trolling. May I invoke the "do not feed the troll" rule? This is absurdity at its finest. I'm serious. I even asked him if my last response to the donkey thing was helpful and I got nothing.

Yeah, I have to agree with this. I mean, c'mon Dave, it's getting a bit silly isn't it? There is a multitude of evolution threads out there if you want to look at them.

 

[Barbarian]

This is why evolutionary biologists need to be very careful in designating drug resistant bacteria as a new species

You know almost all biologists accept evolution, don't you? It's a little hard to decide when a strain of bacteria is changed enough to be a new species (since they reproduce asexually, the biological species concept doesn't apply to them) but there are useful procedures for doing this. I'd suggest you go to a good library, go check out the different Bergey's Manuals over the years and see how it actually happens. Hint: it's not the way you seem to think it is.

This research indicates that the drug resistance was built into the species, and is in fact part of the species genome.

No, it doesn't. And Luria/Delbruck ruled that one out decades ago.

In fact the cite article says that it wasn't built into the "species genome."

Research led by the University of Warwick has uncovered exactly how the bacterium Streptococcus pneumoniae has become resistant to the antibiotic penicillin.

Other populations of this species don't have the ability to do that. In many cases, bacteriologists have been able to pinpoint the mutation that caused resistance.

Antimicrob Agents Chemother. 2003 September; 47(9): 2892–2896.
doi: 10.1128/AAC.47.9.2892-2896.2003.

Resistance to the Peptidyl Transferase Inhibitor Tiamulin Caused by Mutation of Ribosomal Protein L3
Jacob Bøsling,1 Susan M. Poulsen,1 Birte Vester,2 and Katherine S. Long1*

The antibiotic tiamulin targets the 50S subunit of the bacterial ribosome and interacts at the peptidyl transferase center. Tiamulin-resistant Escherichia coli mutants were isolated in order to elucidate mechanisms of resistance to the drug. No mutations in the rRNA were selected as resistance determinants using a strain expressing only a plasmid-encoded rRNA operon. Selection in a strain with all seven chromosomal rRNA operons yielded a mutant with an A445G mutation in the gene coding for ribosomal protein L3, resulting in an Asn149Asp alteration. Complementation experiments and sequencing of transductants demonstrate that the mutation is responsible for the resistance phenotype. Chemical footprinting experiments show a reduced binding of tiamulin to mutant ribosomes. It is inferred that the L3 mutation, which points into the peptidyl transferase cleft, causes tiamulin resistance by alteration of the drug-binding site. This is the first report of a mechanism of resistance to tiamulin unveiled in molecular detail.

 

[Rick W]

Barbarian,
What good has come from research of mutation driven resistance? What treatments of value have been developed? It all sounds good and very complicated but if nothing can come of it then what good is it?
A change is observed. Without knowing the exact mechanics of the change the label "mutation" is used to explain that change because it doesn't fit any known cause and effect mechanism.

It all sounds scientific and very complex as it needs to be to address an unknown change or to come up with a reason why the change occurred in the first place without knowing the specific cause. Again, what practical treatments have come from concluding mutant driven resistance?

 

[Barbarian]

Barbarian,
What good has come from research of mutation driven resistance? What treatments of value have been developed?

Antibiotic protocols are designed according to evolutionary theory, to minimize the likelihood of antibiotic resistance developing. That's why, when your doctor gives you antibiotic pills, he says "take all of these, don't stop until they are all gone."

Now, people like Barry Hall are observing what the descendants of single bacterial cells do in response to antibiotics, to predict what future forms of resistance will evolve. Drug companies are already working on this. The breakthrough you've cited is part of that process. Specific new antibiotics are being developed with this data in mind.

 

[Rick W]

Antibiotic protocols are designed according to evolutionary theory, to minimize the likelihood of antibiotic resistance developing. That's why, when your doctor gives you antibiotic pills, he says "take all of these, don't stop until they are all gone."

Protocols?
I'm not talking about protocols. I'm talking about real treatment like the University of Warwick is developing.
Nowhere in the video do they talk about protocols. They are developing real treatment to eliminate a bacteria's ability to become drug resistant.

Evolutionary resistance rests on mutation. As far as I can tell nothing much has come of this except the excuse, "It mutates therefore we are powerless against it and must continually devise new drugs." The only ones benefiting are the drug companies coming up with these new drugs and the reseachers getting an annual salary.

I have a feeling all this research done concerning "mutations" is only to support the belief in evolution with no or very little motivation to actually find a worthwhile and practical treatment. That and to preserve a lot of egos for those who want to prove evolution through a bacteria's inherent ability to become drug resistant. Where is the payoff for all this research? Will we ever see any results that can be used to actually help people with these diseases? Or will we keep tossing money at the evolutionists so they can stir their data and come up with some sort of results to appease an appropriations committee?

Evolutionary resistance is a dead end. It's not going anywhere much less come to any good.

 

[Barbarian]

Protocols?
I'm not talking about protocols. I'm talking about real treatment like the University of Warwick is developing.

They are real treatments, and they work. By using antibiotics in specfic ways, it is possible to greatly reduce the likelihood of resistance developing. And it uses evolutionary theory.

Nowhere in the video do they talk about protocols. They are developing real treatment to eliminate a bacteria's ability to become drug resistant.

It's one particular way that bacteria can outflank one particular drug. The approaches now being used from research by people like Barry Hall are applicable over a wide range of resistance strategies used by bacteria.

Evolutionary resistance rests on mutation. As far as I can tell nothing much has come of this except the excuse, "It mutates therefore we are powerless against it and must continually devise new drugs."

Turns out we can, and now we are starting to use that to anticipate and work around likely new mutations. And that should work against a wide variety of mutations.

The only ones benefiting are the drug companies coming up with these new drugs and the reseachers getting an annual salary.

The protocols are already saving lives. And new antibiotics are being developed with the knowledge of the likely sorts of mutations they will have to overcome.

I have a feeling all this research done concerning "mutations" is only to support the belief in evolution with no or very little motivation to actually find a worthwhile and practical treatment.

The dirty little truth is, scientists do research because they want to find out how things work. It's nice that it so often has useful application, but that's not why they do it.

That and to preserve a lot of egos for those who want to prove evolution through a bacteria's inherent ability to become drug resistant.

Luria/Delbruck showed that a long time ago. No one doubts it now.

Where is the payoff for all this research?

Slower development of resistance, more people surviving infections, and new antibiotics that will be more difficult for bacteria to devise defenses against.

Will we ever see any results that can be used to actually help people with these diseases?

Already have.

 

[Rick W]

I see protocols as cautionary measures to a bacteria's inherent ability to resistant drugs. Threaten the bacteria with strong doses or widespread use and the bacteria reacts to that threat. Doesn't have to be attributed to "evolution" at all.



For years Streptococcus pneumoniae resistance to penicillin has been toted as a common model of evidence of evolution. No longer. We now know why the bacteria develops it's resistance and it's not evolution. Evolutionists can no longer make that claim.



Streptococcus pneumoniae causes bacterial meningitis as well as acute sinusitis, otitis media, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

And again, tuberculosis is also being studied. As work continues I have little doubt many more diseases will be added to the list.

 

[Barbarian]

I see protocols as cautionary measures to a bacteria's inherent ability to resistant drugs.

That's what I said. By using the drugs in the proper way, you can keep the few useful mutations from becoming established in the population. That's why the doctor is so emphatic about the way you are to take the antibiotics.

Threaten the bacteria with strong doses or widespread use and the bacteria reacts to that threat.

No. Luria/Debruck showed that favorable mutations like resistance occurred just as frequently when there was no threat at all. It's just that the mutation didn't become widespread in non-threatened populations because there was no selective value for it there. On the other hand, if there was phage present, these mutations would quickly become established. It's been done with antibiotic, BTW. Same result.

Doesn't have to be attributed to "evolution" at all.

That's what evolution is.

For years Streptococcus pneumoniae resistance to penicillin has been toted as a common model of evidence of evolution

There are actually several modes of resistance. We know how some of them evolved:

Antimicrobial Agents and Chemotherapy, May 2004, p. 1848-1855, Vol. 48, No. 5
Biochemical Characterization of Streptococcus pneumoniae Penicillin-Binding Protein 2b and Its Implication in ß-Lactam Resistance
Estelle Pagliero,1 Laurent Chesnel,1 Julie Hopkins,2 Jacques Croizé,3 Otto Dideberg,2 Thierry Vernet,1* and Anne Marie Di Guilmi1

Laboratoire d'Ingénierie des Macromolécules,1 Laboratoire de Cristallographie Macromoléculaire, Institut de Biologie Structurale Jean-Pierre Ebel (CEA-CNRS UMR 5075-UJF), 38027 Grenoble Cedex 1,2 Service de Bactériologie et Virologie, Centre Hospitalier Universitaire, 38043 Grenoble Cedex 09, France3

Extensive use of ß-lactam antibiotics has led to the selection of pathogenic streptococci resistant to ß-lactams due to modifications of the penicillin-binding proteins (PBPs). PBP2b from Streptococcus pneumoniae is a monofunctional (class B) high-molecular-weight PBP catalyzing the transpeptidation between adjacent stem peptides of peptidoglycan. The transpeptidase domain of PBP2b isolated from seven clinical resistant (CR) strains contains 7 to 44 amino acid changes over the sequence of PBP2b from the R6 ß-lactam-sensitive strain. We show that the extracellular soluble domains of recombinant PBP2b proteins (PBP2b*) originating from these CR strains have an in vitro affinity for penicillin G that is reduced by up to 99% from that of the R6 strain. The Thr446Ala mutation is always observed in CR strains and is close to the key conserved motif (S443SN). The Thr446Ala mutation in R6 PBP2b* displays a 60% reduction in penicillin G affinity in vitro compared to that for the wild-type protein. A recombinant R6 strain expressing the R6 PBP2b Thr446Ala mutation is twofold less sensitive to piperacillin than the parental S. pneumoniae strain. Analysis of the Thr446Ala mutation in the context of the PBP2b CR sequences revealed that its influence depends upon the presence of other unidentified mutations.

No longer. We now know why the bacteria develops it's resistance and it's not evolution. Evolutionists can no longer make that claim.

Turns out, it's evolution. In some cases, we even know the specific mutation.

 

[Barbarian]

Luria/Delbruck:

The Luria-Delbrück experiment (1943) (also called the Fluctuation Test) demonstrates that in bacteria, genetic mutations arise in the absence of selection, rather than being a response to selection. Therefore, Darwin's theory of natural selection acting on random mutations applies to bacteria as well as to more complex organisms. Max Delbrück and Salvador Luria won the 1969 Nobel Prize in Physiology or Medicine in part for this work.

In their experiment, Luria and Delbrück inoculated a small number of bacteria into separate culture tubes. After a period of growth, they plated equal volumes of these separate cultures onto phage (virus) containing agar. If virus resistance in bacteria were caused by a spontaneous activation in bacteriaâ€â€i.e., if resistance were not due to heritable genetic components, then each plate should contain roughly the same number of resistant colonies. This, however was not what Delbrück and Luria found. Instead, the number of resistant colonies on each plate varied drastically.

Luria and Delbrück proposed that these results could be explained by the occurrence of a constant rate of random mutations in each generation of bacteria growing in the initial culture tubes. Delbrück developed a sophisticated mathematical model based on this hypothesis that was entirely consistent with these results. The conclusion was that mutations in bacteria, as in other organisms, are random rather than directed.[1]
Wikipedia

 

[Rick W]

Going to have to wait and see what comes from the university. If they're on the wrong track of attacking the mechanism I'm sure it'll show up through results.

 

[Dave Slayer]

If evolution is true, why do pigs roll in the mud?

If evolution is true, why do pigs roll in the mud? Couldn't they take their bath in clean water like farm ponds?

 

[John]

Re: If evolution is true, why do pigs roll in the mud?

This has nothing to do with evolution. Pigs roll in mud because it keeps bugs of them and cools them down longer then water does.

 

[Dave Slayer]

When will the evolutionary clock stop ticking?

 

[Crying Rock]

When will the evolutionary clock stop ticking?

The macroevolutionary clock never existed. It's all fantasy based on philosophy versus science.