Posts by QC

Speculative books on abiogenesis do not make it a fact. Why MUST we read them? When abiogenesis reaches the bar set by Einstein and Newton I’ll be glad to read its books.

All animals, birds, bacteria arose out of the primeval sea from a common ancestor due to abiogenesis, that life arose from inorganic [non-living] matter, — This is still a work in progress. You would still be 100% wrong to deny common ancestry of all living things through evolution over millions of years

You say it's “still a work in progress” that means it’s now speculation, not proven. So why is it “100% wrong to deny common ancestry of all living things…from a common ancestor due to abiogenesis evolution over millions of years”? That's over the top 1975 hyperbole, “FDS is right, right or wrong.”

What you need for abiogenesis to be viableis: non-living (inorganic) matter would move from dead state toward a live state, according to some invisible natural law, eventually arriving as evolvable living (organic) matter; similar to how invisibly the law of gravity causes two particles to move towards each other.

Smarter than me explain it better:

Abiogenesis answers.yahoo.com

How can abiogenesis be a fact if no one knows how it happened?

Some think that forming life's building blocks in the lab helps prove abiogenesis. This is absurd. Scientists have found the minimum complexity of life to be about 2000 genes for a self-supporting microbe, and about 400 genes for the simplest parasitic microbe, not capable of surviving on its own. So it is not enough that there be life's building blocks present - they must be arranged in a precise order (and all amino acids must be left-handed) in order for life to function at all.

Creating amino acids or nucleotides in the lab and saying it proves abiogenesis is like someone saying the complete works of Shakespeare arose from naturalistic processes by pointing to a bowl of alphabet soup.

It is one thing to create life's building blocks in the lab, it is another for us to believe that those building blocks will be stable long enough for life to spontaneously arise from them. Many people know of the Miller-Urey experiment that produced amino acids from a hypothetical (now known to be wrong) early earth atmosphere. What many people don't know, however, is that those building blocks of life were unstable. Miller stopped the experiment when he got the most favorable results. If the experiment continued, the building blocks of life were broken down by the same environment that produced them. [This is Behe’s point. Lenski’s E. coli lab work is broken down specimen change, not evolved change upward.]

Also, from what is now known of the early earth, life had to have formed under hostile conditions. And while life, if appropriately designed, can survive under extreme physical and chemical conditions, it cannot originate under those conditions. There are extremophiles that can live in harsh environments, but these organisms have mechanisms built in to them to survive those conditions. If the building blocks of life were present, they would have a very short half-life. Also, the early earth was very acidic. Acidic conditions frustrate key prebiotic reactions. Acidic conditions also promote the breakdown of key biomolecules like proteins and DNA.

There is not enough time for life to have arisen on its own. After the molten earth had cooled, there is evidence that there was some water on earth between 4.4 and 4.2 billion years ago. Then the Late Heavy Bombardment occurred from 4.1 to 3.8 billion years ago, causing the crust to become molten again. The first evidence for life that we have is from 3.8 billion years ago. Allowing for the possibility that extremophiles could have survived the Late Heavy Bombardment, the best case scenario for the time the origin of life had is between 400 and 600 million years. But during the majority of this time period, the earth's environment was extremely unfit for life.

And for those who say that abiogenesis has nothing to do with evolution:

Evolution and abiogenesis are both the products of the philosophy of naturalistic materialism. Although not formally part of Darwin's theory, abiogenesis forms the core of the evolutionary paradigm. Life must have its beginning in exclusively physical and chemical processes for evolutionists to legitimately explain life’s diversity throughout Earth’s history from a strictly materialistic standpoint. If abiogenesis lacks scientific credibility, the foundation of evolutionary theory crumbles. Moreover, if life can be shown to have a supernatural origin, then the door opens for viewing all phenomena in biology from an intelligent design perspective.

Some scientists are trying to create life from 'scratch' in the laboratory. (It is not really from 'scratch,' but based heavily on design concepts already found in living cells.) This is different from abiogenesis and has no bearing on it because the life they are trying to create would be *designed.* Recently scientists have created an enzyme from scratch. But it took about 30 researchers working hard and the use of supercomputers to do it. This shows obvious DESIGN, not abiogenesis: which is life arising on its own from strictly naturalistic processes, and without intelligent direction.

Now I better understand what your fuss is all about. Your situation is JW 2.0 replacing the JW 1.0, Dawkins is now Rutherford. I’m way past that!

17

144,000 Ain't Going to Heaven!!!

by The Searcher in

don't take my word for it, the gb (d.c.of c.) inadvertantly let's the cat out of the bag with the inspired statements found in these publications.. in these, they categorically claim that "the meek who inherit the earth" are none other than 144,000 + 1.

(christ).

w09 2/15 p. 7 par.

QC

Very interesting

273

greatest show on earth

by unstopableravens in

i wanted to start this thread two weeks ago,however i have had alot going on with wifey and the elders,that is another thread.

to be honest my mind has been on my family.

i will be able to discuss the book tommorow morning.

QC

@cofty

Here’s an opposing view to Dawkins’ citing Richard Lenski’s LTEE using E. coli

Excerpts from Evolution News:

Richard Lenski's Long-Term Evolution Experiments with E. coli

http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html

ID readily allows that natural selection and random mutation can effect SOME changes in populations. The right question is not 'Can natural selection do anything?' but rather 'Can natural selection do EVERYTHING ?'

Behe's 2010Quarterly Review of Biology paper specificity:

By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.

Several years later, when the cultures had surpassed their 20,000th generation, Lenski's group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that "The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)" (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein's activity.

The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.

If you weren't following all the technical language, here's what's going on: For the first 20,000 generations of Lenski's LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity -- in essence, a decrease in specificity .

Behe summarizes:

The fact that multiple point mutations in each gene could serve an adaptive role -- and that disruption by IS insertion was beneficial -- suggests that the point mutations were decreasing or eliminating the protein's function.

Behe closes with another specific example that involved decreasing gene activity in Lenski's LTEE:

In an investigation of global protein profiles of the evolved E. coli, Lenski's group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.

Looking at Table 3 of Behe's QRB paper, not a single example of an adaptive mutation in Lenski's LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail "loss-of-function" mutations.

E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:

Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it's not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a "citrate permease" which can transport citrate from outside the cell through the cell's membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, "The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions." (1)

Likewise, Behe's recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski's LTEE showed the evolution of a new pathway that could metabolize citrate.

Behe explains:

Recently, Lenski's group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.

Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren't anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:

As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.

Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused "by the loss of the activity of a normal genetic regulatory element."

Here's what is likely going on here:

Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy . But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can't normally uptake citrate .

If Lenski's citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions .

In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian "evolution" entails the loss of a molecular function, not the gain of a new one .

In fact, as Behe notes, we don't really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.

This example hardly shows the Darwinian evolution of a "new function," especially since E. coli already had the ability to uptake and metabolize citrate.

What do Lenski's LTEE Really Tell Us?

Behe goes on to explain that to date, the known adaptations that have occurred in Lenski's LTEE are either modification-of-function or loss-of-function changes:

The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT .

Behe's paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations.

He concludes:

Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene .

The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation .

Consider an imaginary order of insects, the Evolutionoptera . Let's say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium . The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years . At these rates, every thousand years 1000 species of Evolutionoptera will die off , while one new species will develop-- a net loss of 999 species . If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth .

If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.

But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:

Mere possibility is not an adequate basis for asserting scientific plausibility . A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, "Yes." ... One chance in 10 200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.

(David L. Abel, "The Universal Plausibility Metric (UPM) & Principle (UPP),"Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)

What is the probability for Evolution of one cell? (Use IE9)

http://youtu.be/nyTUSe99z6o

27

Another probe of the Governing Body theory

by QC in

note the activity topology of spiritually "gifted" faithful religiously pure network of individual christians sustaining the therapeia (qerapeiavhousehold for spiritual cure) lu 12:42under the leadership of jesus in heaven.

all accomplished by autonomous ecclesia without central control from jerusalem.

this is the model antecedent for today's class of individual "faithful discreet" slaves.

QC

A few additional thoughts:

The 1 st century distribution of the entire Biblical NT was by individuals circulating their writings through a network of various self-sufficient ecclesia nodes, e.g. Rome, Corinth, Thessalonica, Ephesus, etc. These writings were not funneled to Jerusalem for editing and then distribution. Jerusalem did not model a centralized control of Christianity like the JW BORG power base in NY, or the Pope power base in Rome. "Spirit gifted" individuals in unison with a special message are what led Christianity to become the powerful force it is today.

Document of individuals dispensing spiritual information through a network eliminates the idea that a GB with central control is responsible for 1 st century Christianity.

How should we view the Society today? In reality the JW GB controls a real-estate empire. The COs, DOs and ZOs managers imitate the corporate business manager model. The Bible takes a back seat to corporate BOE policy instructions. Elder emphasis is to become "company men" lording policy over people, the opposite of shepherding and teaching. This leadership style is similar to the Pharisee "letter of the law" traditions; which became Talmudic micromanagement mind control causing spiritual ruin. Mat 16:12; 23:13,15

27

Another probe of the Governing Body theory

by QC in

note the activity topology of spiritually "gifted" faithful religiously pure network of individual christians sustaining the therapeia (qerapeiavhousehold for spiritual cure) lu 12:42under the leadership of jesus in heaven.

all accomplished by autonomous ecclesia without central control from jerusalem.

this is the model antecedent for today's class of individual "faithful discreet" slaves.

QC

>metatron,

>prologos

>Mum

>Pterist

>cantleave

>shadow

>Heathen

thanks guys,

>DDOG

>frankiespeakin

Both of you sum up my position perfectly

>EOne,

We agree in spirit. You think the Society is doing a lousy job and I agree . I will be so glad when it’s over.

27

Another probe of the Governing Body theory

by QC in

note the activity topology of spiritually "gifted" faithful religiously pure network of individual christians sustaining the therapeia (qerapeiavhousehold for spiritual cure) lu 12:42under the leadership of jesus in heaven.

all accomplished by autonomous ecclesia without central control from jerusalem.

this is the model antecedent for today's class of individual "faithful discreet" slaves.

QC

>metatron,

>prologos

>Mum

>Pterist

>cantleave

>shadow

>Heathen

thanks guys,

>DDOG

>frankiespeakin

Both of you sum up my position perfectly

>EOne,

We agree in spirit. You think the Society is doing a lousy job and I agree . I will be so glad when it’s over.

85

Will you attend the Memorial this year? Why? Why not?

by Open mind in

jw
friends

.

om.

QC

I'm thinking of going to one of the foreign congregations. They have the date right for the most important day in the history of the world. And, I like a celebration atmosphere. Also I'm curious to take the temperature of hostility when others partake along with me.

I'll report my experience.

QC

Posts by QC

What is the probability for Evolution of one cell? (Use IE9)http://youtu.be/nyTUSe99z6o

What is the probability for Evolution of one cell? (Use IE9)

What is the probability for Evolution of one cell? (Use IE9)
http://youtu.be/nyTUSe99z6o