If I ever meet a "Darwinist religious fanatic", I'll be sure to check them out and see whether they match your description.
If, however, you meant to slur the millions of people who know that evolutionary biology is valid, then you're just engaging in silly ad hominem. Tell ya what, son, you'd probably write me off as a "Darwinist religious fanatic" -- look over any or all of my hundreds of posts on evolutionary biology and see if you can support the charge that I'm "ignorant, dishonest, or both".
If not, and if you fail to retract your libel, then it should be clear that you yourself are being "ignorant, dishonest, or both".
Darwinism is a religious belief that has nothing to do with science.
Wow, you've never actually cracked open a science journal relating to biology, have you? I've read several thousand biology research papers, and evolutionary biology is very much "real science". Only someone incredibly ignorant (or, indeed, dishonest) could make the kinds of claims you make here, because they are very transparently not true.
Darwinists have adopted the beliefs of various groups and covered them with a pseudo scientific veneer.
What's "pseudoscientific" about, say, this for example? Be specific. Once you've warmed up on that, take a stab at these:
Accelerated Evolution of the ASPM Gene Controlling Brain Size Begins Prior to Human Brain ExpansionAbstract: Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume. The microcephalic brain has a volume comparable to that of early hominids, raising the possibility that some MCPH genes may have been evolutionary targets in the expansion of the cerebral cortex in mammals and especially primates. Mutations in ASPM, which encodes the human homologue of a fly protein essential for spindle function, are the most common known cause of MCPH. Here we have isolated large genomic clones containing the complete ASPM gene, including promoter regions and introns, from chimpanzee, gorilla, orangutan, and rhesus macaque by transformation-associated recombination cloning in yeast. We have sequenced these clones and show that whereas much of the sequence of ASPM is substantially conserved among primates, specific segments are subject to high Ka/Ks ratios (nonsynonymous/synonymous DNA changes) consistent with strong positive selection for evolutionary change. The ASPM gene sequence shows accelerated evolution in the African hominoid clade, and this precedes hominid brain expansion by several million years. Gorilla and human lineages show particularly accelerated evolution in the IQ domain of ASPM. Moreover, ASPM regions under positive selection in primates are also the most highly diverged regions between primates and nonprimate mammals. We report the first direct application of TAR cloning technology to the study of human evolution. Our data suggest that evolutionary selection of specific segments of the ASPM sequence strongly relates to differences in cerebral cortical size.Identification of paralogous HERV-K LTRs on human chromosomes 3, 4, 7 and 11 in regions containing clusters of olfactory receptor genesAbstract: A locus harboring a human endogenous retroviral LTR (long terminal repeat) was mapped on the short arm of human chromosome 7 (7p22), and its evolutionary history was investigated. Sequences of two human genome fragments that were homologous to the LTR-flanking sequences were found in human genome databases: (1) an LTR-containing DNA fragment from region 3p13 of the human genome, which includes clusters of olfactory receptor genes and pseudogenes; and (2) a fragment of region 21q22.1 lacking LTR sequences. PCR analysis demonstrated that LTRs with highly homologous flanking sequences could be found in the genomes of human, chimp, gorilla, and orangutan, but were absent from the genomes of gibbon and New World monkeys. A PCR assay with a primer set corresponding to the sequence from human Chr 3 allowed us to detect LTR-containing paralogous sequences on human chromosomes 3, 4, 7, and 11. The divergence times for the LTR-flanking sequences on chromosomes 3 and 7, and the paralogous sequence on chromosome 21, were evaluated and used to reconstruct the order of duplication events and retroviral insertions. (1) An initial duplication event that occurred 14-17 Mya and before LTR insertion - produced two loci, one corresponding to that located on Chr 21, while the second was the ancestor of the loci on chromosomes 3 and 7. (2) Insertion of the LTR (most probably as a provirus) into this ancestral locus took place 13 Mya. (3) Duplication of the LTR-containing ancestral locus occurred 11 Mya, forming the paralogous modern loci on Chr 3 and 7.Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter fluxAbstract: The enzyme glutamate dehydrogenase (GDH) is important for recycling the chief excitatory neurotransmitter, glutamate, during neurotransmission. Human GDH exists in housekeeping and brain-specific isotypes encoded by the genes GLUD1 and GLUD2, respectively. Here we show that GLUD2 originated by retroposition from GLUD1 in the hominoid ancestor less than 23 million years ago. The amino acid changes responsible for the unique brain-specific properties of the enzyme derived from GLUD2 occurred during a period of positive selection after the duplication event.A uniquely human consequence of domain-specific functional adaptation in a sialic acid–binding receptorAbstract: Most mammalian cell surfaces display two major sialic acids (Sias), N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc). Humans lack Neu5Gc due to a mutation in CMP-Neu5Ac hydroxylase, which occurred after evolutionary divergence from great apes. We describe an apparent consequence of human Neu5Gc loss: domain-specific functional adaptation of Siglec-9, a member of the family of sialic acid–binding receptors of innate immune cells designated the CD33-related Siglecs (CD33rSiglecs). Binding studies on recombinant human Siglec-9 show recognition of both Neu5Ac and Neu5Gc. In striking contrast, chimpanzee and gorilla Siglec-9 strongly prefer binding Neu5Gc. Simultaneous probing of multiple endogenous CD33rSiglecs on circulating blood cells of human, chimp, or gorilla suggests that the binding differences observed for Siglec-9 are representative of multiple CD33rSiglecs. We conclude that Neu5Ac-binding ability of at least some human CD33rSiglecs is a derived state selected for following loss of Neu5Gc in the hominid lineage. These data also indicate that endogenous Sias (rather than surface Sias of bacterial pathogens) are the functional ligands of CD33rSiglecs and suggest that the endogenous Sia landscape is the major factor directing evolution of CD33rSiglec binding specificity. Exon-1-encoded Sia-recognizing domains of human and ape Siglec-9 share only 93–95% amino acid identity. In contrast, the immediately adjacent intron and exon 2 have the 98–100% identity typically observed among these species. Together, our findings suggest ongoing adaptive evolution specific to the Sia-binding domain, possibly of an episodic nature. Such domain-specific divergences should also be considered in upcoming comparisons of human and chimpanzee genomes.Lineage-Specific Gene Duplication and Loss in Human and Great Ape EvolutionAbstract: Given that gene duplication is a major driving force of evolutionary change and the key mechanism underlying the emergence of new genes and biological processes, this study sought to use a novel genome-wide approach to identify genes that have undergone lineage-specific duplications or contractions among several hominoid lineages. Interspecies cDNA array-based comparative genomic hybridization was used to individually compare copy number variation for 39,711 cDNAs, representing 29,619 human genes, across five hominoid species, including human. We identified 1,005 genes, either as isolated genes or in clusters positionally biased toward rearrangement-prone genomic regions, that produced relative hybridization signals unique to one or more of the hominoid lineages. Measured as a function of the evolutionary age of each lineage, genes showing copy number expansions were most pronounced in human (134) and include a number of genes thought to be involved in the structure and function of the brain. This work represents, to our knowledge, the first genome-wide gene-based survey of gene duplication across hominoid species. The genes identified here likely represent a significant majority of the major gene copy number changes that have occurred over the past 15 million years of human and great ape evolution and are likely to underlie some of the key phenotypic characteristics that distinguish these species.Sequence Variation Within the Fragile X LocusAbstract: The human genome provides a reference sequence, which is a template for resequencing studies that aim to discover and interpret the record of common ancestry that exists in extant genomes. To understand the nature and pattern of variation and linkage disequilibrium comprising this history, we present a study of ~31 kb spanning an ~70 kb region of FMR1, sequenced in a sample of 20 humans (worldwide sample) and four great apes (chimp, bonobo, and gorilla). Twenty-five polymorphic sites and two insertion/deletions, distributed in 11 unique haplotypes, were identified among humans. Africans are the only geographic group that do not share any haplotypes with other groups. Parsimony analysis reveals two main clades and suggests that the four major human geographic groups are distributed throughout the phylogenetic tree and within each major clade. An African sample appears to be most closely related to the common ancestor shared with the three other geographic groups. Nucleotide diversity, [pi], for this sample is 2.63 ± 6.28 × 10-4. The mutation rate, [mu], is 6.48 × 10-10 per base pair per year, giving an ancestral population size of ~6200 and a time to the most recent common ancestor of ~320,000 ± 72,000 per base pair per year. Linkage disequilibrium (LD) at the FMR1 locus, evaluated by conventional LD analysis and by the length of segment shared between any two chromosomes, is extensive across the region.Structural and evolutionary analysis of the two chimpanzee alpha-globin mRNAsAbstract: Two distinct alpha-globin mRNAs were detected in chimpanzee reticulocyte mRNA using a primer extension assay. DNA copies of these two mRNAs were cloned in the bacterial plasmid pBR322, and their sequence was determined. The two alpha-globin mRNAs have obvious structural homology to the two human alpha-globin mRNAs, alpha 1 and alpha 2. Comparison of the two chimpanzee alpha-globin mRNAs to each other and to their corresponding human counterparts revealed evidence of a recent gene conversion in the human alpha-globin complex and a marked heterogeneity in the rate of structural divergence within the alpha-globin gene.Differential Alu Mobilization and Polymorphism Among the Human and Chimpanzee LineagesAbstract: Alu elements are primate-specific members of the SINE (short interspersed element) retroposon family, which compriseAdaptive Evolution of MRG, a Neuron-Specific Gene Family Implicated in Nociception10% of the human genome. Here we report the first chromosomal-level comparison examining the Alu retroposition dynamics following the divergence of humans and chimpanzees. We find a twofold increase in Alu insertions in humans in comparison to the common chimpanzee (Pan troglodytes). The genomic diversity (polymorphism for presence or absence of the Alu insertion) associated with these inserts indicates that, analogous to recent nucleotide diversity studies, the level of chimpanzee Alu diversity is
Abstract: The MRG gene family (also known as SNSR) belongs to the G-protein-coupled receptor (GPCR) superfamily, is expressed specifically in nociceptive neurons, and is implicated in the modulation of nociception. Here, we show that Ka/Ks (the ratio between nonsynonymous and synonymous substitution rates) displays distinct profiles along the coding regions of MRG, with peaks (Ka/Ks > 1) corresponding to extracellular domains, and valleys (Ka/Ks < 1) corresponding to transmembrane and cytoplasmic domains. The extracellular domains are also characterized by a significant excess of radical amino acid changes. Statistical analysis shows that positive selection is by far the most suitable model to account for the nucleotide substitution patterns in MRG. Together, these results demonstrate that the extracellular domains of the MRG receptor family, which presumably partake in ligand binding, have experienced strong positive selection. Such selection is likely directed at altering the sensitivity and/or selectivity of nociceptive neurons to aversive stimuli. Thus, our finding suggests pain perception as an aspect of the nervous system that may have experienced a surprising level of adaptive evolution.
The idea that current species once looked different comes from various North American beliefs.
No, it comes from the overwhelming evidence.
The idea of humans being descended from monkeys/apes comes from ancient Tibetan beliefs.
No, it comes from the fossil evidence and the DNA evidence, which exists in massive abundance and cross-validates along multiple independent lines.
The Darwinist belief that all life has a common origin is pure religion and is scientifically impossible if life developed without the aid of some Intelligence.
Nonsense. It's clear in the DNA and biochemistry for anyone who chars to look.
A "natural" process would have been able to produce many different life forms from scratch independently from each over a long period of time.
Probably not, actually. Once the original life forms reached a moderately advanced stage, any further "life from scratch" events wouldn't have a chance -- they'd get eaten by the life that had already gotten a head start, most likely.
Furthermore, when life first appeared on Earth, there was no oxygen in the atmosphere. After a while, the new life produced enough oxygen to change the atmosphere significantly. This may well have altered the Earth in a way that forever removed the chemical conditions which allowed life to form from scratch again. It's well known that the earliest unicellular life on Earth was oxygen-intolerant.
You really need to think things through more before you try to pontificate upon them. These topics have been covered at length in the science journals -- try reading a few for a change.
The life forms observed after mass extinctions could have developed from scratch as new species if life developed "naturally".
Probably not -- see above.
Most Darwinists seem incapable of understanding what Intelligent Design means.
Actually, they understand it better than most of the IDers.
Critique of “Intelligent Design” (ID)
I.D. looks at biological life and recognizes that the only physical systems that are comparable to biological organisms in terms of structure and regularity of operation are the machines constructed by human beings, generally considered to be intelligent beings.
For a really good critique of what's wrong with that line of reasoning, see:
The advantages of theft over toil: the design inference and arguing from ignorance
The biological cell is a biochemical computer with molecular memory that is organized in a manner that can be expressed as "0's" and "1's".
No, actually, it isn't. I know computers, and I know biology, and they are very much *not* alike.
Here's what I wrote in reply to a prior example of the same kind of argument:
In general, the fact of reuse of large amounts of genetic material is nothing more than something "consistant with" an evolutionary historical hypothesis, and in no way proves it or makes it scientific. It is just another level of the forensic-type science where, when we do a DNA test and find results much different than expected, it doesn't change in any way the "theory of evolution", but has a large effect on the historical evolution hypothesis.
You're missing the point -- although we're occasionally surprised by the DNA implications for a particular evolutionary history (i.e., which species diverged from which ancestors when), we have not yet *ever* been surprised by finding a genetic difference between species which was *not* entirely compatible with evolutionary origins. And we *would* very quickly and very obviously find such discordance between the contents of the DNA and evolutionary theory if, in fact, the DNA of modern living things was *not* the result of evolutionary processes.
It's nothing as simple as just "reuse of large amounts of genetic material" which provides support for evolution, it's the very specific *kinds* and exact *patterns* of DNA which support an evolutionary origin to the exclusion of alternative hypotheses (except for the ad hoc one which postulates that some designer *purposely* crafted our DNA in order to *fake* an evolutionary origin).
[...]
This is analogous to computer programming. If you look at a lot of computer programs, you will find common code. This does not suggest that one program "evolved" into another, or even that one programmer extended the one program into the other. It could be that the same programmer wrote both, or that somebody wrote a snippet of code and published it and others used it. It is not predictive to determining the history of a piece of code. It is also common in looking at code to find that two programs which have the same function don't use the same code, even if they are written by the same programmer.
That's a common argument, but it doesn't stand up to close examination. I've written thousands of computer programs, *and* produced code via genetic algorithms (aka "evolutionary computing"). No one could possibly mistake the one type of program for the other. The results are vastly different in form and character, and each contains features which clearly distinguish it from the other.
Similarly, the evolutionary character of DNA is clear and distinctive. The hallmarks of evolution go far beyond mere "reuse of code". For example, it contains features that no sane designer would ever use (such as silent codon differences which vary in exact evolutionary patterns -- it's as if you, as a programmer, randomly changed characters in the variable names in source used in common between all your programs, while having no effect on the compiled code, *and* did it in a way that falsely implied an evolutionary relationship between all the programs you wrote...) Furthermore, a designer has *vastly* more design options to him than *just* the ones which could result from evolutionary processes, and yet "oddly" enough, such structures are not found in DNA -- if there's a designer, why would he restrict himself in that way? *I* certainly don't write my programs in only those ways that could have been produced by genetic algorithms...