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PEER REVIEWED AlanCFAs idea of evidence for evolution (Read 39783 times)
GoodScienceForYou
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Re: AlanCFAs idea of evidence for evolution
Reply #30 - Mar 12th, 2011 at 7:22pm
 
"Children receive far less genetic mutations from their parents that it was previously believed, a new study suggests.

Scientists at the Seattle-based Institute for Systems Biology, the University of Utah and the University of Washington studied the entire family genome and found that each parent passes around 30 gene mutations to their children. Previously, scientists thought that children receive as much as 75 gene mutations from each parent, while the actual mutations rate is less than a half.

Scientists say that in most cases, genetic mutations do not affect child's health. The real number of gene mutations will also vary depending on the age of the parents. Father's age at conception plays a significant role in how many gene mutations will be passed. The risk of genetic disorders increases as father's age rises.

The study was published in the March 11 issue of Science Express."

Here is the problem with this use of the word "mutations".
Parents cannot pass on mutations.  Repeat that 100 times until you get it.  They pass on genetic information.
The mother has all her eggs at the time of birth.  Do you know that. This is common genetic knowledge. That means the eggs are fully made before the mother can screw them up. This is by design and to protect the progeny from the mothers mistakes.
This is one of the main reasons why sonomic mutations are made to take place separate from the genetic mutations. Thus reducing the chances of passing on the mistakes of the parents.
If 70% of all mutations are bad, then these 75 mutations  cannot be random, otherwise the child would never be born alive.  UNDERSTAND?
70% bad mutations  out of 75 = 52 random bad mutations.

Because the child lives and is healthy, these ARE NOT MUTATIONS.  They are genetic information from the parents genealogy.  These are programmed from the ancestors of the parents and now show up.

This means that part of the genetic information stored in the genome is not known to genetic scientists.  There are 3.2 billion base pairs, but only 25,000 or so that are active.  The other are there as, an unknown factor that no scientist has any clue about until they see some "action" from them.

I think we have a whole level of genetic coding that is unknown to "scientists" contained in the 3 plus billion unknown base pairs. 

So if a child is born healthy and has "different" gene coding they are not mutations, but are information contained in the parents genetics from ancestors.  This mixing is also part of what make people utterly unique.

Get this...There are no two people ever exactly alike. Not ever in all the time people have been reproducing.  They may have similarity, but never exact clones.
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Re: AlanCFAs idea of evidence for evolution PEER Papers.
Reply #31 - Apr 7th, 2011 at 3:05am
 
http://www.ncbi.nlm.nih.gov/pubmed/14525925

Gene loss, protein sequence divergence, gene dispensability, expression level, and interactivity are correlated in eukaryotic evolution.
Krylov DM, Wolf YI, Rogozin IB, Koonin EV.

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20894, USA.
Abstract
Lineage-specific gene loss, to a large extent, accounts for the differences in gene repertoires between genomes, particularly among eukaryotes. We derived a parsimonious scenario of gene losses for eukaryotic orthologous groups (KOGs) from seven complete eukaryotic genomes. The scenario involves substantial gene loss in fungi, nematodes, and insects. Based on this evolutionary scenario and estimates of the divergence times between major eukaryotic phyla, we introduce a numerical measure, the propensity for gene loss (PGL). We explore the connection among the propensity of a gene to be lost in evolution (PGL value), protein sequence divergence, the effect of gene knockout on fitness, the number of protein-protein interactions, and expression level for the genes in KOGs. Significant correlations between PGL and each of these variables were detected. Genes that have a lower propensity to be lost in eukaryotic evolution accumulate fewer substitutions in their protein sequences and tend to be essential for the organism viability, tend to be highly expressed, and have many interaction partners. The dependence between PGL and gene dispensability and interactivity is much stronger than that for sequence evolution rate. Thus, propensity of a gene to be lost during evolution seems to be a direct reflection of its biological importance.
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #32 - Apr 7th, 2011 at 11:09am
 
Here we see the premise is to show evolution but the results show gene loss or stability.  The "revolving door" is the same thing repeating or gene loss only.
The wording is done in such a vague way as to mask the results, so read it carefully and it is clear that noting is supporting evolution. See the highlighted text.
http://www.ncbi.nlm.nih.gov/pubmed/21466698

"Expansion and functional diversification of a leucyl aminopeptidase family that encodes the major protein constituents of Drosophila sperm.
Dorus S, Wilkin EC, Karr TL.

Abstract
ABSTRACT:

BACKGROUND: The evolutionary diversification of gene families through gene creation (and loss) is a dynamic process believed to be critical to the evolution of functional novelty. Previous identification of a closely related family of eight annotated metalloprotease genes of the M17 Merops family in the Drosophila sperm proteome (termed, Sperm-LeucylAminoPeptidases, S-LAPs 1-8) led us to hypothesize that this gene family may have experienced such a diversification during insect evolution.

RESULTS: To assess putative functional activities of S-LAPs, we (i) demonstrated that all S-LAPs are specifically expressed in the testis, (ii) confirmed their presence in sperm by two-dimensional gel electrophoresis and mass spectrometry, (iii) determined that they represent a major portion of the total protein in sperm and (iv) identified aminopeptidase enzymatic activity in sperm extracts using LAP-specific substrates. Functionally significant divergence at the canonical M17 active site indicates that the largest phylogenetic group of S-LAPs lost catalytic activity and likely acquired novel, as yet undetermined, functions in sperm prior to the expansion of the gene family.

CONCLUSIONS: Comparative genomic and phylogenetic analyses revealed the dramatic expansion of the S-LAP gene family during Drosophila evolution and copy number heterogeneity in the genomes of related insects. This finding, in conjunction with the loss of catalytic activity and potential neofunctionalization amongst some family members, extends empirical support for pervasive "revolving door" turnover in the evolution of reproductive gene family composition and function."
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #33 - Apr 7th, 2011 at 3:03pm
 
Every single scientific paper written on DNA only shows de-evolution.  The use irrefutable, absolute evidence, that is physical and represents the defects which are shown to permeate throughout human kind and all multi cellular creatures.

This completely negates all the old religious BS of Evotards, forcing religious ideas of creatures evolving from some simpler life form and eventually become some complex creatures.

Please note If evolution were true, there would be no defects and no retardation no gene losses. There would only be fixes that continue to make things better.  YOu cannot have it both ways.  Either creatures "magically fix" and "mangically improve" or they don't.

Since we have ZERO
DNA
evidence of any net positive evolution towards more fit, more complex more intelligent, guess what?

Evolution is a pile or religious nonsense.  That is the conclusion, and it is verified in every single DNA study.
The conclusions of these poor believers is crap, because the evidence does not fit with any form of evolution.

You have to look at only the evidence and realize what is going on and forget this word "evolution" it is not even related to any creature on this earth.

Degradation is the real word. When you see one of these articles, just put in "genetic degradation" in place of "evolution" and you will see the truth of the matter, pretty clear.

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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #34 - Apr 23rd, 2011 at 12:48am
 
MORE DE-EVOLVED humoids found:
(This crap dating system has to go.)

22 April 2011
Another missing link in human evolution?
Skeletons of Australopithecus sediba display a unusual mix of modern and primitive traits - sharing more features with early Homo specimens than any other known Australopithecus species, according to Darryl de Ruiter of Texas A&M University in College Station, USA.
     Researchers found the remains of at least four individuals - a youth, an older female, an 18-month-old infant and at least one other adult - who died when they fell into a 'death trap' in a cave about 2 million years ago at Malapa (South Africa).
     These particular individuals could not be ancestors of Homo because members of our genus were already living at the time when they fell into the pit. But, says Lee Berger of the University of the Witwatersrand in Johannesburg (South Africa), they might be late members of the australopithecine species that earlier gave rise to Homo, or a close relative that could shed light on that crucial ancestor.
     Anthropologists have long wondered which of several species of Australopithecus gave rise to the first members of our genus - with Lucy's north African species,  Australopithecus afarensis, as the leading candidate - and evidence is accumulating that the South African species formed an evolutionary connection between relatively apelike members of Australopithecus, and the Homo genus, which includes living people.
     Much uncertainty surrounds the identity of fossil members of the human evolutionary family between 3 million and 2 million years ago, says John Hawks of the University of Wisconsin, Madison (USA).

Edited from ScienceNews (18 April 2011), Science (19 April 2011), PhysOrg (20 April 2011)
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #35 - Apr 23rd, 2011 at 12:53am
 
This is a fine example of people trying, scrambling to avoid the obvious:  These are degenerated humans
It is clear as can be.

=============================================

MINNEAPOLIS, MINNESOTA—Finding one partial skeleton of an ancient member of the human family is the rarest of rare discoveries in human evolution. So, paleoanthropologists murmured in surprise at a meeting here Saturday when South African researchers announced that they had found at least four individuals of a new species of early human, Australopithecus sediba. The discoverers say that this hominin shows some surprisingly modern traits and its species may even be an ancestor of our own genus. “We really have found something very, very odd and very unexpected,” says discovery team leader Lee Berger of the University of the Witwatersrand in Johannesburg, South Africa. But other paleoanthropologists are waiting for more detailed analysis of the still-unpublished fossils before they agree on its identity or place in the human family tree.

The four hominin individuals died when they fell into a “death trap” in a cave about 2 million years ago at Malapa, South Africa, according to new dates reported by Berger in his talk at the annual meeting of the American Association of Physical Anthropologists (AAPA). In addition to the articulated partial skeletons of a youth and an older female unveiled last year in Science, the team members reported the discovery of bones of an 18-month-old infant and at least one other adult. This means they are getting a good look at Au. sediba’s development from infancy to old age. “It is going to be a remarkable record,” Berger said. “And we still haven’t found everything!”

In talks at AAPA and the annual meeting of the Paleoanthropology Society last week, Berger and members of his team sketched a quick portrait of Au. sediba, who lived at the mysterious time right after the emergence of our genus Homo between 2 million to 3 million years ago. Researchers have long wondered which of several species of Australopithecus gave rise to the first members of our genus, with Lucy’s species Au. afarensis as the leading candidate.

The trove of well-preserved bones includes clavicles, shoulder blades, and ribs as well as a complete skull, hand, foot, and two pelvises. The researchers called it an australopithecine—extinct members of the human family that lived 1 million to 4 million years ago in Africa—because it had a small brain the size of an ape's, and its “overall body plan” was like that of an australopithecine, team member Darryl de Ruiter of Texas A&M University in College Station said in a talk. It had long arms and a primitive thorax and heel like an ape, for example.

But the fossils also show some surprisingly modern traits usually found only in members of our own genus, Berger said. Two pelvises, in particular, are capacious and elongated in a way that looks quite Homo-like. In his talk on the fossils, Berger ticked off a list of other traits that were modern, including smaller teeth, short fingers, and an elongated thumb.

In a separate talk at the Paleoanthropology Society, Kristian Carlson of Indiana University, Bloomington, described the endocast, the impression left inside the skull by the brain. He said that the outer surface of the brain suggests that the forebrain, the uppermost part of the brain that extends from the forehead to the base of the skull, might be reorganized in a modern way. If so, Au. sediba’s brain and pelvis would have both begun to evolve into more modern shapes before the brain expanded—countering the view that the expanding brain drove the remodeling of the pelvis to accommodate bigger-brained babies.

These particular individuals could not be ancestors of Homo because members of our genus were already living at the time when these hominins fell into the pit at Malapa. But, Berger says, they might be late members of the australopithecine species that gave rise to Homo earlier, or a close relative that could shed light on that crucial ancestor.

Other researchers, who were able to examine casts of the fossils at the meeting, agreed that on first glance the fossils represent an unusual mix of primitive and more modern traits. But most thought it important to compare Au. sediba directly with other fossils of early Homo and Australopithecus in more detail before placing them on our family tree. “The pelvis does look more modern,” says paleoanthropologist Christopher Ruff of Johns Hopkins University in Baltimore, Maryland. “But that doesn’t mean it looks exactly like a modern human’s or that it gave rise to early Homo.”

Yet even if Au. sediba is an evolutionary dead end, William Kimbel of Arizona State University in Tempe says, “It does still shed light on the evolution of early Homo because we know nothing about the time period 1/2 million to 3/4 million years before Au. sediba.”
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #36 - Apr 23rd, 2011 at 11:43pm
 
There is ONLY shown in DNA evidence a constant degradation to all genomes or some semblance of stability and nothing else.
There are between 7000 to estimated 15000 genetic diseases in the human tribe.  Here is a good quote for you:

"With this array of human diseases that are caused by mutations, what of positive effects? With thousands of examples of harmful mutations readily available, surely it should be possible to describe some positive mutations if macroevolution is true.

These would be needed not only for evolution to greater complexity, but also to offset the downward pull of the many harmful mutations. But, when it comes to identifying positive mutations, evolutionary scientists are strangely silent."

These religious believers will resort back to the fossils and fantasy of belief. When DNA is absolutely irrefutable physical evidence against all this human garbage religion of Evodelusionism.  You would think that humans are smarter than that?  But they are not.  Human stupidness has no limits. 

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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #37 - Sep 3rd, 2011 at 5:29am
 
Now go listen to my video on DNA Mutations and understand that the only pathway we have is gene loss, if we don't work towards fixing and removing all the mutagens we have now. Humans are degrading faster than ever.
GoodScienceForYou 2 weeks ago 3
Pathoadaptive mutations: gene loss
and variation in bacterial pathogens
google it
GoodScienceForYou 2 weeks ago 3
Gene Loss and Movement in the Maize Genome
Google it.
GoodScienceForYou 2 weeks ago 2
Comparative Genomics of Brassica oleracea and Arabidopsis thaliana Reveal Gene Loss, Fragmentation, and Dispersal after Polyploidy
Google it.
GoodScienceForYou 2 weeks ago 2
Gene Loss and Evolutionary Rates Following Whole-Genome Duplication in Teleost Fishes
Google it.
GoodScienceForYou 2 weeks ago
Loss of alleles of loci on the short arm of chromosome 3 in renal cell carcinoma
Google it.
GoodScienceForYou 2 weeks ago
For about 150 years people have been making this Evodelusion religion to be real. In the mean time we found DNA. DNA is the only real evidence we have, and it only shows genetic degradation of all multicellular creatures.
GoodScienceForYou 2 weeks ago
Evolution of mitochondrial gene content: gene loss and transfer to the nucleus
Google it.
GoodScienceForYou 2 weeks ago
When less is more: gene loss as an engine of evolutionary change.
Google it.
This is funny. Gene loss means less able to adapt, less fit, and the environment and foods are far more restricted,
GoodScienceForYou 2 weeks ago
Gene Loss, Protein Sequence Divergence, Gene Dispensability, Expression Level, and Interactivity Are Correlated in Eukaryotic Evolution
Google it.
GoodScienceForYou 2 weeks ago
Up-regulation of hypoxia-inducible factors HIF-1α and HIF-2α under normoxic conditions in renal carcinoma cells by von Hippel-Lindau tumor suppressor gene loss of function
Google it.
GoodScienceForYou 2 weeks ago
EST Analysis of the Cnidarian Acropora millepora Reveals Extensive Gene Loss and Rapid Sequence Divergence in the Model Invertebrates
Google it.
GoodScienceForYou 2 weeks ago
Multiple rounds of speciation associated with reciprocal gene loss in polyploid yeasts.
Google it.
GoodScienceForYou 2 weeks ago
Genetics of gene expression surveyed in maize, mouse and man
Google it.
GoodScienceForYou 2 weeks ago
Dissecting Arabidopsis thaliana DICER function in
small RNA processing, gene silencing and DNA
methylation patterning
Google it.
GoodScienceForYou 2 weeks ago
A role for methylation of the hMLH1 promoter in loss of hMLH1 expression and drug resistance in ovarian cancer.
google it.
GoodScienceForYou 2 weeks ago
S. cerevisiae genes required for cell cycle arrest in response to loss of microtubule function
There are over 88,000 peer reviewed articles on gene loss alone.
GoodScienceForYou 2 weeks ago
Identification of rare DNA variants in mitochondrial disorders with improved array-based sequencing
Google it.
Do independent research and understand what is going on.
GoodScienceForYou 2 weeks ago
A System of Shuttle Vectors and Yeast Host Strains Designed for Efficient Manipulation of DNA in Saccharomyces cerevisiae
google it.
GoodScienceForYou 2 weeks ago
Loss of genomic methylation causes p53-dependent apoptosis and epigenetic deregulation
Google it.
GoodScienceForYou 2 weeks ago
Comparable Rates of Gene Loss and Functional Divergence After Genome Duplications Early in Vertebrate Evolution
google it.
GoodScienceForYou 2 weeks ago
There is only gene loss, atrophy, genetic weakness, in any form of mutation as a result.
GoodScienceForYou 2 weeks ago
Loss of the wild type MLH1 gene is a feature of hereditary nonpolyposis colorectal cancer
Google it.
GoodScienceForYou 2 weeks ago
Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
Google it.
GoodScienceForYou 2 weeks ago
Respiratory deficiency due to loss of mitochondrial DNA in yeast lacking the frataxin homologue
Google it.
GoodScienceForYou 2 weeks ago
Genetics 1651.short
google it.
GoodScienceForYou 2 weeks ago
Silencing of the VHL tumor-suppressor gene by DNA methylation in renal carcinoma 9700.short
google it
GoodScienceForYou 2 weeks ago
S016895259901971X
Google it
GoodScienceForYou 2 weeks ago
SmithFJDetal.1743.pdf
Google it
GoodScienceForYou 2 weeks ago
it's funny because there is no difference between micro and macro evolution. Scientists don't recognize separate terms for the two. Creationists want to say that micro evolution can happen but macro not? That's wrong, because basically macro evolution, is micro evolution happening 1,000,000 times to produce something totally different.
Sanquinity 2 weeks ago
@Sanquinity The reality is that what is produced is reduced in fitness from the ancestor. There is only genetic degradation shown in absolutely irrefutable DNA evidence. In all cases multicellular creatures lose gene, have less fit genes, and have just plain genetic diseases as time go on.
Evolution is not science.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou Um, wrong. Mutations is not the same thing as traits. Though mutations can become traits over time. Traits are the things that set us apart. Hair colour, eye colour, skin colour, ect. Mutations would be babies born without a limb, with a bulge not supposed to be there on their body, act. Traits is what evolution is about, mutations is something different. Still, some rare mutations can be a good thing.
Sanquinity 2 weeks ago
@Sanquinity You are a fool. There is only genetic loss, and de-evolution shown in all complex creatures. They lose features and become less and less able to adapt. Then extinction is the norm. Study real science and real genetics. Evolution is nonsense.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou No, YOU study real science and real genetics. We, as a species of ape (not monkey) are the evidence of evolution, f**kING WORKING. You just ignore the scientific facts and only see what you want to see.
Sanquinity 2 weeks ago
@Sanquinity you are a fool. I pity people so gullible as to believe the religious nonsense of Evotards.
Humans and Apes are de-evolved from a far superior creature.
GoodScienceForYou 2 weeks ago
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AlanCFA 2 days ago
@Sanquinity You are a brainwashed fool. Did anybody ever tell you that getting all your information from the people who indoctrinated you is a cult.
If you want to learn about humanity you need to get away from them and study humanity and all their nonsense from a distance. Emotional controls of society are horrible things.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou If I was even indoctrinated, it was by Christians. I was raised a Christian, then at age 15, now 9 years ago, I started to think for myself and research/explore for myself. I was never indoctrinated in the ways of evolution, I came to my own conclusions. And I have yet to see proper evidence that goes against it.
Sanquinity 2 weeks ago
@Sanquinity Yea! Right! and at your age you are full of wisdom. garbage, I'll bet you can't even wipe your ass correctly. There is no evidence for evolution. The ONLY real evidence we have is DNA. And DNA only shows gene loss with speciation. If you were to look you will see the same thing.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou Right, and you as a...non-evolutionist know so much better than the scientists that have spent years upon years of study, research, tests and god knows what else to get to their conclusion. What do you have? Some obscure sites that try (only TRY) to disprove evolution, but don't have any actual evidence? I'd rather believe in the scientists than in you, thank you very much.
Sanquinity 2 weeks ago
@Sanquinity I am a scientist. I have been studying this for over 43 years and have read over 27,000 peer papers on this. The only thing shown is reduction in fitness. Humans now have over 4500 genetic diseases from "evolution". The experts can only show me 4 positive mutations. That is 1100 to 1 for genetic degradation only.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou You're a scientist...right, sorry if I don't believe someone over the internet, posting in a youtube comment section, saying they're a scientist.
Sanquinity 2 weeks ago
@Sanquinity Why would you believe some moron with a PHD? I want you to wake up about human folly. People believe in Evolution because they don't want the truth that they are destroying their species, by what they do.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou "Why would you believe some moron with a PHD?" You keep claiming that a psychologist with a PhD tested your IQ and you expect that to lend credibility to your ludicrous claim. I don't believe your story, but if it were true, that would be one PhD. The theory of evolution is supported by nearly every biologist with a PhD - only a few YECs like you deny the theory.
AlanCFA 2 days ago
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GoodScienceForYou 1 day ago
@Sanquinity I have to go to bed now. I live in Holland.
GoodScienceForYou 2 weeks ago
@GoodScienceForYou I live in the netherlands too. And hey, I agree that we are de-evolving right now. We're making our own species weaker by allowing all kinds of people procreate that are degrading to our species. Retards, people with mutations, just plain stupid people, gullible people, people with inherit genetic defects, you name it. They're all allowed to procreate, which makes our species weaker. But evolution as a whole, works.
Sanquinity 2 weeks ago
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GoodScienceForYou 2 weeks ago
@GSFY "I am a scientist." That is a lie. You sell hot tubs.
"I have been studying this for over 43 years and have read over 27,000 peer papers on this" More lies. You do not even know the basic principles of science or the theory of evolution. You claimed two years ago to have read 20,000 papers, then 200,000 with 20,000 "in-depth". You've been asked what SPECIFIC items you disagreed with in published papers and NEVER replied with anything. You can't remember with your photographic memory?
AlanCFA 2 days ago
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@AlanCFA The evidence is overwhelming showing only genetic degradation. The papers you pointed out only show opinions. When DNA is the only source of absolutely irrefutable physical evidence, then all the other evidence must be looked at and it must fit the DNA. It does when you stop believing in fairy tales. There are no organic structures that can fix themselves and make their genome better after a mutation has taken away good cell replication and replaced it with "sick" or weak cells.
GoodScienceForYou 1 day ago
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@AlanCFA I told you before the only evidence that counts is physical, obvious, having no opinions in it. Opinions are like asses, everybody has one and they don't put out anything but human waste.
You don't understand what absolutely irrefutable physical evidence is. In all cases the genomes do not improve become more complex no do they gain in fitness for any environment. Speciation causes genetic losses.
GoodScienceForYou 1 day ago 2
@Sanquinity I don't have any beliefs. I only go with the evidence. We have only had DNA for about 30 years and it wasn't until the last 10 that they have done much with it. DNA is the only irrefutable, physical, evidence we have, and it only shows genetic losses and genetic degradation less fitness, less able to adapt and then extinction if the degradation is not stopped.
GoodScienceForYou 2 weeks ago
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AlanCFA 2 days ago
@GoodScienceForYou "There is no evidence for evolution" Liar
"The ONLY real evidence we have is DNA.
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #38 - Nov 1st, 2012 at 1:14am
 
Human amniotic fluid stem cells as a model for functional studies of genes involved in human genetic diseases or oncogenesis
Margit Rosner, Helmut Dolznig, Katharina Schipany, Mario Mikula, Oliver Brandau, Markus Hengstschläger
Oncotarget. 2011 September; 2(9): 705–712. Published online 2011 September 14.
PMCID: PMC3248217
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #39 - Nov 1st, 2012 at 1:18am
 
http://www.plosgenetics.org/article/info%3Adoi/10.1371/journal.pgen.1002607

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits: A Multi-Ethnic Meta-Analysis of 45,891 Individuals
Zari Dastani, Marie-France Hivert, Nicholas Timpson, John R. B. Perry, Xin Yuan, Robert A. Scott, Peter Henneman, Iris M. Heid, Jorge R. Kizer, Leo-Pekka Lyytikäinen, Christian Fuchsberger, Toshiko Tanaka, Andrew P. Morris, Kerrin Small, Aaron Isaacs, Marian Beekman, Stefan Coassin, Kurt Lohman, Lu Qi, Stavroula Kanoni, James S. Pankow, Hae-Won Uh, Ying Wu, Aurelian Bidulescu, Laura J. Rasmussen-Torvik, Celia M. T. Greenwood, Martin Ladouceur, Jonna Grimsby, Alisa K. Manning, Ching-Ti Liu, Jaspal Kooner, Vincent E. Mooser, Peter Vollenweider, Karen A. Kapur, John Chambers, Nicholas J. Wareham, Claudia Langenberg, Rune Frants, Ko Willems-vanDijk, Ben A. Oostra, Sara M. Willems, Claudia Lamina, Thomas W. Winkler, Bruce M. Psaty, Russell P. Tracy, Jennifer Brody, Ida Chen, Jorma Viikari, Mika Kähönen, Peter P. Pramstaller, David M. Evans, Beate St. Pourcain, Naveed Sattar, Andrew R. Wood, Stefania Bandinelli, Olga D. Carlson, Josephine M. Egan, Stefan Böhringer, Diana van Heemst, Lyudmyla Kedenko, Kati Kristiansson, Marja-Liisa Nuotio, Britt-Marie Loo, Tamara Harris, Melissa Garcia, Alka Kanaya, Margot Haun, Norman Klopp, H.-Erich Wichmann, Panos Deloukas, Efi Katsareli, David J. Couper, Bruce B. Duncan, Margreet Kloppenburg, Linda S. Adair, Judith B. Borja, DIAGRAM+ Consortium, MAGIC Consortium, GLGC Investigators, MuTHER Consortium, James G. Wilson, Solomon Musani, Xiuqing Guo, Toby Johnson, Robert Semple, Tanya M. Teslovich, Matthew A. Allison, Susan Redline, Sarah G. Buxbaum, Karen L. Mohlke, Ingrid Meulenbelt, Christie M. Ballantyne, George V. Dedoussis, Frank B. Hu, Yongmei Liu, Bernhard Paulweber, Timothy D. Spector, P. Eline Slagboom, Luigi Ferrucci, Antti Jula, Markus Perola, Olli Raitakari, Jose C. Florez, Veikko Salomaa, Johan G. Eriksson, Timothy M. Frayling, Andrew A. Hicks, Terho Lehtimäki, George Davey Smith, David S. Siscovick, Florian Kronenberg, Cornelia van Duijn, Ruth J. F. Loos, Dawn M. Waterworth, James B. Meigs, Josee Dupuis, J. Brent Richards
PLoS Genet. 2012 March; 8(3): e1002607. Published online 2012 March 29. doi: 10.1371/journal.pgen.1002607
PMCID: PMC3315470

Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P=4.5×10−8–1.2×10−43). Using a novel method to combine data across ethnicities (N=4,232 African Americans, N=1,776 Asians, and N=29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (p<3×10−4). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D (p=4.3×10−3, n=22,044), increased triglycerides (p=2.6×10−14, n=93,440), increased waist-to-hip ratio (p=1.8×10−5, n=77,167), increased glucose two hours post oral glucose tolerance testing (p=4.4×10−3, n=15,234), increased fasting insulin (p=0.015, n=48,238), but with lower in HDL-cholesterol concentrations (p=4.5×10−13, n=96,748) and decreased BMI (p=1.4×10−4, n=121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance.
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #40 - Nov 1st, 2012 at 2:01am
 
Am J Hum Genet. 2010 June 11; 86(6): 904–917.
doi:  10.1016/j.ajhg.2010.05.005
PMCID: PMC3032075
Principal-Component Analysis for Assessment of Population Stratification in Mitochondrial Medical Genetics

Alessandro Biffi,1,2,3,9 Christopher D. Anderson,1,2,3,9 Michael A. Nalls,4,9 Rosanna Rahman,1,2,3 Akshata Sonni,1,2,3 Lynelle Cortellini,1,2,3 Natalia S. Rost,1,2,3 Mar Matarin,4,5 Dena G. Hernandez,4,6 Anna Plourde,1,2,3 Paul I.W. de Bakker,3,7 Owen A. Ross,8 Steven M. Greenberg,2 Karen L. Furie,2 James F. Meschia,8 Andrew B. Singleton,4 Richa Saxena,1,3 and Jonathan Rosand1,2,3,
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Abstract
Although inherited mitochondrial genetic variation can cause human disease, no validated methods exist for control of confounding due to mitochondrial population stratification (PS). We sought to identify a reliable method for PS assessment in mitochondrial medical genetics. We analyzed mitochondrial SNP data from 1513 European American individuals concomitantly genotyped with the use of a previously validated panel of 144 mitochondrial markers as well as the Affymetrix 6.0 (n = 432), Illumina 610-Quad (n = 458), or Illumina 660 (n = 623) platforms. Additional analyses were performed in 938 participants in the Human Genome Diversity Panel (HGDP) (Illumina 650). We compared the following methods for controlling for PS: haplogroup-stratified analyses, mitochondrial principal-component analysis (PCA), and combined autosomal-mitochondrial PCA. We computed mitochondrial genomic inflation factors (mtGIFs) and test statistics for simulated case-control and continuous phenotypes (10,000 simulations each) with varying degrees of correlation with mitochondrial ancestry. Results were then compared across adjustment methods. We also calculated power for discovery of true associations under each method, using a simulation approach. Mitochondrial PCA recapitulated haplogroup information, but haplogroup-stratified analyses were inferior to mitochondrial PCA in controlling for PS. Correlation between nuclear and mitochondrial principal components (PCs) was very limited. Adjustment for nuclear PCs had no effect on mitochondrial analysis of simulated phenotypes. Mitochondrial PCA performed with the use of data from commercially available genome-wide arrays correlated strongly with PCA performed with the use of an exhaustive mitochondrial marker panel. Finally, we demonstrate, through simulation, no loss in power for detection of true associations with the use of mitochondrial PCA.
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #41 - Nov 1st, 2012 at 2:02am
 
Report on the 6th African Society of Human Genetics (AfSHG) Meeting, March 12–15, 2009, Yaoundé, Cameroon
Giorgio Sirugo, Scott M. Williams, Charmaine D. M. Royal, Melanie J. Newport, Branwen J. Hennig, Renato Mariani-Costantini, Franco M. Buonaguro, Digna R. Velez Edwards, Muntaser Ibrahim, Himla Soodyall, Ambroise Wonkam, Raj Ramesar, Charles N. Rotimi
Am J Trop Med Hyg. 2010 August 5; 83(2): 226–229. doi: 10.4269/ajtmh.2010.10-0208
PMCID: PMC2911163
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #42 - Nov 1st, 2012 at 2:04am
 
How to Catch All Those Mutations—The Report of the Third Human Variome Project Meeting, UNESCO Paris, May 2010
Maija R.J. Kohonen-Corish, Jumana Y. Al-Aama, Arleen D. Auerbach, Myles Axton, Carol Isaacson Barash, Inge Bernstein, Christophe Béroud, John Burn, Fiona Cunningham, Garry R. Cutting, Johan T. den Dunnen, Marc S. Greenblatt, Jim Kaput, Michael Katz, Annika Lindblom, Finlay Macrae, Donna Maglott, Gabriela Möslein, Sue Povey, Raj Ramesar, Sue Richards, Daniela Seminara, María-Jesús Sobrido, Sean Tavtigian, Graham Taylor, Mauno Vihinen, Ingrid Winship, Richard G.H. Cotton, Contributors to the Human Variome Project Meeting
Hum Mutat. Author manuscript; available in PMC 2011 December 1.
Published in final edited form as: Hum Mutat. 2010 December; 31(12): 1374–1381. doi: 10.1002/humu.21379
PMCID: PMC3119486
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #43 - Nov 1st, 2012 at 2:09am
 
The long-term clinical implications of clonal chromosomal abnormalities in newly diagnosed chronic phase chronic myeloid leukemia patients treated with imatinib mesylate.
Lee SE, Choi SY, Bang JH, Kim SH, Jang EJ, Byeun JY, Park JE, Jeon HR, Oh YJ, Kim M, Kim DW.
Cancer Genet. 2012 Oct 27. doi:pii: S2210-7762(12)00234-7. 10.1016/j.cancergen.2012.09.003.

p38 (MAPK) stress signalling in replicative senescence in fibroblasts from progeroid and genomic instability syndromes.
Tivey HS, Brook AJ, Rokicki MJ, Kipling D, Davis T.
Biogerontology. 2012 Oct 31. [Epub ahead of print]
PMID: 23112078
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Re: PEER REVIEWED AlanCFAs idea of evidence for evolution
Reply #44 - Nov 1st, 2012 at 2:26am
 
DDX5 is a positive regulator of oncogenic NOTCH1 signaling in T cell acute lymphoblastic leukemia.
Lin S, Tian L, Shen H, Gu Y, Li JL, Chen Z, Sun X, James You M, Wu L.
Oncogene. 2012 Oct 29. doi: 10.1038/onc.2012.482. [Epub ahead of print]
PMID: 23108395
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