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Genetic Recombination Study Defies Human-Chimp Evolution by Jeffrey Tomkins, Ph.D. *

Results from a recent study in human and chimpanzee genetics have shipwrecked yet another Darwinian hypothesis.¹ Genetic recombination is one of the key events that occur during the production of egg and sperm cells, and secular scientists have long thought it to be a major driver of human and ape evolution. 

When sperm and egg cells are formed in humans and various animals, the process of meiosis generates genetic variation. For example, since humans have two sets of chromosomes, when similar ones (i.e., sister chromatids)–one each from your mother and father—pair up together in the cell, they undergo a controlled exchange of DNA segments (maintaining the same linear order of segments). This is one reason why the offspring of two parents are always genetically unique, except for identical twins where the fertilized egg cell splits into two identical embryos. This process of exchanging DNA segments across sister chromatids is called genetic or homologous recombination and does not occur randomly across the genome, but most often occurs in areas called “hotspots.”²

Evolutionists have speculated for years that genetic recombination is one of the key mechanisms generating mutations and resulting in new genes and regulatory DNA sequences. They claim that this process facilitates some sort of mystical evolutionary tinkering and shuffling mechanism.

The problem with this idea is the fact that genetic recombination is now being shown to be a highly regulated and controlled cellular process. It is limited to specific hotspots and directed away from the key regulatory parts of the genome that are critical for gene regulation.^3,4 Unless something goes wrong with the process, recombination typically allows for variations in non-vital traits while protecting core-cellular processes. If this process was not precisely arranged and expertly controlled, severe damage to the genome would result and sexual reproduction would not be possible.

A recent study, published in the journal Molecular Biology and Evolution, evaluated various regions of the chimpanzee and human genomes for genetic recombination frequency by determining the DNA variability (differences) within large populations of both humans and chimpanzees.¹ The researchers found that genetic recombination levels were much higher in regions of the genome between humans and chimps where sequence identity was higher. In the regions of much lower DNA similarity, which occur as differences in gene order, gene content, and other major DNA sequence differences—the recombination rates were much lower.

Interestingly, the authors also searched the DNA sequences between humans and chimpanzees for sections that were “flipped” in their orientation, called inversions. Large inversions, once they occur in a species and if they are tolerated, will stop recombination. However, the researchers found that inverted sequences accounted for very few differences in the regions they examined. 

These results are the exact opposite of what evolutionists expected. According to evolutionary reasoning, the chromosomal areas between humans and chimps that were the most different should have had high levels of genetic recombination that would help explain why they were so different. But these chromosomal areas that were the most different between humans and chimpanzees had the lowest levels!

More recombination equals more evolutionary differences right? Apparently not!

Once again, new scientific data has falsified a prominent evolutionary hypothesis. While this study failed to uphold the hypothetical predictions of evolution, it did vindicate the now well-established fact that genetic recombination is a highly regulated, and complex bio-engineered feature that helps create variability in just the right areas of the genome.

Other recent research has shown that the human and chimpanzee genomes are radically different.⁵ And now this new study has demonstrated that these differences are not due to a mythical evolutionary tinkering and shuffling process associated with genetic recombination, but because humans and chimps were created separately and uniquely.

References

1. Farré, M. et al. 2013. Recombination Rates and Genomic Shuffling in Human and Chimpanzee—A New Twist in the Chromosomal Speciation Theory. Molecular Biology and Evolution. 30 (4): 853-864.
2. Smagulova, F. et al. 2011. Genome-wide analysis reveals novel molecular features of mouse recombination hotspots. Nature. 472 (7343): 375–378.
3. Tomkins, J. 2012. Gene Control Regions Are Protected--Negating Evolution. Posted on icr.org June 11, 2102, accessed May 17, 2013. 
4. Brick, K. et al. 2012. Genetic recombination is directed away from functional genomic elements in mice. Nature. 485 (7400): 642-645. 
5. Tomkins, J. 2013. Comprehensive Analysis of Chimpanzee and Human Chromosomes Reveals Average DNA Similarity of 70%. Answers Research Journal. 6 (2013): 63-69.

* Dr. Tomkins is Research Associate at the Institute for Creation Research and received his Ph.D. in Genetics from Clemson University.

Article posted on May 31, 2013.

http://www.icr.org/article/7526/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+icrscienceupdate+%28Science+Update+from+ICR%29

[grigorije22]

Genomic monkey business—estimates of nearly identical human–chimp DNA similarity re-evaluated using omitted data

by Jeffrey Tomkins and Jerry Bergman

©Eric Isselée/ 123rf.com

A review of the common claim that the human and chimpanzee (chimp) genomes are nearly identical was found to be highly questionable solely by an analysis of the methodology and data outlined in an assortment of key research publications. Reported high DNA sequence similarity estimates are primarily based on prescreened biological samples and/or data. Data too dissimilar to be conveniently aligned was typically omitted, masked and/or not reported. Furthermore, gap data from final alignments was also often discarded, further inflating final similarity estimates. It is these highly selective data-omission processes, driven by Darwinian dogma, that produce the commonly touted 98% similarity figure for human–chimp DNA comparisons. Based on the analysis of data provided in various publications, including the often cited 2005 chimpanzee genome report, it is safe to conclude that human–chimp genome similarity is not more than ~87% identical, and possibly not higher than 81%. These revised estimates are based on relevant data omitted from the final similarity estimates typically presented.

Several recent research reports confirm the conclusions noted above. While the recent Y-chromosome comparison between human and chimp does not lend itself to a genome-wide similarity estimate, the extreme dissimilarity discovered is an insurmountable paradox for common ancestry in primate evolution because it is by far the least variable chromosome in the human genome. Finally, a very recent large-scale human–chimp genome comparison research report spectacularly confirms the data presented in this report. The human–chimp common ancestor paradigm is clearly based more on myth and propaganda than fact.

A common claim is that the DNA of chimpanzees (Pan troglodytes) and humans (Homo sapiens) are about 98% similar. This oversimplified and often-touted estimate can actually involve two completely separate concepts. 1) Gene content (the comparative counts of similar types of coding sequences present or absent between different species) and 2) similarities between the actual base pairs of DNA sequences in alignments. For the most part, the modern similarity paradigm refers to DNA sequence alignment research.

 

Biological sequence data often goes through several levels of prescreening, filtering and selection before being summarized and discussed.

 

One of the major problems with overall research in the field of comparative genetics, as we will show, is that in most studies there is a great deal of preselection applied to the available biological samples and data before the final analysis is undertaken. Only the most promising data from a larger pool is typically extracted for a final analysis. Of course, you can only compare what you know is highly comparable, otherwise there is no available sequence comparison in most cases. Biological sequence data often goes through several levels of prescreening, filtering and selection before being summarized and discussed. Non-alignable regions and gaps in the sequence alignments are often omitted in the final results or their impact is obfuscated. As discussed below, this can be done in a variety of ways and must be evaluated on a case-by-case basis for each published study.

Early human–chimp studies used reassociation kinetics

The initial estimates of high human-chimp DNA similarity came from a field of study called reassociation kinetics. These initial reports fueled early claims by such popular evolutionary luminaries as Oxford Professor Richard Dawkins, who stated “Chimpanzees and we share more than 99 per cent of our genes.”¹ At the time, this statement was presumptuous, because gene numbers for humans and chimps were not known. The initial drafts of the human and chimp genomes were not announced until 2001 and 2005, respectively.^2–5

The supposed gene data Dawkins referred to in 1986 was an indirect estimate based on the reassociation kinetics of mixed human and chimp DNA, not clearly defined genes.¹ In reassociation kinetics, heat and/or chemistry are used to separate double-stranded DNA into single strands. When the DNA is allowed to reassociate in a controlled manner, it can be fractionated using various protocols. The slower the reassociation, the more complex and gene-dense the DNA is thought to be. In general, three types of DNA can be recovered: high-copy (highly repetitive, gene poor), low-copy (moderately repetitive, low levels of genes), and single copy (gene-rich). For comparative studies, the single copy fraction of DNA is collected from two species, mixed together, disassociated and allowed to reassociate so that human and chimp DNA can recombine. The level of complementary base matching between strands can be indirectly measured by a variety of methods that indirectly measure rates/levels of reassociation.

The caveat is that only the single-copy fractions of the human and chimp genomes were utilized to obtain early estimates of similarity. Scientists focused on the single-copy fraction because of the high gene content. However, many genes are located in the other genome fractions and were thus left out of the analysis. Another problem is that virtually the entire genome is now known to be functional in some aspect and the non-coding regions have been shown to provide many critical control features and nucleotide templates.^6,7,8

The first 99% similarity claim, which Cohen calls “The Myth of 1%”, was made in 1975 by Allan Wilson and Mary-Claire King using reassociation kinetics of single-copy DNA.⁹ Other similar studies came up with an average divergence in single-copy DNA that measured about 1.5%, producing the widely spread quotes of 98.5% DNA sequence similarity.^10–12 While a vast majority of the human and chimp genomes were actually excluded in the early quest to compare DNA, the supposed high similarities in the relatively small portions represented by single copy fractions surprised researchers. The eventual consensus, as reviewed by Gibbons, was that the dramatic differences between human and chimp anatomy and behaviour were based on the assumption that small genetic differences produce enormous physical differences.¹³

Genomics research—affirming the myth

Subsequent research using sequenced DNA built upon the early high similarity dogma established by reassociation kinetics. In a companion to this paper, we discuss the possibility that an unspoken dogma-based ‘Gold Standard’ regarding the human–chimp similarity issue was established during the initial studies involving reassociation kinetics.¹⁴

A review paper written by creationist Todd Wood on biological similarity between human and chimp highlighted and supposedly confirmed evolutionary similarity claims, yet ignored the important bioinformatic issues surrounding widespread data omission and selective analyses.¹⁵ Wood’s review did little to support creationist claims that humans were uniquely created in the image of God rather than being a few DNA base pairs from a chimp. Therefore, our focus on DNA sequence similarity will address the same publications listed in Wood’s review in addition to several more recent papers. The summarized data from these studies including estimates of similarity adjusted for omitted data is shown in table 1.

Table 1. Summary of human–chimpanzee genome comparison papers. Where possible, omitted data from the reported alignments is used to produce an actual percent DNA identity.

Reference

Total genomic bases analyzed

Aligned bases

Reported DNA identity

Actual DNA identity*

Britten, 2002

846,016

779,132

95.2%

~ 87%

Ebersberger et al., 2002

3,000,286

1,944,162

98.8%

< 65%

Liu et al., 2003

10,600,000 (total for human, chimp, baboon, and marmoset)

4,968,069 (human–chimp)

98.9% no indels

?

Wildman et al., 2003

~90,000 (exons from 97 genes)

?

98.4–99.4%

?

Chimp. Chrom. 22 Consort.

32,799,845

?

98.5% excluding indels

80–85% including indels

Nielson et al., 2005

?

?

99.4% selected gene regions

?

Chimp. Seq. Consort. 2005

Whole genome (5X redundant coverage)

2.4 Gb

95.8%

81%**

* Based on the amount of omitted DNA sequence in the alignments

** Compared to data from The International Human Genome Sequencing Consortium (2004)—((.9577 x 2.4 Gb) / 2.85 Gb) x 100

? Cannot calculate actual percent identity because data was not provided.

 

One of the first human–chimp DNA sequence papers that appeared at the beginning of the chimpanzee genome project was perhaps one of the most objective. Roy Britten, one of the early pioneers in DNA reassociation kinetics, compared the genomic sequence from five chimp large-insert DNA clones (Bacterial Artificial Chromosomes, or BACs¹⁶) to human genomic sequence using an atypical fortran-based computer program that was/is not publicly available.¹⁷ These five chimp BAC sequences were chosen because they were the only ones then available.¹⁸ Researchers typically choose initial seed BACs for genome sequencing because of their single-copy DNA content, which makes them easier to assemble and compare to other species. The total length of the DNA sequence for all 5 BACs was 846,016 bases. However, only 92% of this was alignable to human DNA, thus the final statistics reported on only 779,132 bases. To his credit, Britten included the alignment data on insertions and deletions (indels) and reported a human–chimp similarity of ~95%. However, a more realistic figure would include the complete high-quality sequence of all five BACs, which is just as legitimate as the indels within the alignments; giving a final DNA similarity of 87% (table 1). See figure 1, which graphically illustrates the concept of indels and substitutions in a pair-wise alignment between two DNA sequences.

Figure 1. Illustration showing the caveats of a hypothetical pairwise alignment between homologous sequences from two different species (seq1 and seq2). The first caveat is that in nearly all alignments there are portions of compared sequences outside the aligned regions that are typically omitted, but represent valid differences. Insertions and deletions (indels) within alignments represent the addition or loss of DNA sequence in one sequence compared to the other. Indels can vary in size from a single base to thousands of bases. Sometimes they are accounted for in alignments and sometimes they are omitted. Substitutions are bases that are different between two sequences and in most cases are included in the alignment results.

 

Another notable study published by Ebersberger et al. the same year as Britten’s paper utilized chimp genome sequence obtained from randomly sheared, size-selected fragments in the 300 to 600 base range.¹⁹ These DNA sequences were aligned to an early version of the human genome assembly using the BLAT (Blast-Like Alignment Tool) algorithm. Researchers selected two-thirds of the total sequence for more detailed analyses. One-third of the chimp sequence would not align to the human genome and was discarded. The methods section in the paper¹⁹ describes how the subset of prescreened data was further filtered to obtain only the very best alignments. The resulting data was then subjected to a variety of comparative analyses that, for all practical purposes, are completely meaningless given the extremely high level of selection, data masking, and filtering applied. Not surprisingly, they report only a 1.24% difference in only highly similar aligned areas between human and chimp. A more realistic sequence similarity based on the researchers’ own numbers for discarded data in the alignments alone is not more than 65% (table 1).

Shortly after these initial human–chimp comparison papers, a disturbing trend quickly emerged. This trend involved only reporting final alignment results and omitting the specific details of how such data was filtered, masked and selected. Key data to allow critical readers of human–chimp similarity papers to calculate a more accurate overall similarity began to be consistently omitted. For example, Liu et al. reported on the alignment of human genomic sequence with chimp, baboon, and marmoset.²⁰ Important information concerning the starting set of sequences and specific data for the alignments was omitted. They state only that they used a total amount of 10.6 Mb of sequence for all species combined. Their similarity estimate on the final alignment, omitting indels and non-aligned areas, was 98.9%. Including indels, we derived a value of 95.6% for the alignments, similar to Britten’s research. Important data outside the aligned areas was impossible to evaluate because of the omitted sequence data.

Another disturbing trend is that only highly conserved protein-coding sequence (exons) are often utilized to report genome-wide similarity. We now know that non protein-coding sequences, which comprise greater than 95% of the genome, are critical to all aspects of genetics and genome function.⁸ Typical of the trend to only align exonic sequences, Wildman, et al. reported on a study that compared only human and chimp protein coding regions of 97 exon fragments for a total of 90,000 bases.²¹ The preselected exons were based on the fact that they were present in both humans and chimps and already known to be highly alignable. Because of these bias issues and a lack of detail in the materials and methods, it is impossible to arrive at a valid estimate of omitted data and actual similarity in this case (table 1).

In 2004, Watanabe et al. used a variety of BAC libraries to select clones for DNA sequencing representing chimp chromosome 22.²² The sequence was then compared to its similar human homolog. The caveat is that the individual chimp BAC clones were only selected if they each contained 6 to 10 human DNA markers. Once again, we have an initial level of biased pre-selection occurring. In this case, it is happening before the DNA sequence data is even generated. Unfortunately, critical overall DNA alignment statistics are not given in the paper or in the supplemental information. The authors state a nucleotide substitution rate of 1.44% in aligned areas, but do not give similarity estimates to include indels. While indels are omitted from the alignment similarity, the authors indicate that there were 82,000 of them and provide a histogram that graphically shows the size distribution based on binned data groupings. Oddly, no data for average indel size or total indel length was provided. Likewise, the number of sequence gaps were given, but nothing about cummulative gap size. Despite the fact that supposedly well-sequenced orthologous chromosomal regions are being compared, specific data that would allow one to calculate overall DNA similarities are conspicuously absent. Based on an estimate using the limited graphical data provided regarding base substitutions and indels, a rough and fairly conservative estimate of about 80 to 85% overall similarity can be inferred (table 1).

One of the most ambiguous of all human–chimp studies was published by Nielson et al.²³ In keeping with the established obfuscational trend, only highly conserved exons were used and no data were given to allow one to calculate any type of real overall similarity. Of the total starting number of gene sequences in the analysis (20,361) the researchers decided to throw out 33% (6,630) in an ambiguously stated “very conservative quality control”. In other words, one third of the initial chimp data did not align to human, so it got tossed out. In fact, no hard data was actually given to even assess the final two-thirds of chimp data that was compared. The authors only report on sequence substitution divergence beyond ‘silent sites’. These ‘silent sites’ are the areas where the data was thrown out; representing locations where genetic variation supposedly exhibits little to no effect on genome function. This is an errant presupposition that is coming under scrutiny due to the fact that the majority of the non-coding portions of the genome are now proven to be functionally active. Data for important indel differences was also completely omitted. Unfortunately, there was not enough data provided in this highly obfuscated report to obtain even a rough calculation of similarity.

Chimpanzee rough draft genome assembly data—81% similarity?

The major milestone publication regarding human–chimp genome comparisons was the 2005 Nature paper from the International Chimpanzee Genome Sequencing Consortium.⁴ Unfortunately, this paper followed the previously established trend where most of the comparative data was given in a highly selective and obfuscated format and detailed information about the alignments was absent. The majority of the paper was primarily concerned with a variety of hypothetical evolutionary analyses for various divergence rates and selective forces. Hence, the critical issue of overall similarity was carefully avoided.

However, based on the numbers given in the chimp genome paper, one can determine a rough overall genome similarity between humans and chimp by including published concurrent information from the human genome project. In regards to the overall alignment, the authors state, “Best reciprocal nucleotide-level alignments of the chimpanzee and human genomes cover ~2.4 gigabases (Gb) of high-quality sequence”.²⁴ At this time, the human euchromatic assembly was estimated to be 99% complete at 2.85 Gb and had an error rate of 1 in 100,000 bases.²⁵ The chimp genome authors state, “The indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions.”²⁶

In summary, only 2.3 Gb of chimp sequence aligned onto the highly accurate and complete human genome (2.85 Gb) an operation that included the masking of low complexity sequences. For the chimp sequence that aligned, the data for substitutions and indels indicates 95.8% similarity, a biased figure which excludes the masked regions. Using these numbers, an overall estimate of chimp compared to human DNA produces a conservative estimate of genome-wide similarity at 80.6%. In 2005, a five-fold redundant coverage of the chimp genome had been attained, which should have represented greater than 95% of the overall sequence.

Wood’s report features an analysis that attempts to validate the entire 2005 chimp genome assembly.²⁷ Wood’s comparison between human and chimp used deduced amino-acid sequences from gene orthologs already known to be similar, thus alignable. Protein amino acid comparisons between electronically translated coding sequences of known orthologs is hardly an accurate indicator of genome-wide DNA sequence similarity. Orthologs are genes in different species that are assumed to have evolved from a common ancestral gene primarily because they have the same function and similar sequence in both species. Amino acid comparisons between electronically translated coding sequence of known orthologs is also not an accurate indicator of genome-wide sequence similarity because less than 5% of the human genome actually contains protein-coding sequence. Yet another problem with using electronically generated proteins for comparisons is highlighted by the fact that a majority of mammalian genes undergo alternative transcription and translational start/stop sites, multiple mechanisms of exon splicing, intragene regulatory RNA coding segments, enhancer elements and many other complex transcriptional splicing code features.^28,29 In light of our current knowledge of how the genome actually functions, the antiquated approach of using electronically deduced nuclear protein sequences for intergenome comparisons needs to be seriously reconsidered by both evolutionists and creationists.

The human–chimp paradigm starts to crumble

Following Wood’s summary¹⁵ of some of the major papers involved in the human–chimp similarity myth, several key reports emerged that called into question the dogma of the human-primate evolutionary paradigm. The first was a study by Ebersberger et al., in which a large pool of human, chimp, orangutan, rhesus and gorilla genomic sequences was used in constructing phylogenies (multiple alignments analyzed in evolutionary tree format).³⁰ The original pool of DNA sequences actually went through several levels of selection to preanalyze, trim and filter them for optimal alignment. First, a set of 30,112 sequences were selected that shared homology (overlapping similarity) between the five species. These sequences were aligned and only those which produced ≥ 300 base alignments were retained for another series of alignments and only the sequences that produced superior statistical probabilities > 95% were used in the final analysis. This filtering process removed over 22% of already-known, pre-selected homologous sequence. Despite all of this data filtering designed to produce the most favourable evolutionary alignment and trees, the results did not show any clear path of ancestry for humans with chimps or any of the great apes. What emerged was a true mosaic of unique human and primate DNA sequences; discounting any clear path of common ancestry. Perhaps the best summary of the research can be found in the author’s own words.

“For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee.

“Thus, in two-thirds of the cases a genealogy results in which humans and chimpanzees are not each other’s closest genetic relatives. The corresponding genealogies are incongruent with the species tree. In accordance with the experimental evidences, this implies that there is no such thing as a unique evolutionary history of the human genome. Rather, it resembles a patchwork of individual regions following their own genealogy.”

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The authors add that the lack of support for a consistent and clear evolutionary tree among humans and other primates is due to the “inclusion of alignments with no clear phylogenetic signal,”³² a significant statement given the fact that they used extremely high levels of data filtering and selection designed to provide enormous levels of “phylogenetic signals”.

The Y-chromosome bombshell

One of the most dogma-damaging reports to surface in recent years is the Y-chromosome comparison between humans and chimps.³³ In this study, the male-specific region (MSY), a large region of the Y-chromosome, was compared between human and chimp. To accomplish this, a fair amount of resequencing had to be performed due to the fact that the chimp sequence in this area was fragmented and incomplete. The end result was 25,800,000 bases of highly accurate chimp Y-chromosome sequence distributed among eight contiguous segments. When compared to the human Y-chromosome, the differences were enormous. The authors state, “About half of the chimpanzee ampliconic sequence has no homologous, alignable counterpart in the human MSY, and vice versa.”³⁴ The ampliconic sequence contains ornate repeat units (called palindromes) that read the same forwards as they do backwards. Dispersed within these palindromes are families of genes that are expressed primarily in the male testes. Not only did 50% of this type of sequence fail to align between human and chimp in the Y-chromosome, humans had over twice as many total genes (60 in humans vs 25 in chimp). There were also three complete categories of genes (gene families) found in humans that were not even present in chimps. Related to this large difference in gene content, the authors note, “Despite the elaborate structure of the chimpanzee MSY, its gene repertoire is considerably smaller and simpler than that of the human MSY,”³⁵ and “the chimpanzee MSY contains only two-thirds as many distinct genes or gene families as the human MSY, and only half as many protein-coding transcription units.”³⁵

Besides these distinctively male-type genes, there were other areas characterized that contained genes labelled as ‘X-degenerate’, a somewhat misleading term based on the assumption that the X-degenerate genes have homologs on the female X chromosome from which they are postulated by evolutionists to have evolved. A comparison of X-degenerate gene regions between humans and chimps also showed distinct organizational and locational differences in addition to differences in gene content. In fact, humans have three types (classes) of X-degenerate genes that are not even present in chimps.

Besides the large differences in gene content between human and chimp MSY regions, the overall structural differences were enormous. Take note of some of the additional comments from the authors:

“Moreover, the MSY sequences retained in both lineages have been extraordinarily subject to rearrangement: whole chromosome dot-plot comparison of chimpanzee and human MSYs shows marked differences in gross structure.

“The chimpanzee ampliconic regions are particularly massive (44% larger than in human) and architecturally ornate, with 19 palindromes (compared to eight in human) and elaborate mirroring of nucleotide sequences between the short and long arms of the chromosome, a feature not found in the human MSY.

“Of the 19 chimpanzee palindromes, only 7 are also found in the human MSY; the other 12 are chimpanzee-specific. Unlike the human MSY, nearly all of the chimpanzee MSY palindromes exist in multiple copies.”

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The large differences in both structural arrangements of unique DNA features and gene content described in the Y-chromosome study, is particularly damaging to human-chimp DNA similarity mythos and the dogma of primate evolution. In fact, the authors shockingly note that given “ … 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation.”³⁵

 

The main problem with these drastic differences between human and chimp Y-chromosomes is that the evolutionary dogma cannot account for it.

 

The main problem with these drastic differences between human and chimp Y-chromosomes is that the evolutionary dogma cannot account for it. A large study of genetic variation in the human genome showed that the Y-chromosome was exceptionally stable and had five times less genetic variation than the autosomes.³⁶ This data makes perfect sense because the Y-chromosome has no similar homolog in the genome and undergoes very little recombination with the X-chromosome during meiosis. Given this lack of recombination and sequence diversity on the Y-chromosome, the primate evolution model encounters a serious problem, because the human and chimp Y-chromosomes should be considerably more similar to each other. Evolutionists consider high levels of DNA sequence variation as positive indicators of places in the genome that evolve rapidly. Therefore, the Y-chromosome should have signatures of such activity because it is so markedly different from chimp, but it has not. Instead, it appears to be very static and stable, with very few structural differences and little sequence diversity among human males worldwide. The proven stability of the Y-chromosome compared to the rest of the human genome, combined with the large differences between human and chimp, is an insurmountable enigma for the human–chimp common ancestry paradigm.

Some cases of high similarity may be due to contamination

Another factor to consider in the human-chimp similarity debate is that some cases of high sequence similarity may be due to contamination. Not only is the chimpanzee genome assembly still largely based on the human genomic framework, it also now appears that the wide-spread contamination of non-primate databases with human DNA is a serious problem and can run as high as 10% in some cases.³⁷ Human contamination results from the process of cloning DNA fragments in the lab for sequencing where airborne human cells come from coughing, sneezing, and physical contact with contaminated fingers. The detection and characterization of human DNA contamination in primate databases could be a difficult and highly subjective endeavour because of the overriding dogma of primate evolution. It is also noteworthy that the chimpanzee genome was sequenced during the time period where wide-spread human DNA contamination was not well exposed. The contamination problem is also confounded by the use of the human framework for chimp sequence assembly and annotation.

In fact, contamination is not only possible via laboratory error, but is introduced on purpose during chimpanzee genome assembly and annotation based on Darwinian dogma. On a recent website at the Ensembl database (joint bioinformatics project between EMBL-EBI and the Wellcome Trust Sanger Institute), a webpage titled ‘Chimp Genebuild’ provides the following information as to one of the ways in which the human genome is used as a guide to assemble and annotate the chimp genome:

“Owing to the small number of proteins (many of which aligned in the same location) an additional layer of gene structures was added by projection of human genes. The high-quality annotation of the human genome and the high degree of similarity between the human and chimpanzee genomes enables us to identify genes in chimpanzee by transfer of human genes to the corresponding location in chimp.

“The protein-coding transcripts of the human gene structures are projected through the WGA [whole genome assembly] onto the chromosomes in the chimp genome. Small insertions/deletions that disrupt the reading-frame of the resultant transcripts are corrected for by inserting ‘frame-shift’ introns into the structure.”

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Not only is the chimpanzee genome assembled using the human genome as framework, human sequence contamination is admitted to exist because it was electronically added to fill in putative missing chimp sequences. Based on the myth and dogma that human DNA is supposedly nearly identical to chimp, bits and pieces of human DNA have been fitted into gaps and regions of the chimp genome, making it appear more human. As a result, when downloading the assembled and annotated chimp genome sequence for independent study, the researcher does not have 100% unbiased chimp sequence, as often assumed. Instead, there is a patchwork of human and chimp sequence pieced together, aligned, and oriented based on the human genome.

Conclusion—human and chimp DNA not so similar after all

The chimpanzee genome in its final annotated and assembled state is clearly a biased product. In addition, nearly all research reports on human–chimp DNA similarity omit significant amounts of data that do not align or represent gaps in the sequence. In fact, a significant number of papers do not even include enough data to allow an independent reader the ability to factor in how much original dissimilarity existed before the final, highly filtered numbers are given. In regards to an estimate of human–chimp genome similarity from data provided (but often buried) in published reports, it is safe to say that it is not more than 81 to 87% and quite possibly lower.

In support of this conclusion, a large-scale human–chimp genome comparison research project was just recently published in a separate journal.³⁹ This study completely substantiates and confirms the data presented in this report. In this study, author Tomkins reports on the pair-wise alignment data of 40,000 random chimpanzee genomic sequences compared to four different versions of the human genome using the blastn algorithm run under 30 different parameter combinations. This effort produced a total of 1.2 million attempted alignments—4.8 million if you factor in the four different human genome assemblies. Excluding data for the large amount of chimp sequence that did not align, Tomkins reported a very conservative estimate of human–chimp DNA similarity in just the aligned regions at 86–89% (depending on algorithm parameters). Results from this extensive and very objective study unequivocally indicate that the human and chimpanzee genomes are at least 10–12% less identical than is commonly claimed. The human-chimp common ancestor paradigm, which claims a nearly identical DNA content, is clearly based more on myth and propaganda than real factual data.

http://creation.com/human-chimp-dna-similarity-re-evaluated

[grigorije22]

Genetics Research Confirms Biblical Timeline by Jeffrey Tomkins, Ph.D. *

Exciting research from the summer of 2012 described DNA variation in the protein coding regions of the human genome linked to population growth. One of the investigation's conclusions was that the human genome began to rapidly diversify not more than 5,000 years ago.^1,2 This observation closely agrees with a biblical timeline of post-flood human diversification. Yet another study, this one published in the journal Nature, accessed even more extensive data and unintentionally confirmed the recent human history described in Genesis.³

Differences in human DNA can be characterized across populations and ethnic groups using a variety of techniques. One of the most informative genetic technologies in this regard is the analysis of rare DNA variation in the protein coding regions of the genome. Variability in these regions is less frequent than the more numerous genetic differences that occur in the non-coding regulatory regions. Researchers can statistically combine this information with demographic data derived from population growth across the world to generate time scales related to human genetic diversification.⁴

What makes this type of research unique is that evolutionary scientists typically incorporate hypothetical deep time scales taken from the authority of paleontologists or other similar deep-time scenarios to calibrate models of genetic change over time. Demographics-based studies using observed world population dynamics do not rely on this bias and are therefore more accurate and realistic.

In a 2012 Science report, geneticists analyzed DNA sequences of 15,585 protein-coding gene regions in the human genome for 1,351 European Americans and 1,088 African Americans for rare DNA variation.^1,2 This new study accessed rare coding variation in 15,336 genes from over 6,500 humans—almost three times the amount of data compared to the first study.³ A separate group of researchers performed the new study.

The Nature results convey a second spectacular confirmation of the amazingly biblical conclusions from the first study. These scientists confirmed that the human genome began to rapidly diversify not more than 5,000 years ago. In addition, they found significant levels of  variation to be associated with degradation of the human genome, not forward evolutionary progress. This fits closely with research performed by Cornell University geneticist John Sanford who demonstrated through biologically realistic population genetic modeling that genomes actually devolve over time in a process called genetic entropy.⁵

According to the Bible, the pre-flood world population was reduced to Noah's three sons and their wives, creating a genetic bottleneck from which all humans descended. Immediately following the global flood event, we would expect to see a rapid diversification continuing up to the present. According to Scripture, this began not more than 5,000 years ago. We would also expect the human genome to devolve or degrade as it accumulates irreversible genetic errors over time. Now, two secular research papers confirm these biblical predictions.

References

1. Tomkins, J. 2012. Human DNA Variation Linked to Biblical Event Timeline. Creation Science Update. Posted on icr.org July 23, 2012, accessed December 31, 2012.
2. Tennessen, J. et al. 2012. Evolution and Functional Impact of Rare Coding Variation from Deep Sequencing of Human Exomes. Science. 337 (6090): 64-69.
3. Fu, W, et al. Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Nature. Published online before print, July 13, 2012.
4. Keinan, A and A. Clark. 2012. Recent Explosive Human Population Growth Has Resulted in an Excess of Rare Genetic Variants. Science. 336 (6082): 740-743.
5. Sanford, J. C. 2008. Genetic Entropy and the Mystery of the Genome, 3rd ed. Waterloo, NY: FMS Publications.

* Dr. Tomkins is a Research Associate and received his Ph.D. in Genetics from Clemson University.

Article posted on January 9, 2013.

http://www.icr.org/article/7231/282/  

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Are Rotifers Gene Stealers or Uniquely Engineered? by Jeffrey Tomkins, Ph.D. *

The tools of DNA sequencing are becoming cheaper to use and more productive than ever, and the deluge of DNA comparison results between organisms coming forth are becoming a quagmire for the evolutionary paradigm. To prop it up, biologists resort to ever more absurd explanations for discrepancies. A prime example of this trickery is in a recent DNA sequencing project performed in a microscopic aquatic multi-cellular animal called a rotifer.¹

In this effort, the researchers targeted those gene sequences that are expressed as proteins for DNA sequencing because the genome was too large and complex to sequence and assemble all of its DNA. They recorded over 61,000 gene sequences that were expressed from rotifers grown in stressed and non-stressed conditions. Of these, they could only find sequence similarities between rotifers and other creatures for 28,922 sequences (less than half). The researchers tossed the unknown DNA sequences out of their analysis since the non-similar genes were novel, apparently specific to rotifer, and essentially difficult for evolution to explain.

Of the 28,922 sequences for which they could obtain a match in a public database of other creature's DNA and protein sequences, a significant proportion (more than in any other creature sequenced) did not fit evolutionary expectations of common descent. Further complicating this picture, the rotifer gene sequences were found in a diverse number of non-rotifer creatures!

Some of the creatures that had gene matches to rotifers included a variety of plants, other multicellular animals, protists (complex single celled animals), archaea, bacteria, and fungi.

Evolutionists have two options in which to categorize these unusual gene matches based on their naturalistic presuppositions. First, they can say that these genes evolved independently in separate creatures in a hypothetical process called "convergent evolution." However, in cases where there are literally hundreds of these DNA sequences popping up in multiple organisms, this scenario becomes so unlikely that even evolutionists have too much difficulty imagining it. The second option is called "horizontal gene transfer," or HGT. This involves the transfer of genes, perhaps via some sort of microbial host vector such as a bacterium.²

In the present report, the rotifer under study was asexual, limiting heredity as an option for aiding in gene transfer. So the researchers concluded that it stole hundreds of genes via HGT from a plethora of other creatures.

HGT is considered somewhat common among bacteria because they form connective tubes (called pili) and exchange little bits of DNA, like sharing software. Also, HGT can occur rarely between a bacterium and a multicellular host that it interacts with during its life cycle.³

How will rotifer researchers account for the massive transfer of hundreds of genes from a broad range of hosts that they believe includes 533 supposed source genomes for which no biological host-based relationships exists? Some sort of causal host relationship must occur for the transfer of one gene, let alone hundreds of genes from hundreds of sources.¹

Another problem is that the researchers showed that the so-called "stolen genes" were well-integrated into the rotifer cell biochemistry and its environmental adaptation mechanisms. A separate 2012 study showed that highly expressed native genes could not be shared via HGT, even among bacteria, because they would severely disrupt essential cell biochemistry.⁴ And these are exactly the types of genes that were surveyed in the rotifer.

In this case, evolutionary biologists have resorted to fictional stories cloaked in technical terminology to escape the straightforward conclusion that rotifer DNA was purposefully crafted. If a large bunch of newly discovered genes don't make evolutionary sense, then evolution proponents ascribe their origin to HGT despite the fact that HGT is not known to operate without any host-based relationship. HGT is also not known to occur en masse, and HGT of essential genes is in theory impossible.⁴

The unique mix of rotifer genes along with their flawless biochemical integration into the rotifer's cell system, clearly and abundantly supports the special creation described in the Bible.

References

1. Boschetti, C. et al. 2012. Biochemical Diversification through Foreign Gene Expression in Bdelloid Rotifers. PLOS Genetics. 8 (11): e1003035.
2. For example, this author contributed to a report describing HGT from Wolbachia bacteria to fruit flies, parasitic wasps, and soil roundworms. See Dunning Hotopp, J. C. et al. 2007. Widespread Lateral Gene Transfer from Intracellular Bacteria to Multicellular Eukaryotes. Science 317 (5845): 1753-1756.
3. HGT is also sometimes called lateral gene transfer, as opposed to the transfer of genes vertically through the germ line (heredity).
4. Park, C. and J. Zhang. 2012. High Expression Hampers Horizontal Gene Transfer. Genome Biology and Evolution. 4 (4): 523-532.

* Dr. Tomkins is Research Associate at the Institute for Creation Research and received his Ph.D. in Genetics from Clemson University.

Article posted on December 3, 2012.

 

 http://www.icr.org/article/7132/282/

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Gene Networks Are Intolerant of Mutation by Jeffrey Tomkins, Ph.D. *

Fish supposedly evolved into people by gene mutations, but a recent report shows that mutations have disastrous effects.¹ Not only are individual genes essential, but when they are inhibited, entire gene networks are disrupted, resulting in severe growth and development problems in the organism.

One of the main model organisms used to study gene and genome function is the small soil worm called a nematode. Nematodes are the most abundant type of animal on earth and live in many different environments. They also make excellent test animals for genetic study in the lab because they are easy to raise, have a small genome size, and much is known about their biology.

In the past, scientists used a variety of technologies to sequentially inhibit individual genes in the nematode genome.^{2, 3} Their goal was to ascertain which genes are essential to its survival. However, in these early studies, researchers only analyzed the effects of gene mutation by looking at individual nematodes for observable changes. They also only evaluated the effects of mutation on a single generation. Therefore, they missed detecting the results of disabling genes where the effects were subtle.

In this recent study, scientists observed the effects of 550 sequentially inhibited genes on the overall fitness of nematodes over eight generations. Fitness is the ability of a population of organisms to grow and reproduce over time compared to a control population that does not have the mutation. Fitness can also be tested in different environments that apply various stresses.

In the majority of cases, the disruption of single genes reduced the fitness of the nematode populations. This was an effect that kept increasing with successive generations. Theoretically, this would have eventually led to extinction.

As a result, researchers concluded that most every gene tested was essential to survival of the nematode. Because the mutant worms' fitness decreased over successive generations, the researchers also concluded that even single mutations negatively impact entire gene networks.

The researchers wrote,

In contrast to previous estimates, we find that, in these multigeneration population assays, the majority of genes affect fitness, and this suggests that genetic networks are not robust to mutation. Our results demonstrate that, in a single environmental condition, most animal genes play essential roles.¹

In the biological evolution model, the process of genome mutation not only involves the hypothetical alteration of gene sequences, but the idea that not all genes are essential to life. In other words, there is room in the cell system for DNA to randomly change, so that once in a while it can spit out some useful new gene sequence to advance evolutionary progress. However, this new study shows that even though the cell systems in roundworms are dynamic and environmentally responsive, the fine-tuned DNA-based informational system that underlies it cannot be corrupted without diminishing its ability to survive.

So in addition to refuting evolution, nematode gene networks show every sign of carefully crafted system engineering.

References

1. Ramani, A. K. et al. 2012. The Majority of Animal Genes Are Required for Wild-Type Fitness. Cell. 148 (4): 792-802.
2. Kamath, R. L. et al. 2003. Systematic Functional Analysis of the Caenorhabditis elegans Genome Using RNAi. Nature. 421 (6920): 231-237.
3. Sonnichsen, B. et al. 2005. Full-Genome RNAi Profiling of Early Embryogenesis in Caenorhabditis elegans. Nature. 434 (7032): 462-469.

* Dr. Tomkins is Research Associate at the Institute for Creation Research and received his Ph.D. in Genetics from Clemson University.

Article posted on December 17, 2012. 

 

 http://www.icr.org/article/7166/282/

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Natural selection ≠ evolution

by Marc Ambler

This is an important ‘equation’¹ that all people should be aware of, namely ‘Natural Selection does not equal (≠) Evolution’.² Christians should know it so they do not get conned, and evolutionists should know it as a reminder that they still have lots of work to do to be able to claim that they have a mechanism for evolution.

How often we hear an example of natural selection being used as proof of evolution. Changing sizes, colours, skin patterns and shapes are often paraded as evolution’s honour roll. This bait-and-switch tactic has been so often exposed for what it is, it’s a wonder that it is still used, or that people are still taken in by it.

The very term should put people on their guard that something is missing. If we think of the word ‘selection’, in our common, daily experience, we select from something pre-existing. Think of being asked to select cards from a pack. You could select cards from a pack every second for the rest of your life and all you would only ever produce is different groups of the same cards. You would not have created anything new—only re-arranged cards, or removed cards or added cards from another pack.

If we think of the word ‘selection’, in our common, daily experience, we select from something pre-existing.

If an illusionist asks you to select a card from a pack, and surprises you with something new, you know it is an illusion, a sleight of hand. We need to learn to see the evolutionists’ sleight of hand when they claim to have pulled something ‘new’ out of the pack. Selection is always from a pre-existing series or range; it creates nothing new.

This illustration applies equally to ‘selection’ in the biological context. The all-wise Creator knew the different environments that His creatures would have to adapt to after the Fall and Curse, and particularly after the Flood of Noah, in order to survive. He included in the genetic information of each ‘kind’ of creature He created, a smorgasbord of variety in their makeup. This includes those features that would interact with the environment: the overall size of a plant, animal or person; the size of individual organs or limbs such as beaks and noses, leaf sizes, skin colours, hair and feather lengths, textures and colours. All of these and many more variations were programmed into the DNA of His creatures in order that as populations of the various kinds moved into new environments, expression of those variations enabled individuals to survive those environments. Individuals with those variations then passed them on to their young. When these variations and the habitat of the population expressing that variation are distinct enough, we might distinguish different ‘species’. In all of this selection process, new information is never added. It can be conserved or lost, but never gained.

The creationist chemist/zoologist Edward Blyth (1810–1873) wrote about natural selection about 25 years before Darwin misappropriated it to support his theory of evolution. Blyth clearly saw this remarkable phenomenon as arising from the providence of the all-wise, all-knowing, ingenious Creator God.

Knowing God’s love for beauty (reflected in men and women who are made in His image), God probably also had in mind the spectacular array of birds, fish, dogs and cats that we have varied by ‘artificial selection’ purely for the sake of ‘beauty’ rather than survival.³

But whether variation is selected naturally by the environment, or artificially by breeders for a particular trait, it remains just that, ‘selection’ from existing genetic information. Nothing new is created.

Evolution desperately needs ‘Natural Invention’, ‘Natural Novelty’ and ‘Natural Creation’.

Patent law calls for a product to have an ‘inventive step’ in order for it to be patented. Mere changes in design of an existing product cannot be patented. Many legal battles over patent rights have been waged over this point. Evolution requires the same thing—an ‘inventive step’, a novel organ or body part, facilitated by new information in the DNA that wasn’t there before. Despite the huge resources thrown at evolution in universities and research institutions, natural selection has never been shown to bring about this type of ‘inventive step’.

Today’s Darwinists point to mutations as the mechanism which provides this novelty from which ‘Natural Selection’ selects. Evolutionists should then focus on mutations to defend their theory, instead of ‘Natural Selection’. When pressed for examples of novel genetic information or body organs created by mutation, they typically point to instances such as wingless beetles⁴ on islands, or the flightless cormorant on the Galapagos islands.⁵ The problem with these examples is obvious. While they may confer a benefit to the creatures in a specific, very unusual environment, nothing ‘new’ is added to the DNA or creatures’ body parts. They actually involve a loss or corruption of existing genetic information.⁶

Evolution desperately needs ‘Natural Invention’, ‘Natural Novelty’ and ‘Natural Creation’. ‘Natural Selection’ just does not pass muster as exhibit A for evolution. Rather, it is a wonderful tribute to God’s design, and His providence for a fallen world. Natural Selection ≠ Evolution.

Related Articles

• Refuting Evolution
• Muddy Waters
• Defining terms

http://creation.com/natural-selection-evolution

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Stark Differences Between Human and Chimp Brains by Brian Thomas, M.S. *

New research adds to an ever-lengthening stream of discoveries that confirm exactly what a Bible-believing scientist would expect—humans are distinct from chimpanzees. They should be, if they were created in the image of God, not as an imaginary pre-human primate. The study, published in American Journal of Human Genetics, investigated DNA methylation patterning in human and chimpanzee brains.¹ Two observations from this research support the biblical origins of mankind.

In a process called methylation, cell systems add methyl groups to some regions of chromosomes. DNA methylation patterns are different in brain cells than they are in muscle cells, for example, and they differ between individuals and species. They do not change the genetic code, but they regulate some genetic functions. Therefore, they comprise a level of information separate from the genetic code. Studies show that they provide critical regulation of the activity of DNA-manipulating enzymes both during embryonic development and during the daily life of adult cells. When methylation patterns are errant, they cause gene malfunction and can lead to disease. Some types of abnormal methylation patterns are lethal.

The researchers used a new technique to peer in unprecedented detail at the methylation patterns of human and chimp DNA that they harvested from brain tissue of three cadavers of each species. They compared only those DNA sequences already known to have basically the same genes, ignoring the vast majority of DNA. If humans and chimps are close relatives, then they should have similar DNA methylation patterns in the areas of chromosomes that they have in common such as similar gene sequences.² However, this team found major differences.

In particular, human and chimp DNA methylation patterns, called "methylomes," were very different between the two species’ brain tissue. The data statistically indicated that "major principal components separate humans and chimpanzees," according to their report in American Journal of Human Genetics.^1,3

A second observation is that the very genes that were differently methylated "exhibit striking associations with several disorders, including neurological and psychological disorders and cancers."¹ These data show that methylation patterns in many cases can tolerate very little disruption, thus presenting another impossible hurdle for the evolutionary model to overcome.

If humans evolved from chimpanzee-like creatures, then some unknown evolutionary process must have altered their methylomes. But since methylomes apparently cannot tolerate that much alteration, then the evolutionary story must be in error.

Human and chimp species-specific and irreducibly complex methylomes refute human evolution. On the other hand, the origin of mankind as a special creation of an omnipotent and loving kind Creator who made man after His likeness is consistent with the newly described uniquely human methylome.

References

1. Zeng, J. et al. 2012. Divergent whole-genome methylation maps of human and chimpanzee brains reveal epigenetic basis of human regulatory evolution. American Journal of Human Genetics. 91 (3):455-465.
2. Human and chimp DNA sequences are overall much more different than widely held. See Tomkins, J. 2011. Evaluating the Human-Chimp DNA Myth—New Research Data. Acts & Facts. 40 (10): 6; and Tomkins, J. and B. Thomas. 2010. New Chromosome Research Undermines Human-Chimp Similarity Claims. Acts & Facts. 39 (4): 4-5.
3. Specifically, 474 homologous genes that were either heavily methylated or weakly methylated in one species was just the opposite in the other species. Similarly, 468 gene promoters in human were significantly less methylated than the same gene promoter regions in chimpanzees.

* Mr. Thomas is Science Writer at the Institute for Creation Research. 

http://www.icr.org/articles/view/7067/372/

 

[Avocado]

Natural selection ≠ evolution

by Marc Ambler

 

The very term should put people on their guard that something is missing. If we think of the word ‘selection’, in our common, daily experience, we select from something pre-existing. Think of being asked to select cards from a pack. You could select cards from a pack every second for the rest of your life and all you would only ever produce is different groups of the same cards. You would not have created anything new—only re-arranged cards, or removed cards or added cards from another pack.

 

 

Ništa ne nedostaje i sam autor ovog pamfletića je toga svestan budući da to pominje na kraju teksta, pominjući mutacije.

 

U pitanju je čista igra reči sa neadekvatnim primerima. Da, tačno je da izborom drugačijih karata ne nastaje "ništa novo" OSIM drugačijeg rasporeda i broja karata... međutim, između mačke i krokodila nema nikakve razlike OSIM drugačijeg rasporeda i broja nukleotida u DNK... te je umanjivanje značaja drugačijeg rasporeda nukleotida prosto glupo.

 

 

All of these and many more variations were programmed into the DNA of His creatures in order that as populations of the various kinds moved into new environments, expression of those variations enabled individuals to survive those environments.

 

 

 

Ova tvrdnja je možda nekada bila zabavna... kada nismo imali dešifrovan genom... danas ništa ne sprečava kreacioniste da demonstriraju da su varijacije unapred programirane u DNK... a da u suprotnom ne pričaju takve budalaštine.

[RYLAH]

između mačke i krokodila nema nikakve razlike OSIM drugačijeg rasporeda i broja nukleotida u DNK

 

 

Шутни крокодила, паш да видиш разлику

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NEURONS IN THE BRAIN AND A SIMULATED IMAGE OF THE UNIVERSE..

One is micrometers wide, there other is so large it's beyond human comprehension.Two very similar patterns but in two very different natural forms, one in space the other on Earth. Why else would there be such a similar pattern? Because they had the same Creator.  

 

 

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SIMILARITIES THAT DISPROVE EVOLUTION

Lysozyme is the enzyme in tears that bites holes in the cell walls of bacteria so that they explode. This same enzyme is also in egg white, and protects baby chicks from infection. Neither human eyes nor baby chicks become infected easily. But does this mean that man is descended from baby chicks? Does it mean they are closely related?

One researcher, *Richard E. Dickerson, wanted to locate the exact point at which humans branched off the family tree. He decided, after comparing lysozyme and lactalbumin, that we are the direct descendants of chickens; for, in this one respect, people are more closely related to chickens than they are to any other kind of living creature.

Eye of the Octopus. The octopus has an eye that is very similar to the one that humans have. In contrast the eyes of fish are totally different from the eyes of an octopus. Are we then descended from the octopus? But..Dickerson said we were the offspring of baby chicks? It doesn't take a genius to see evolution is just plain wrong. We are the product of a Common Designer, and as such we share some similarities.   

 

 

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DVD makers copy mantis shrimp eye design

by Jonathan Sarfati

©iStockPhoto.com/Klaus-bodo

We have already reported on the amazing mantis shrimp,¹ highlighting its powerful punch due to a catapult mechanism—it can accelerate up to 10,600 g (humans pass out at 10g). Its superb colour vision system includes 12 primary colour receptors—four times as many as humans have. Australian satellite designers wanted to design satellite cameras based on that, making the pithy comment, “Instead of throwing a shrimp on the barbie, I want to put a prawn into space.”

A 2009 update² pointed out that the mantis shrimp also has remarkable light-sensitive cells that rotate the plane of polarization³ in light. Manmade systems can do this, but work well only in one colour; the mantis shrimp worked almost perfectly throughout the visible spectrum and even beyond: near ultra-violet to infra-red.

Transferring the same multi-colour ability into a DVD player could enable it to handle far more information.

The mechanism we have found in this eye is unknown to human synthetic devices. It works much, much better than any attempts that we’ve made to construct a device.—University of Bristol researcher Nicholas Roberts.

“The mechanism we have found in this eye is unknown to human synthetic devices. It works much, much better than any attempts that we’ve made to construct a device,” said University of Bristol researcher Nicholas Roberts.

4

He and his colleagues observed that the mantis shrimp had cell membranes rolled into tiny tubes (nanorods).

Now some engineers from National Taipei University of Technology, Taiwan, have made waveplates based on the mantis shrimp eye lenses. Waveplates change polarization, and these new ones could highly improve DVD definition and storage capacity. A report explains:

“The research team’s waveplate is made of two layers of nanorods that are structurally similar to those in the eye of the peacock mantis shrimp.”

5

Waveplates change polarization, and these new ones could highly improve DVD definition and storage capacity.

These layers (of tantalum pentoxide) are deposited by different methods. Both produce parallel layers of nanorods, but one is upright. Each stage of the waveplate comprises a sandwich of the non-upright layer between two upright layers. Then these sandwiches are stacked to make the required waveplate.

Furthermore, this ingenious technique uses relatively inexpensive methods within the thin-film industry.

This is only one in a long list in the field of biomimetics (or biomimicry)—human designers copying the ingenious designs of the Master Designer, i.e. the One who made the heavens and the earth and the seas and all that is in them (Exodus 20:11).^6,7  

 

  http://creation.com/mantis-shrimp-eye