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« Odgovor #210 poslato: Novembar 23, 2012, 12:33:20 pm »

 Nije zamena teza posto niko nije tvrdio da "oziljci" postoje kod razlicitih vrsta na razlicitim mestima. Receno je da ERV okupira iste lokuse kod razlicitih vrsta gde je nemoguce uspostaviti zajednicko poreklo. 

 Inace evo kako je argument o ERV virusima razbijen. 

  Do Shared ERVs Support Common Ancestry?

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees, as well as the other members of Hominidae (great apes), the members of Hylobatidae (gibbons), and even the members of Cercopitheciodae (old world monkeys) (Kurdyukov et al., 2001; Lebedev et al., 2000; Medstrand and Mager, 1998; Anderssen et al., 1997; Steinhuber et al., 1995). Since humans don't and/or can't regularly procreate and have fertile offspring with members of these species, and thus don't make sizable contributions to their gene pools, and vice versa, their inheritance cannot have resulted from unions of modern species. As previously mentioned, parallel integration is ruled out by the highly random target selection of integrase. And even if it was far more target-specific than observed, it would require so many simultaneous insertion and endogenizations that the evolutionary model would still be tremendously more parsimonious. This leaves only one way an ERV could have been inherited: via sexual reproduction of organisms of a species that later diverged into the one the organisms that share the ERV belong to, i.e. an ancestral species--simply put, humans and the other primates must share common ancestry.
Just how target-specific are these ERV integrations? In the portion of the article headed "common creationist responses," we are told that,
...while proviral insertion is not purely random, it is also not locus specific; due to the way it directly attacks the 5' and 3' phosphodiester bonds, with no need to ligate (Skinner et al., 2001). So relative to pure randomness, insertion is non-random, but relative to locus specificity, insertion is highly random.

Let's take a few moments to do what any good student of biology would do -- and briefly survey some of the literature.

In one relevant study, Barbulescu et al. (2001) report that,
We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus. [emphasis added]
It seems that the most plausible explanation for this is an independent insert in the gorilla and chimpanzee lineages. Notice that the intact preintegration site at the pertinent locus in humans precludes the possibility of the HERV-K provirus having been inserted into the genome of the common ancestor of humans, chimpanzees and gorillas, and subsequently lost from the human genome by processes of genetic recombination. The inserts in the chimpanzee and gorilla lineages must be independent events.

But there's more.

Another study, by Sverdlov (1998) reports,

But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically. [emphasis added]
In addition,Yohn et al. (2005) report that,

Horizontal transmissions between species have been proposed, but little evidence exists for such events in the human/great ape lineage of evolution. Based on analysis of finished BAC chimpanzee genome sequence, we characterize a retroviral element (Pan troglodytes endogenous retrovirus 1 [PTERV1]) that has become integrated in the germline of African great ape and Old World monkey species but is absent from humans and Asian ape genomes.
I could continue in a similar vein for some time. Other classes of retroelement also show fairly specific target-site preferences. For example, Levy et al. (2009) report that Alu retroelements routinely preferentially insert into certain classes of already-present transposable elements, and do so with a specific orientation and at specific locations within the mobile element sequence. Moreover, a study published in Science by Li et al.(2009) found that, in the waterflea genome, introns routinely insert into the same loci, leading the internationally-acclaimed evolutionary biologist Michael Lynch to note,

Remarkably, we have found many cases of parallel intron gains at essentially the same sites in independent genotypes. This strongly argues against the common assumption that when two species share introns at the same site, it is always due to inheritance from a common ancestor.
Finally, Daniels and Deininger (1985) suggest that,

...a common mechanism exists for the insertion of many repetitive DNA families into new genomic sites. A modified mechanism for site-specific integration of primate repetitive DNA sequences is provided which requires insertion into dA-rich sequences in the genome. This model is consistent with the observed relationship between galago Type II subfamilies suggesting that they have arisen not by mere mutation but by independent integration events.
Such target-site preferences are also documented here, here, and here.

Why might these ERV site-preferences exist? Presumably because these sites are most conducive to their successful reproduction (e.g. the necessitude for expression of the ERV's regulatory elements; the activity of the host's DNA correction system, etc). Mitchell et al. (2004) suggest "that virus-specific binding of integration complexes to chromatin features likely guides site selection."

Out of tens of thousands of ERV elements in the human genome, roughly how many are known to occupy the same sites in humans and chimpanzees? According to this Talk-Origins article, at least seven. Let's call it less than a dozen. Given the sheer number of these retroviruses in our genome (literally tens of thousands), and accounting for the evidence of integration preferences and site biases which I have documented above, what are the odds of finding a handful of ERV elements which have independently inserted themselves into the same locus?

A Nested Hierarchy?
What about this "nested hierarchy" of which we are told?

We are (incorrectly) told that "There is only one, solitary known deviation of the distributional nested hierarchy; a relatively recently endogenized/fixed ERV called HERV-K-GC1."

This claim, however, is false.

In addition to the case mentioned, Yohn et al. (2005) report:
We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely (Figure S3).


Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists.

As irritating to the evolutionary model as it might be, there are, in fact, a significant number of deviations from the orthodox phylogeny.

In the final part of this blog series, I will discuss the argument based on "shared mistakes" in these ERV elements, as well as the argument based on degrees of mutational divergence between the retroviral 5' and 3' long terminal repeats (LTRs). 

 More Points on ERVs

Shared Mutations?
Regarding shared "mistakes" between primate genomes, this argument again assumes that mutations are random and are unlikely to occur convergently. Cuevas et al. (2002), however, have documented, in retroviruses, the occurrence of molecular convergenes in 12 variable sites in independent lineages. Some of these convergent mutations even took place in intergenic regions (changes in which are normally thought to be selectively neutral) and also in synonymous sites. The authors also note that this observation is fairly widespread among HIV-1 virus clones in humans and in SHV strains isolated from macaques, monkeys and humans.

As the authors note,
One of the most amazing features illustrated in Figure 1 is the large amount of evolutionary convergences observed among independent lineages. Twelve of the variable sites were shared by different lineages. More surprisingly, convergences also occurred within synonymous sites and intergenic regions. Evolutionary convergences during the adaptation of viral lineages under identical artificial environmental conditions have been described previously (Bull et al. 1997; Wichman et al. 1999; Fares et al. 2001). However, this phenomenon is observed not only in the laboratory. It is also a relatively widespread observation among human immunodeficiency virus (HIV)-1 clones isolated from patients treated with different antiviral drugs; parallel changes are frequent, often following a common order of appearance (Larder et al. 1991; Boucher et al. 1992; Kellam et al. 1994; Condra et al. 1996; Martinez-Picado et al. 2000). Subsequent substitutions may confer increasing levels of drug resistance or, alternatively, may compensate for deleterious pleiotropic effects of earlier mutations (Molla et al. 1996; Martinez-Picado et al. 1999; Nijhuis et al. 1999). Also, molecular convergences have been observed between chimeric simian-human immunodeficiency viruses (strain SHIV-vpu+) isolated from pig-tailed macaques, rhesus monkeys, and humans after either chronic infections or rapid virus passage (Hofmann-Lehmann et al. 2002).
I could cite several other similar studies. For another case example, see Bull et al. (1997).

LTRs And Phylogeny
The other argument offered by the article pertains to primate phylogenies in relation to long terminal repeat (LTR) sequences. Because LTRs are identical at the time of integration, it is argued, if the 5' and 3' LTR sequences are very different with respect to one another, this should correspond with an older insertion. The problem is that the pattern is nothing like as neat and tidy as many Darwinists would like us to think.

One of the main difficulties associated with trying to construct phylogenies based on the divergence between the 5' and 3' LTRs is that it is based on the assumption that the two LTRs accumulate point mutations independently and, therefore, the divergence reflects the time since the insertion event. However, if gene conversion occurs between LTRs, the nucleotide divergence will be much smaller than expected under the supposition given above. By applying a comparative genomic approach to primates and rodents, one paper by Kijima and Innan (2010) set out to investigate the extent of gene conversion between LTRs.

The authors note,
We found that gene conversion plays a significant role in the molecular evolution of LTRs in primates and rodents, but the extent is quite different. In rodents, most LTRs are subject to extensive gene conversion that reduces the divergence, so that the divergence-based method results in a serious underestimation of the insertion time. In primates, this effect is limited to a small proportion of LTRs. The most likely explanation of the difference involves the minimum length of the interacting sequence (minimal efficient processing segment [MEPS]) for interlocus gene conversion. An empirical estimate of MEPS in human is 300-500 bp, which exceeds the length of most of the analyzed LTRs. In contrast, MEPS for mice should be much smaller. Thus, MEPS can be an important factor to determine the susceptibility of LTRs to gene conversion, although there are many other factors involved. It is concluded that the divergence method to estimate the insertion time should be applied with special caution because at least some LTRs undergo gene conversion. [emphasis added]
To summarise, we have observed over the last three blog posts that the case for primate common ancestry is not nearly as cut and dried as many evolutionary biologists would like to make out. While one can find a handful of ERVs which occupy the same loci, further inspection reveals that they are often independent events.

In the absence of a feasible naturalistic mechanism to account for how evolution from a common ancestor could have occurred, how can we be so sure that it did occur? In such a case, one ought to reasonably expect there to be some quite spectacular evidence for common ancestry. Unfortunately for Darwinists, however, the evidence for common ancestry is paper thin on the ground.

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« Odgovor #211 poslato: Novembar 23, 2012, 01:09:18 pm »

 Zakljucak je da ERV okupiraju istu genetsku lokaciju ali oni su na osnovu svih obzervacija nezavisni dogadjaji, tj nisu nasledjeni vec svaki primat i sisar generalno poseduje odredjene ERV koje je nasledio nezavisno od ostalih grupa sisara. Slicnost Endogenih retrovirusa izmedju ljudi i primata moze da se objasni i inteligentnim dizajnom posto ljudi dele istu okolinu sa drugim primatima logicno je da ce sa njima da dele odredjene biohemijske pa i virusoloske slicnosti. Da toga nema doslo bi do izumiranja odredjenih vrsta sisara jer dele zajednicku okolinu. 

 Drugo prica o ERV virusima je bazirana na junk DNK odnosno smatra se da da tidelovi DNK koji okupiraju ERV virusi nisu aktivni i da ne sluze nicemu. Medjutim, najnovija istrazivanja pokazuju da je 80% DNK za koje se smatralo da je djubre ustvari aktivno, tako da moze vrlo lako da se desi i da su ovih 12 lokacija kod ljudi i primata aktivne.   

 Trece ako uzmemo da ima 98 000 ljudski ERV i da od toga samo 12 zauzima istu lokaciju to znaci da 99,99986% nisu isti.
 Takodje treba pomenuti da da jedna od najbogatijih porodica endogenih retrovirusa PTERV1 se nalaze kod simpanzi i velikih africkih majumuna ali ne i kod ljudi.
Van mreže Van mreže

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« Odgovor #212 poslato: Novembar 23, 2012, 06:20:13 pm »

Refuting Ken Miller on Chromosome 2
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« Odgovor #213 poslato: Novembar 23, 2012, 06:24:16 pm »

 It's Cherry Picking Season (Updated)
Evolution News & Views July 24, 2012 6:18 AM | Permalin  

 In our exchange with Darwinist critics on the subject of human chromosome 2, at issue are "interstitial telomeric sequences (ITSs)." The critics argue that one of these, 2q13 ITS, provides evidence for a chromosomal fusion event that proves humans and chimps are descended from a common ancestor.

But there are hundreds of ITSs in mammalian genomes (including those of humans and chimps) that are clearly NOT due to a fusion event. Rather, these appear to be due to the action of an enzyme (telomerase) in repairing chromosome damage. Darwinists have picked the one case that happens to fit their argument, and ignored all the others. This is cherry picking.

Cherry picking has been used by Darwinists to prop up other arguments, too. An example was Francisco Ayala's choice of one particular coding region of the HLA-DRB1 gene to prove that the human species could not have originated with one man and one woman. As Ann Gauger wrote in Science and Human Origins, the gene region Ayala chose -- unlike the many gene regions he ignored -- was "guaranteed" to yield the sort of result he wanted. Similarly, Jerry Coyne argued that similarities in the vitamin C pseudogene proved the common ancestry of chimps and humans. As Jonathan Wells pointed out in The Myth of Junk DNA, however, Coyne ignored many dissimilarities in the chimp and human genomes that do not fit a pattern of common ancestry.

Returning to the chromosome 2 story, this is ground we've covered here already, long before the publication of Science and Human Origins. Back in 2009, Richard Sternberg wrote in "Guy Walks Into a Bar and Thinks He's a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity":

    I try to outline all the functions of telomeric repeats, but my friend tells me that I am getting off the subject.

    He wants to me to focus on the ITSs, the tracks of the hexamer TTAGGG that reside within chromosome arms or around the centromere, not at the ends. I tell him that I was just coming to that topic. The story, you see, is that in the lineage leading up (or down, I forget which) to chimps and humans, a fusion of chromosome ends occurred -- two telomeres became stuck together, the DNA was stitched together, and now we find the remnants of this event on the inside of chromosomes. And to be fair, I concede at this point that the 2q13 ITS site shared by chimps and humans can be considered a synapomorphy, a five-dollar cladistic term meaning a genetic marker that the two species share. As this is said, it is apparent that the countenance of my acquaintance lightens a bit only to darken a second later. For I follow up by saying that of all the known ITSs, and there are many in the genomes of chimps and humans, as well as mice and rats and cows..., the 2q13 ITS is the only one that can be associated with an evolutionary breakpoint or fusion. The other ITSs, I hasten to add, do not square up with chromosomal breakpoints in primates (Farré M, Ponsà M, Bosch M. 2009, "Interstitial telomeric sequences (ITSs) are not located at the exact evolutionary breakpoints in primates," Cytogenetic and Genome Research 124(2): 128-131.). In brief, to hone in on the 2q13 ITS as being typical of what we see in the human and chimp genomes seems almost like cherry-picking data. Most are not DNA scars in the way they have been portrayed.

Read the rest from Dr. Sternberg here.  
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« Odgovor #214 poslato: Decembar 04, 2012, 10:38:35 pm »


One of the biggest attempts at a pseudo-scientific snow-job has to be the Laetoli prints. Evolutionists attempting to play 'sleight of hand' with spin disguised as science like to make us believe
that the Laetoli prints are those of an extinct chimp-like hominid, Australopithecus Afarensis. There only connection in reality with this idea is the supposed radiometric age of the prints of 3.6 million years is contemporaneous, in long-age terms, with the supposed time that A. Afarensis supposedly lived. So, by verbal 'sleight of hand' they piously pontificate that the Laetoli prints were that of a family of extinct bipedal apes. That's really funny if one considers that all of the anatomical features of Afarensis are actually very chimp-like and not human-like at all...
 Further damning evidence for Laetoli being evidence of supposed ape-like ancestors are the x-rays taken at 90 degrees from top-dead-center of the fossil itself...
"Based on previous analyses of the skeletons of Australopithecus afarensis, we expected that the Laetoli footprints would resemble those of someone walking with a bent knee, bent hip gait typical of chimpanzees, and not the striding gait normally used by modern humans...the Laetoli footprints fall completely within the range of normal human footprints. The fossil footprints at Laetoli preserve a remarkably even depth at the toe and heel, just like those of modern humans." 

 The truth is that when we go back to the ' beginning', from an anatomical vantage point, man has always been man and never an ape, or a fish, or anything other than man!
Photo: EVOLUTIONARY SNOW-JOB *TREADING * ON FACTS One of the biggest attempts at a pseudo-scientific snow-job has to be the Laetoli prints. Evolutionists attempting to play 'sleight of hand' with spin disguised as science like to make us believe that the Laetoli prints are those of an extinct chimp-like hominid, Australopithecus Afarensis. There only connection in reality with this idea is the supposed radiometric age of the prints of 3.6 million years is contemporaneous, in long-age terms, with the supposed time that A. Afarensis supposedly lived. So, by verbal 'sleight of hand' they piously pontificate that the Laetoli prints were that of a family of extinct bipedal apes. That's really funny if one considers that all of the anatomical features of Afarensis are actually very chimp-like and not human-like at all... http://www.answersingenesis.org/assets/images/campaigns/lucy-exhibit.jpg Further damning evidence for Laetoli being evidence of supposed ape-like ancestors are the x-rays taken at 90 degrees from top-dead-center of the fossil itself... "Based on previous analyses of the skeletons of Australopithecus afarensis, we expected that the Laetoli footprints would resemble those of someone walking with a bent knee, bent hip gait typical of chimpanzees, and not the striding gait normally used by modern humans...the Laetoli footprints fall completely within the range of normal human footprints. The fossil footprints at Laetoli preserve a remarkably even depth at the toe and heel, just like those of modern humans." http://www.sciencedaily.com/releases/2010/03/100319202526.htm The truth is that when we go back to the ' beginning', from an anatomical vantage point, man has always been man and never an ape, or a fish, or anything other than man! 

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« Odgovor #215 poslato: Decembar 08, 2012, 07:36:56 pm »


  Neandertals Apparently Knew Medicinal Plants
by Brian Thomas, M.S. *

The Institute for Creation Research has long identified Neandertals as fully human.1 But for decades, evolutionists had labeled this extinct variety of humankind as sub-human, alleging that they had eaten mostly meat.

A 1970 book titled Early Man illustrated a migrating Neandertal family wearing animal skins and carrying clubs. Part of the caption reads, "At left a man is carrying small game for provisions—a rabbit and a waterfowl—indicating that Neanderthalers hunted other creatures besides cave bears and woolly rhinoceroces."2 The book doesn't mention Neandertals eating plants for food or for medicine. But a recent forensic analysis of Neandertal teeth takes a bite out of this old evolutionary story.

Researchers studied tooth calculus, or tartar, from the teeth of five Neandertals found in El Sidrón Cave in North Spain. They used advanced techniques that detect trace amounts of certain chemicals. They wrote in the journal Naturwissenschaften,

By using these methods in conjunction with the extraction and analysis of plant microfossils, we have found chemical evidence consistent with wood-fire smoke, a range of cooked starchy foods, two plants known today for their medicinal qualities, and bitumen or oil shale entrapped within the dental calculus. Yet within the same calculus, chemical evidence for lipids/proteins from meat was low to absent.3 


 Neandertals ate starchy foods for nutrition and plants that provided medicinal benefits, too? The study authors wrote that these ancients "had a sophisticated knowledge of their natural surroundings which included the ability to select and use certain plants."3

Whoever suggested that Neandertals were anything less than fully human must be motivated by dogma, because decades of forensics analyses have demonstrated their humanity ad nauseum. For example, they used musical instruments and jewelry, and their DNA was fully human.4,5

Importantly, Neandertals eating starch refutes the standard excuse that evolutionists use to explain why human population burgeoned starting only about 5,000 years ago, after mankind had supposedly existed for over a hundred thousand years.6 The authors of the Naturwissenschaften study began their report with doctrinaire fare, asserting that "Neanderthals disappeared sometime between 30,000 and 24,000 years ago."3 If fully human beings have been alive for 30,000 years or more, what caused them to wait for 25,000 years before their historical population growth?

For evolutionists, , calories from starch in grain were supposedly the key.7 They maintain that the earliest humans were mere hunters for ages, only recently able to farm crops and glean the calories required for population growth. The problem now is that the Neandertal peoples at El Sidrón Cave, given an evolutionary age of 50,000 years, ate grains. If these early people ate "a range of cooked, starchy foods," it is reasonable that others around the world could have also.

Fitting this evidence into biblical history instead of an ever-changing man-made history substitute is plain. Neandertal and other human populations descended ultimately from the first created man and woman who were made in the image of God, complete with the ability to make jewelry, play instruments, and "select and use certain plants" for food and medicine.

And the reason for the recent population growth is simply that it reflects the time since the Flood described in Genesis, when men began multiplying and filling the earth. No story about calories is required. And that's good, because evidence that Neandertal people ate enough starch to cause tooth tartar shows that calories were available too early to be used as an excuse for why human population growth began later than evolutionary assumptions expect.


    Gish, D. 1975. Man...Apes...Australopithecines...each Uniquely Different. Acts & Facts. 4 (11).
    Howell, F. C. 1970. Early Man. Morristown, NJ: Silver Burdett Company, Time Inc., 132.
    Hardy, K. et al. 2012. Neanderthal medics? Evidence for food, cooking, and medicinal plants entrapped in dental calculus. Naturwissenschaften. 99 (Cool :617–626.
    Zilhão, J. et al. Symbolic use of marine shells and mineral pigments by Iberian Neandertals. Proceedings of the National Academy of Sciences. Published online before print January 11, 2010.
    Green, R. E. et al. 2010. A Draft Sequence of the Neandertal Genome. Science. 328 (5979): 710-722
    Thomas, B. 2012. A Recent Explosion of Human Diversity. Acts & Facts. 41 (9): 17.
    For example, one study said, "What, in the agricultural economy, had an impact on human biology that ultimately determined the growth of the population? The increase in natural maternal fertility, through a reduction in the birth interval, is mainly determined by the energy balance and the relative metabolic load. It implies a positive return of the postpartum energy balance, which occurred earlier in farming than in foraging societies due to the energy gain from the high-calorie food of sedentary farmers (wheat, lentils, peas, maize, rice, and millet) compared to the low-calorie food of mobile foragers (mainly game), coupled with a decrease in the energy expenditure of carrying infants. This signal is interpreted as the signature of a major demographic shift in human history and is known as the Neolithic Demographic Transition (NDT) or, synonymously, the Agricultural Demographic Transition." See Bocquet-Appel, J.-P. 2011. When the World's Population Took Off: The Springboard of the Neolithic Demographic Transition. Science. 333 (6042): 560-561.

* Mr. Thomas is Science Writer at the Institute for Creation Research.
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« Odgovor #216 poslato: Januar 19, 2013, 01:46:24 pm »

 The Amazing Human Hair
by David Menton, Ph.D.
July 4, 2007


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Rest assured, God didn’t make anything simple in our body. A human hair is so complex that man will never fully understand it, much less explain its origin by chance evolutionary processes.

Hair is mentioned over 100 times in the Bible, often in the context of God’s loving care and protection for His people. For example, when God delivered Shadrach, Meshach, and Abednego from the fiery furnace, “the hair of their head was not singed” (Daniel 3:27, KJV). In Luke 21:18, Jesus warned His disciples of persecution but told them not to fear because “not a hair of your head shall be lost.” Finally, Jesus declared that even “the very hairs of your head are all numbered” (Matthew 10:30, KJV). How personally and intimately our Savior knows and loves us!
Lots of Hairs

The human head has an estimated 100,000 hairs, though the number varies from individual to individual. While hair appears to be largely confined to our head and a few other scattered locations, it is actually rather uniformly distributed over all our skin (with the exception of our palms and soles, which are truly hairless). On the entire surface of the human body, there are about 5 million hairs; but many of them are difficult to see.
Types of Hairs

While some areas of our skin appear to lack hair (e.g., on the forehead and nose), they actually have tiny, colorless hairs called vellus hairs. We have about as many hairs per square inch on our nose and forehead as we do on the top of our head—we just don’t notice them. 

 The long and often pigmented hairs (e.g., those of our scalp or beard) are called terminal hairs.

Several other types of hair, such as eyelashes, form during the course of our life.

The first hair follicles begin to form by the third month in the womb. The follicles produce lanugo hair. These rather long, silky hairs are usually shed in the womb a few weeks prior to birth and are replaced with vellus hairs, which grow out of the same hair follicles. A premature baby may appear surprisingly hairy because of unshed lanugo hair.
You Never Lose a Hair Follicle

Amazingly, we are born with all the hair follicles we are ever going to have, and these follicles normally continue to produce hairs throughout our lives.

Why then do so many of us get bald with age? Beginning at puberty, some follicles that had been producing terminal hairs begin to replace them with almost invisible vellus hairs. So you don’t lose hairs as you age, your hair just gets smaller.
Why Don’t Animals Need a Barber?

While many of us make periodic trips to the barber, most nonhuman mammals always appear in perfect trim without a barber. The reason for this is that hair grows in a cyclic manner. A relatively long period of growth (that varies with the type and location of the hair) is followed by a short period of rest after which the hair is released from the follicle, and a new growth cycle begins forming a new hair (see The Growth of Human Hair below). Thus the length of the growth cycle determines the length of the hair.

If hair grew longer and longer without being released from the follicle, it would be disastrous for the mammals that don’t visit a barber. Can you imagine, for example, a squirrel dashing through the branches, dragging a couple feet of hair? The Lord thinks of everything!

Hair grows about .3 mm per day (about three tenths the thickness of a dime). Within a year, our scalp and beard can produce nearly five inches (13 cm). By comparison, the longest hairs on our arm have a growth cycle of less than two months.

The growth cycle of scalp and beard hairs varies from individual to individual but can be several years. A Vietnamese man was reported to have the longest scalp hair, which measured over 20 ft. (6 m) long. According to a BBC News report in June 2004, he claimed not to have cut his hair in more than 30 years.

We stand in awe of Christ our Creator, who has lavished such exquisite design and complexity on even the hairs of our body. We are greatly comforted by Christ our Protector, who has numbered the very hairs of our head and will not permit one hair to be harmed if it is not His will. And finally, we are eternally grateful for the amazing grace of Christ our Savior who allowed His own hairs to be plucked from His cheeks as He endured taunting, torment, and death for our sins.

“I gave my back to the smiters, and my cheeks to them that plucked off the hair: I hid not my face from shame and spitting” (Isaiah 50:6, KJV).
The Growth of the Human Hair

Hair grows from tube-like depressions in the skin called hair follicles. The hair shaft is formed from living cells deep in the follicle. These fragile living cells subsequently die to form the remarkably strong fiber we call a hair. The same follicle is capable of producing more than one type of hair during the course of our lives.


Hair grows from the bottom of the follicle at a rate of 3 tenths the thickness of a dime per day.
   Hair growth period


Hair grows to a certain length specific to each follicle then stops growing for a short period of time.
   Hair resting period

New Growth

When growth begins again in the hair follicle, the resting hair is released from the follicle and a new hair is produced.
   New hair growth period
The Hair Cuticle

All hairs are covered with a layer of flattened dead cells (called the cuticle) that help to keep the hair from knotting up (imagine the knotted mess if our hair was made from comparably thin nylon thread). Under the microscope the cuticle looks like overlapping shingles or roof tiles.

Wigs made from natural human hair must have all their hairs facing in the proper direction (the free edges of the cuticle cells facing away from the scalp), if they are to be groomed and lie properly.

The shape of the cuticle has an added benefit—perhaps its most important function—it locks the hair in its follicle.
  (Top Left) Magnified view of a human hair showing both mid-shaft and tip. The hair is covered with a layer of overlapping shingle-like cells called the cuticle.
The Incredible “Hair Lock”

The hair needs to be locked inside the hair follicle to prevent it from being easily pulled out. Without a “hair lock,” hair loss would likely prove fatal for most mammals
 The hair follicle is lined with a cuticle whose overlapping cells face the opposite direction of the cuticle on the hair shaft. The precise interlock of the two cuticles makes it impossible to pull out a hair without tearing out a large part of the follicle with it. But don’t worry; this event immediately triggers the rebuilding of the damaged follicle and a new hair growth cycle.

The question arises, if the hair is locked in place, how does it slide out as it grows? Amazingly, tens of thousands of little “buttons,” called desmosomes, line the hair follicle. These buttons are quickly buttoned and unbuttoned in a precise sequence to allow the hair to slide out in a controlled fashion. Before the hair emerges from the surface of the skin, the lock (the cuticle lining the hair follicle) is digested with special enzymes.

Hair locked in by follicle Hair Unlocked hair next to follicle

Click to enlarge

Cuticle cells, lining the innermost layer of the hair follicle, interlock with the cuticle on the hair shaft. On the left is a magnified view of the follicle cuticle in contact with the hair cuticle. Below is a magnified view of the follicle cuticle peeled away from the hair showing a perfect match.

Dr. David Menton holds his Ph.D. in cell biology from Brown University and is a well-respected author and teacher. He is Professor Emeritus at the Washington University School of Medicine in St. Louis. Dr. Menton has many published works and is one of the most popular speakers for Answers in Genesis-USA.
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« Odgovor #217 poslato: Januar 27, 2013, 01:14:43 pm »

 Our Top 10 Evolution-Related Stories: #5, Publication of the Gorilla Genome
Casey Luskin December 28, 2012 5:00 AM | Permalink



Editor's note: A memorable and unwelcome news development for Darwinian evolutionists this year was the publication of the gorilla genome. Casey Luskin gave us his report and analysis ("30% of the Gorilla Genome Contradicts the Supposed Evolutionary Phylogeny of Humans and Apes").

A whopping 30% of the gorilla genome -- amounting to hundreds of millions of base pairs of gorilla DNA -- contradicts the standard supposed evolutionary phylogeny of great apes and humans. That's the big news revealed last week with the publication of the sequence of the full gorilla genome. But there's a lot more to this story.

Eugenie Scott once taught us that when some evolutionary scientist claims some discovery "sheds light" on some aspect of evolution, we might suspect that's evolution-speak for 'this find really messed up our evolutionary theory.' That seems to be the case here. Aylwyn Scally, the lead author of the gorilla genome report, was quoted saying, "The gorilla genome is important because it sheds light on the time when our ancestors diverged from our closest evolutionary cousins around six to 10 million years ago." NPR titled its story similarly: "Gorilla Genome Sheds Light On Human Evolution." What evolutionary hypothesis did the gorilla genome mess up?

The standard evolutionary phylogeny of primates holds that humans and chimps are more closely related to one-another than to other great apes like gorillas. In practice, all that really means is that when we sequence human, chimp, and gorilla genes, human and chimp genes have a DNA sequence that is more similar to one-another's genes than to the gorilla's genes. But huge portions of the gorilla genome contradict that nice, neat tidy phylogeny. That's because these gorilla genes are more similar to the human or chimp version than the human or chimp versions are to one-another. In fact, it seems that some 30% of the gorilla genome contradicts the standard primate phylogeny in this manner. New Scientist explains:

    But despite the ancient split, the remaining 30 percent of [the gorilla's] genome turned out to be more closely related to humans or chimp than those species are to one another...

    (Sara Reardon, "DNA from the last of the great apes decoded," New Scientist, March 10-16, 2012, p. 12)

Nature news put it this way:

    But the genome sequencing has thrown up surprises, too. The standard view of the great-ape family tree is that humans and chimps are more similar to each other than either is to the gorilla -- because chimps and humans diverged more recently. But, 15% of human genes look more like the gorilla version than the chimp version.

Scally's interview with NPR stated:

    And what we see that as is in fact this 15 percent figure that you may have mentioned or that people might have seen, which is that humans are actually closer to gorillas in 15 percent of their genome, of the human genome. So overall we're closer to chimpanzees, and 70 percent of our genome is closer to chimpanzees. That's consistent with the speciation of the species tree.

    But there are these regions all across the genome where the ancestry is different, and that amounts to 15 percent where humans and gorillas are closest and then another 15 percent where chimpanzees and gorillas are closest.

Likewise, the technical paper in Nature stated: "In 30% of the genome, gorilla is closer to human or chimpanzee than the latter are to each other." As a result, now they must qualify assertions that chimps are our "closest" relatives, as the paper stated "Molecular studies confirmed that we are closer to the African apes than to orangutans, and on average closer to chimpanzees than gorillas." (emphasis added) "On average," of course, is wiggle-language, because huge portions parts of our genomes don't fit with the standard evolutionary phylogeny. As one of the researchers put it, "We can't just conform to a simple tree on a gene-by-gene basis."

As always, they try to explain why hundreds of millions of base pairs in the gorilla genome contradict the standard phylogeny. As we saw in an ENV post from last year titled, "Study Reports a Whopping '23% of Our Genome' Contradicts Standard Human-Ape Evolutionary Phylogeny," their explanation is that interbreeding between populations of chimps, humans, and gorillas after the initial splits of these lines caused different genes to become fixed in different lineages at different times. Called incomplete lineage sorting, it provides a convenient after-the-fact explanation for why different genes carry different phylogenetic signals. Of course, this is merely an ad hoc hypothesis invoked to explain away inconvenient data which contradicts the standard phylogeny.

The bottom line is that the gorilla genome has confirmed that there is not a consistent story of common ancestry coming from the genomes of the great apes and humans. Hundreds of millions of base pairs in the gorilla genome conflict with the supposed phylogeny of great apes and humans. They might think their explanation salvages common ancestry, but clearly the gorilla genome data badly messes up the supposedly nice, neat, tidy arguments which they use to claim humans are related to the great-apes.

Genes Don't Talk

What's also interesting is that one of the gorilla genes which conflicted with the standard primate phylogeny was highly similar to a human gene, thought by evolutionists to be involved in the origin of human speech. But obviously gorillas don't talk. So if this gorilla gene is highly similar to the human version, it stands to reason that those human genes may not be as important for the evolution of speech after all. As Nature news explained:

    Much of the 15% is in sections of the genome that do not code for proteins. But the researchers also looked at functional gene changes. They found that certain genes -- including some involved in hearing and brain development -- had gone through more rapid changes than expected in both the gorilla and human lineage.

    Some of these rapid changes are puzzling: the gene LOXHD1 is involved in hearing in humans and was therefore thought to be involved in speech, but the gene shows just as much accelerated evolution in the gorilla. "But we know gorillas don't talk to each other -- if they do they're managing to keep it secret," says Scally.

    This weakens the connection between the gene and language, says Enard. "If you find this in the gorilla, this option is out of the window."

Gorilla Genome Researchers Fall Back to Weaker Arguments for Common Ancestry

Since the gorilla genome didn't fit nicely with the standard phylogeny of higher primates, evolutionary scientists sought to put some spin on the situation to support common ancestry. They thus fell back to making the old "we're 98% ape" argument:

    "The big picture is that we're perhaps 98 percent identical in our sequences to gorillas. So that means most of our genes are very similar, or even identical to, the gorilla version of the same gene," said Chris Tyler-Smith, a geneticist at Wellcome Trust.

Of course, the "big-picture" implication that Tyler-Smith wants you to take is that if we're 98% genetically similar to gorillas, then we must be related to them. Of course this argument is full of logical fallacies and factual inaccuracies.

First, we're less than 98% similar to chimpanzees, which are supposedly "on average" more closely related (e.g. genetically similar) to humans than gorillas. So Tyler-Smith has overstated the percent genetic similarity between humans and gorillas.

Second, even if humans and gorillas actually were 98% genetically similar, why should that demonstrate common ancestry? We might reasonably ask the evolutionist why 98% similarity is considered powerful evidence for common ancestry, and at what point does the comparison cease to support common descent? What about 97% different? 95%? 90%? 80%? Is there an objective metric for falsification here, or is Tyler-Smith implying a fallacious argument for human / gorilla common ancestry?

Finally, intelligent design is certainly compatible with human/gorilla common ancestry, but the percent difference says nothing about whether humans and gorillas share a common ancestor. Just as intelligent agents re-use functional components that work over and over in different systems (e.g., wheels for cars and wheels for airplanes, or keyboards for computers and keyboards for cell phones), genetic similarities between humans and other apes like gorillas could also be explained as the result of the re-usage of common genetic programs due to functional requirements of the hominid body plan. The percent genetic similarity between humans and apes does not demonstrate Darwinian evolution, unless one excludes the possibility of intelligent design.




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« Odgovor #218 poslato: Januar 27, 2013, 01:21:14 pm »

 eptional” As “Justifying Animal”
By Wesley J. Smith
January 4, 2013 12:27 A.M.

An interesting blog entry over at Psychology Today focuses on the crucial issue of human exceptionalism (and also, this less crucial blog). The author, Gregg Henriques, Ph.D., agrees with me that, “We are unique beings that warrant special moral value,” and much to my delight, justifies the belief from an explicitly “secular humanist”perspective. From, “On Human Exceptionalism:”

    The system I have developed for unifying psychology argues strongly that humans are a unique kind of animal. However, in contrast to many traditional positions that differentiate animals from humans (e.g., Descartes’ substance dualism), the unified theory claims animals are mental and most are conscious (see here for a recent declaration on animal consciousness by some well-known neuroscientists). Humans are unique in that they have a self-consciousness system on top of the conscious system shared with other animals.

What does Henriques mean?

    Humans are as different from other animals as animals are different from plants. Whether it is writing a blog, composing a sonnet, leading a revolution, attending a class, building a computer, and on and on, it is an empirical fact that human behavior exhibits a whole separate dimension of complexity. To deny this or to claim that this observation is only based on speciest wishful thinking lacks intellectual integrity.

Bingo!  He goes on:

    Human cognition advanced to allow for human language (an open symbolic syntactical system of information processing that is, despite some claims to the contrary, a fundamentally different kind of communication/information processing system). Although language was a great advantage, a problem emerged because human language affords a window into the mind. This is the problem of social justification—for the first time in evolutionary history, our ancestors were asked about and thus had to justify (give reasons for) their behavior. I have explained elsewhere why the problem of justification gave rise to the human self-consciousness system and the human culture.

    We are the justifying animal. And that opens up a whole new, qualitative dimension of existence. It is not that other animals don’t have minds. That is an obviously misguided claim. Instead, it is better to think of it in terms of humans having two minds, whereas other animals only have one. Thus, the answer to HE is not that humans are exceptional because they are conscious and feel—other animals are conscious and feel. But humans are exceptional in that they have the capacity for self-conscious justification, which in turn is the engine that builds human cultures and knowledge systems about truth, goodness and evil. In short, HE is ultimately justified by the fact that humans alone can justify.

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« Odgovor #219 poslato: Januar 27, 2013, 01:30:40 pm »

 Is ‘Mitochondrial Eve’ Consistent with the Biblical Eve?

Posted on January 5, 2013


Read more: http://creationrevolution.com/2013/01/is-mitochondrial-eve-consistent-with-the-biblical-eve/#ixzz2JB7VSwkN


 B.R. from Australia writes:

    Dr Carl Wieland is very confused about the subject of ‘mitochondrial Eve’.

    Mitochondrial Eve and biblical Eve are looking good: criticism of young age is premature

    His very first sentence on this page is strange.

        “Mitochondrial DNA (mtDNA) indicates that all women have descended from a single woman, called mitochondrial Eve.”

    Why only women? A very strange thing to say.

        “the mitochondrial Eve findings were in line with biblically based expectations. While not proving the biblical Eve, they were consistent with her reality, and were not predicted by evolutionary theory”

    the existence of a mitochondrial Eve is by definition necessary according to evolution theory. Only a person who does not understand it would claim the opposite.

    My question is: Is Carl Wieland as ignorant as he appears to be? Or perhaps just dishonest?


    B.R. Genetics BSc. Bioinformatics MSc

CMI biologist Dr Robert Carter responds:

Dear B.,

Dr. Wieland asked me to answer this for him because he thought it might look strange for him to be defending himself against false accusations.

First, Carl does admit that he slipped in the first sentence. It probably should have read “people”, but he was not incorrect by saying “women”. It is true, but, as you say, a strange way to put it. He did not say “only women”. But that is a very minor point….

Read more: http://creationrevolution.com/2013/01/is-mitochondrial-eve-consistent-with-the-biblical-eve/#ixzz2JB7v61vP

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« Odgovor #220 poslato: Januar 27, 2013, 01:36:04 pm »

 Four-strand DNA structure found in cells

Unusual nucleic-acid structure may have role in regulating some genes.

    Alison Abbott

20 January 2013


 Four DNA strands come together in this model, built using data from x-ray crystallography.

Jean-Paul Rodriguez
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There is no more iconic image in biology than that of DNA's double-stranded helix, which coils and supercoils on itself to form dense chromosomes.

But a quite different, square-shaped type of DNA structure can easily be created in the laboratory by the folding of synthetic DNA strands rich in guanine, one of the building blocks of DNA. Scientists have long believed that these so-called 'G-quadruplex structures' may occasionally form in the DNA of living cells. A G-quadruplex comprises four guanines from different places along a G-rich strand held together by a special type of hydrogen bonding to form a compact square structure that interrupts the DNA helix.

In a paper published online today in Nature Chemistry1, researchers led by Shankar Balasubramanian at the University of Cambridge, UK, provide strong evidence that G-quadruplexes do occur in cells — and that these unusual structures may have important biological functions.
Protecting the chromosome

The protective tips of chromosomal DNA, known as telomeres, are rich in guanine and so are likely candidates for G-quadruplex structures. In fact, studies in cancer cells have shown that small molecules that bind and stabilize G-quadruplex structures cause DNA damage at telomeres, supporting the argument2.

After trawling through human genome data in search of other guanine-rich sequences, some scientists have suggested that quadruplexes could also be created in other areas of the genome involved in regulating genes, particularly some cancer-causing genes.
G-quadruplex visualized

This seems likely to be the case, Balasubramanian and colleagues found. They engineered an antibody that binds tightly and specifically to G-quadruplex structures and does not bind to double-stranded helical DNA. When they incubated the antibody with human cells in culture, they found that it bound to many different sites in the chromosomes, only around a quarter of them in telomeres.

“It’s early days, but if we can map exactly where these G-quadruplex structures pop up in the genome, we may learn how better to control genes or other cellular processes that go awry in diseases like cancer,” he says. “That’s the long-term vision anyway.’’

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