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originally posted by: Phantom423
a reply to: Phantom423
Have to make a separate post for videos as citation update post getting too long - thanks to all who are contributing great stuff.
VIDEOS
There was no first human
Contributed by BoyMonkey74
Minds Blown: Scientists Develop Fish That Can Walk on Land
Contributed by Akragon
Evolution in Action
Contributed by BoyMonkey74
Evolution: It's a Thing – Crash Course Biology #20
Contributed by BoyMonkey74
How Evolution Works
Contribued by flyingfish
Sea Slugs that Eat the Sun
Contributed by sapien2
Leonard Susskind: Is the Universe Fine Tuned for Life?
Contributed by Phantom423
originally posted by: Isurrender73
Things that science needs to prove before a natural cause and evolution past Class/Phylum is anything more than your imagination.
1. Abiogenesis
2. Single Cell to Multi Cell
3. Physically observe cross Kingdom - a plant physically observed to become an animal. Since plants and animals are both DNA based, either they have a common creator or common ancestor.
4. Physically observe the separation of cellular organisms from asexual to male/female
5. Physically observe an animal cross Phylum
6. Physically observe an animal cross Class
7. Physically observe an animal cross Order
8. Physically observe an animal cross Family
9. Physically observe an organism cross Genius
originally posted by: Masterjaden
a reply to: OpenEars123
Do you have ANY idea how laughably hilarious this post is....
" I starred and flagged this thread, because of all the people who will supply the irrefutable and overwhelming evidence that hasn't been supplied yet".
ROTFLMAO....
Jaden
originally posted by: Phantom423
CATEGORY
ORIGINS
Self Assembly:
1. Link to board discussion: www.abovetopsecret.com...
2. Summary: The self-organization properties of DNA-like molecular fragments four billion years ago may have guided their own growth into repeating chemical chains long enough to act as a basis for primitive life.
3. www.sciencedaily.com...
4. www.nature.com...
5. www.science20.com...
GENOMICS
1. Board discussion link: www.abovetopsecret.com...
2. www.abovetopsecret.com...
3. www.genome.gov...
4. science.nasa.gov...
DEVELOPMENTAL EVOLUTION
1. Board discussion link: www.abovetopsecret.com...
2. www.washingtonpost.com...
3. Developmental Plasticity and the Origin of Tetrapods
www.nature.com... 5DI4S1NeV2yxE7_gEI11m4Xs9v5VT3MMEx27bkZz2E6-VNa6yzuzed3HbeTLGgkXC5Oozxl95i-VUSOh-fv4LhgruzPs8n8pXPRxQ-tPXI0v4FYDSVEQcOMRFoV2liRWbu33EcFXO3oOnLl20JXGg5 7zmSmz1kKSjscpvuRCVAfl9I2USCqlIbYp8BSETqUKC9vYMB5culdnGMycGTAMvXmGby8%3D&tracking_referrer=www.washingtonpost.com
4. Your Brain Evolved from Bacteria
www.scientificamerican.com... on+%28Topic%3A+Evolution%29
5. From fish to man: Research reveals how fins became legs
www.eurekalert.org...
6. 10 Popular Fallacies and Misconceptions About Evolution
Thread link: www.abovetopsecret.com...
Contributed by krazysh0t
Evidence for Evolution - www.google.com...
C-14 dating is unreliable and therefore cannot be trusted - en.wikipedia.org...
Evolution Violates the Second Law of Thermodynamics - en.wikipedia.org...
Evolution doesn't adequately explain the origin of life - atheism.about.com...
Mutations are only harmful -
en.wikipedia.org...
Evolution has never been observed - en.wikipedia.org...
www.cdc.gov...
Evolution doesn't answer such and such question about the universe and the origin of life - No scientific theory answers 100% of the questions in science. Sorry I don't have a link for this one, but it is just so absurd that it doesn't really need one. If you find a theory or idea that claims to answer every question imaginable (religion) then it is HIGHLY suspect. The idea of science is that it works to answer a question, but then when that question is answered many new questions appear that the scientists then work to answer. It is an infinite process, but it certainly doesn't discredit the information gained and answers to questions that it does answer.
Evolution is just a theory - www.livescience.com...
Evolution doesn't explain the diversity of life on the planet - www.nhm.ac.uk...
en.wikipedia.org...
en.wikipedia.org...
Any number of hoaxes about evolution (ex: piltdown man) -
Ok, unfortunately this one won't have any links either because it is rather obvious. Thanks to the peer review process once a hoax is identified, it is removed from the scientific knowledge base and is no longer regarded as evidence for anything. HOWEVER, because a hoax exists is NOT proof that the prevailing theory that is for is also untrue. In order for that to be the case, ALL the evidence for that theory would have to be exposed as fradulent, and this is simply not the case for evolution. In fact new evidence surfaces all the time that proves evolution is true, while literally zero evidence surfaces that completely contradicts it.
Every now and then there is some evidence that shows that evolution doesn't work EXACTLY how we originally thought, but in this case we just modify the theory to account for the new information. An example of this would be the punctuated equilibrium idea that I posted in the last point. Originally evolution was thought to happen at the same rate across the species, but evidence kept surfacing that contradicted this account. So now, the theory was updated to include this and show that not all species evolve at the same rate. What DIDN'T happen however is that evolution was completely discredited by this new evidence.
7. From chicken to dinosaur: Scientists experimentally reverse the evolution of the perching toe
22 May 2015 Universidad de Chile
www.alphagalileo.org...
Board discussion link: www.abovetopsecret.com...
Contributed by flyingfish
After analyzing the genomes of members of three Chinese families with CGHT and one person with CGHT and gingival hyperplasia, researchers pinpointed the genetic defects to chromosome 17. In the three families, members had DNA deletions on this chromosome, meaning they were missing pieces in their genes. On the other hand, the individual with enlarged gums had extra pieces of DNA, called DNA duplications, a type of mutation in which sequences of DNA appear multiple times. These genetic abnormalities affected four to eight genes on chromosome 17.
Since the Middle Ages, when this condition was first reported, there has been much speculation over the root causes of CGH. Some have argued that CGH is an example of atavism, or an evolutionary ‘throwback’ to a more primitive ancestor. Others have reasoned (incorrectly) that individuals suffering from CGH represented the missing link between apes and humans, and thus further evidence to support Darwin’s theory of evolution. Read more at blog.23andme.com...
CGHT is an extremely rare but highly heritable disorder. Scientists are unsure how many people have the condition, but there are at least 30 cases in China's billion-strong population. Affected men and women develop excessive dark hair across their bodies and faces. Some sufferers also have a broad, flat nose, large ears, a large mouth, and thick lips, and, occasionally, an enlarged head and jaw.
a : recurrence in an organism of a trait or character typical of an ancestral form and usually due to genetic recombination
originally posted by: Phantom423
originally posted by: Phantom423
a reply to: Phantom423
Have to make a separate post for videos as citation update post getting too long - thanks to all who are contributing great stuff.
SECTION II
VIDEOS
There was no first human
Contributed by BoyMonkey74
Minds Blown: Scientists Develop Fish That Can Walk on Land
Contributed by Akragon
Evolution in Action
Contributed by BoyMonkey74
Evolution: It's a Thing – Crash Course Biology #20
Contributed by BoyMonkey74
How Evolution Works
Contribued by flyingfish
Sea Slugs that Eat the Sun
Contributed by sapien2
Leonard Susskind: Is the Universe Fine Tuned for Life?
Contributed by Phantom423
Bio116 Crash Course Evo Devo
Contributed by flyingfish
originally posted by: Phantom423
a reply to: Wolfenz
The condition is called generalized hypertrichosis. It's a pathogenic copy-number mutation and is a trisomy 17 genomic disorder. Similar to Down's Syndrome which is a trisomy 21 disorder, there are 2 copies of chromosome 17 which is the root of the disorder. So instead of 46 chromosomes, the person has 47 chromosomes. Here's a research paper describing the disorder: www.ncbi.nlm.nih.gov...
I didn't see anything in the literature to suggest that hypertrichosis is an "atavistic" disorder, i.e. a throwback to earlier evolutionary models. I think it's just a chromosomal disorder where the physical expression of the extra genetic component is very "apelike". But the person is totally human. The condition also exists in primates - but the primate physical appearance looks more like Down's Syndrome (to me anyway). Would have been really strange if the primate expression of the gene disorder caused them to look more human (good subject for a sci fi novel!)
Interesting stuff - thanks for posting.
X-linked congenital generalized hypertrichosis (Online Mendelian Inheritance in Man 307150) is an extremely rare condition of hair overgrowth on different body sites.
We previously reported linkage in a large Mexican family with X-linked congenital generalized hypertrichosis cosegregating with deafness and with dental and palate anomalies to Xq24-27. Using SNP oligonucleotide microarray analysis and whole-genome sequencing,
Inherited hypertrichoses are rare human disorders characterized by excessive hair growth that does not depend on androgen stimulation and is independent of age, sex, and ethnicity (1). Hypertrichosis syndromes fall under the larger umbrella of ectodermal dysplasias, or abnormal development of the hair, skin, nails, teeth, and/or eccrine glands, and are often associated with additional anomalies including gingival hyperplasia, deafness, cardiomegaly, and bone abnormalities (2).
It has been suggested that inherited hypertrichoses represent examples of atavisms, or the recurrence of an ancestral phenotype, where the genes that promote a full coat of hair in other mammals and were silenced throughout evolution have become “reactivated” in human hypertrichosis, invoking unusual genetic mechanisms to explain their occurrence
Researchers are familiar with other atavistic genetic behavior. Some rare examples include additional nipples, and small tail-like extrusions at the end of the spine. The defective gene in CGH is passed by both sexes, to 50% of their offspring. Typically, fetuses lose their fine body hair, called lanugo, by the end of the seventh and eight month of gestation. Babies afflicted with CGH are born with this body hair intact, which occasionally fades in adulthood, but typically lastis a lifetime. Currently, the best known cases of CGH occurs in a family living in Mexico. Sadly, much of this family has resorted to working in circuses and “freak” shows to earn a living. This Mexican family grows an even thicker, darker body hair than their Asian, and European counterparts. Men have thicker and denser hair than the women in this family, suggesting an X-linked dominant pattern of inheritance, cardiagra.blogspot.com reports. - See more at: english.pravda.ru...
originally posted by: Phantom423
a reply to: Wolfenz
Atavism isn't reverse evolution. There's obviously a mutation event occurring, but I don't think it's a reversion to some pre-existing organism. I don't think you can label it reverse evolution. It's just like a human being born with a small tail - we know the code is there in the genome, but it takes a mutation and a whole cascade of events for it to appear. But that doesn't imply that the human is reversing evolutionary course. Remember - evolution is a population event, not an individual event. If whole populations started to breed ape-like characteristics, then we would be looking at a whole new dynamic. But these are very isolated events which suggest that it's a mutation which can be either inherited or occur in a single individual.
Humans and primates have about 98% genetic similarity.
Trisomy 17 occurs in primates too. If the chromosome 17 duplicate was a normal genetic configuration in the primate genome, then you wouldn't expect it to turn up as an "anomaly", or genomic abnormality. It would be considered normal. But it isn't. So whatever triggers the Trisomy 17 mutation in humans - whether it's inherited or a single generation - isn't duplicating some normal condition that existed previously in primates. It's an abnormal mutation.
At least that's how I would interpret the research.
Atavism isn't reverse evolution. There's obviously a mutation event occurring, but I don't think it's a reversion to some pre-existing organism. I don't think you can label it reverse evolution.
Humans and primates have about 98% genetic similarity.
We conclude that the locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2.
originally posted by: Wolfenz
originally posted by: Phantom423
a reply to: Wolfenz
Atavism isn't reverse evolution. There's obviously a mutation event occurring, but I don't think it's a reversion to some pre-existing organism. I don't think you can label it reverse evolution. It's just like a human being born with a small tail - we know the code is there in the genome, but it takes a mutation and a whole cascade of events for it to appear. But that doesn't imply that the human is reversing evolutionary course. Remember - evolution is a population event, not an individual event. If whole populations started to breed ape-like characteristics, then we would be looking at a whole new dynamic. But these are very isolated events which suggest that it's a mutation which can be either inherited or occur in a single individual.
Humans and primates have about 98% genetic similarity.
Trisomy 17 occurs in primates too. If the chromosome 17 duplicate was a normal genetic configuration in the primate genome, then you wouldn't expect it to turn up as an "anomaly", or genomic abnormality. It would be considered normal. But it isn't. So whatever triggers the Trisomy 17 mutation in humans - whether it's inherited or a single generation - isn't duplicating some normal condition that existed previously in primates. It's an abnormal mutation.
At least that's how I would interpret the research.
Atavism isn't reverse evolution. There's obviously a mutation event occurring, but I don't think it's a reversion to some pre-existing organism. I don't think you can label it reverse evolution.
Atavism is the development of on ancestor traits
and then the modern traits take control ( Game change )
wiki terms he he
Evolutionarily, traits that have disappeared phenotypically do not necessarily disappear from an organism's DNA. The gene sequence often remains, but is inactive. Such an unused gene may remain in the genome for many generations.[4] As long as the gene remains intact, a fault in the genetic control suppressing the gene can lead to it being expressed again. Sometimes, the expression of dormant genes can be induced by artificial stimulation.
en.wikipedia.org...
I showed Legit Sites in Science saying it is,
Atavism is a revert back to what we originally were
in the DNA coding Sequence aka Add ons
as i see it when the interruption of Missing Genes.
perhaps those dormant genes , become active to to replace
those missing genes. in julia Pastrana's case.
and that is basically what Scientist are debating.
like Whale Dolphins have leg stubs and snakes with leg stub
all from what they original had !
Atavism a Perfect example is what jack Horner explained
about the Embryo fetus stages of a Bird
it grows Tail but stops and most of the tail is adsorbed
, a fingered like limb then fuses to a wing
he explained this on TED. that in that process.
there is something stopping it in the Genes.
its the Same for Humans.
There is some left over parts aka useless parts
from our ancestors that proved evolution within our selves
as in tails, body hair, 3rd eyelid, wiggle in the ears controlled
muscle movement extra ribs , extra neck bone etc..
evidence we are not 100% created !
Humans and primates have about 98% genetic similarity.
but what gets me that the chromosome 2
what science proved that it actually 2 chromosome fused to one
end for end of the telomers. making it 46 instead of 48
like our primate cousins Chimps %98 Orangutan 97%
Gorilla 96-97% and Gibbons 95% shared makeup.
so the closest of the highest percentage in the great apes is
the chimpanzee..
I never mention that the Human Race is reversing back to its
ancestral course , it just sometimes the traits come out from
usually ways a genetic distorter.
Right evolution is a Population event from a Group
from a certain locations from the effect of the species surroundings
like one group of ( for example ) Big cats like the Tiger
but theirs multiple from all over in Asia from Siberia to a Bengal and
to the extinct Caspian. all different sizes some stronger or weaker
some thicker or thinner coat . all adapted to their environment it lives in
over the thousands of years.
Tiger Subspecies (image)
blogs.evergreen.edu...
species of tiger
for individual that's called mutation but also can lead to a Group
causing a Heredity trait.
what i referring too, isn't the duplication but the Missing genes
and what is missing , what is replacing it ? or just the plain gap
is causing it .
Phantom 423 im not the perfect apple in the bunch
but i try to related and make sense of it .
Creation and evolution gotta love it ,
love to know what cause that fusion of
chromosome 2
Origin of human chromosome 2: an ancestral telomere-telomere fusion.
www.ncbi.nlm.nih.gov...
We conclude that the locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2.
I also want to point out phantom423
im going into detail for those reading this post
that are not in the knowedit on 12015MondayfAmerica/Chicago9249 by Wolfenz because: (no reason given)edit on 12015MondayfAmerica/Chicago9249 by Wolfenz because: (no reason given)edit on 12015MondayfAmerica/Chicago9249 by Wolfenz because: (no reason given)
Chromosomal translocations that encode fusion oncoproteins have been observed consistently in leukemias/lymphomas and sarcomas but not in carcinomas, the most common human cancers. Here, we report that t(2;3)(q13;p25), a translocation identified in a subset of human thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX8 to domains A to F of the peroxisome proliferator–activated receptor (PPAR) γ1. PAX8-PPARγ1 mRNA and protein were detected in 5 of 8 thyroid follicular carcinomas but not in 20 follicular adenomas, 10 papillary carcinomas, or 10 multinodular hyperplasias. PAX8-PPARγ1 inhibited thiazolidinedione-induced transactivation by PPARγ1 in a dominant negative manner. The experiments demonstrate an oncogenic role for PPARγ and suggest that PAX8-PPARγ1 may be useful in the diagnosis and treatment of thyroid carcinoma.
originally posted by: Phantom423
a reply to: Wolfenz
I see what you're driving at. But expressing genes that are already in the genome, whether dormant or not, seems to me just playing an old record - it gets played once in a while for unknown reasons.
I'm not sure what you mean by "missing genes" - do you mean the reduction from 48 chromosomes in the primates to 46 in humans? It's interesting to consider that nature may be reducing the number of chromosomes during the evolutionary process and concomitantly increasing the complexity - sort of like an artificial intelligence or self programming computer that reduces waste, increases efficiency and complexity.
It's an interesting topic - I want to do more reading and research. The fusing on chromosome 2 is intriguing mainly because of the outcome. Genetic fusing has been identified in a number of cancers and other disease processes.
Chromosomal translocations that encode fusion oncoproteins have been observed consistently in leukemias/lymphomas and sarcomas but not in carcinomas, the most common human cancers. Here, we report that t(2;3)(q13;p25), a translocation identified in a subset of human thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX8 to domains A to F of the peroxisome proliferator–activated receptor (PPAR) γ1. PAX8-PPARγ1 mRNA and protein were detected in 5 of 8 thyroid follicular carcinomas but not in 20 follicular adenomas, 10 papillary carcinomas, or 10 multinodular hyperplasias. PAX8-PPARγ1 inhibited thiazolidinedione-induced transactivation by PPARγ1 in a dominant negative manner. The experiments demonstrate an oncogenic role for PPARγ and suggest that PAX8-PPARγ1 may be useful in the diagnosis and treatment of thyroid carcinoma.
www.sciencemag.org...
Keep digging this stuff up! Very intriguing and worth researching.
After analyzing the genomes of members of three Chinese families with CGHT and one person with CGHT and gingival hyperplasia, researchers pinpointed the genetic defects to chromosome 17. I n the three families, members had DNA deletions on this chromosome, meaning they were missing pieces in their genes. On the other hand, the individual with enlarged gums had extra pieces of DNA, called DNA duplications, a type of mutation in which sequences of DNA appear multiple times. These genetic abnormalities affected four to eight genes on chromosome 17.
I'm not sure what you mean by "missing genes" - do you mean the reduction from 48 chromosomes in the primates to 46 in humans? It's interesting to consider that nature may be reducing the number of chromosomes during the evolutionary process and concomitantly increasing the complexity - sort of like an artificial intelligence or self programming computer that reduces waste, increases efficiency and complexity.