It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Some features of ATS will be disabled while you continue to use an ad-blocker.
Mutated protein can have single amino acid change (minor, but still in many cases significant change leading to disease) or wide-range amino acid changes by e.g. truncation of C-terminus after introducing premature stop codon.
Missense mutations can render the resulting protein nonfunctional, and such mutations are responsible for human diseases such as Epidermolysis bullosa, sickle-cell disease, and SOD1 mediated ALS.
A missense mutation is a mistake in the DNA which results in the wrong amino acid being incorporated into a protein because of change, that single DNA sequence change, results in a different amino acid codon which the ribosome recognizes. Changes in amino acid can be very important in the function of a protein. But sometimes they make no difference at all, or very little difference. Sometimes missense mutations cause amino acids to be incorporated, which make the protein more effective in doing its job. More frequently, it causes the protein to be less effective in doing its job. But this is really the grist of evolution, when missense mutations happen, and therefore small changes, frequently small changes in proteins, happen, and it happens to be that it improves the function of a protein. That will sometimes give the organism that has it a competitive advantage over its colleagues and be maintained in the population.
Some genetic disorders, such as thalassemia and cystic fibrosis result from point-nonsense mutations.
Nonsense-mediated mRNA decay (NMD) is a quality-control mechanism that selectively degrades mRNAs harboring premature termination (nonsense) codons. If translated, these mRNAs can produce truncated proteins with dominant-negative or deleterious gain-of-function activities.
Dominant negative mutations (also called antimorphic mutations) have an altered gene product that acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular function (often inactive) and are characterized by a dominant or semi-dominant phenotype. In humans, dominant negative mutations have been implicated in cancer (e.g., mutations in genes p53, ATM, CEBPA and PPARgamma). Marfan syndrome is caused by mutations in the FBN1 gene, located on chromosome 15, which encodes fibrillin-1, a glycoprotein component of the extracellular matrix. Marfan syndrome is also an example of dominant negative mutation and haploinsufficiency.
originally posted by: TheRedneck
I read it over quickly... actually, the more I read the quicker I read. I saw no research or even detailed hypothesis; the paper reads to me like a lot of "maybe," "might," and "possibly." That's not what i expect from an actual paper. ...
The people conducting this study are psychologists, and their essay provides no evidence that they did any empirical studies to determine if the behaviors being studied actually produced more offspring than other behaviors. They simply spin tales about how — possibly, maybe, perhaps — it might be so. Neither did they provide any scientific studies of genes, to see if there actually are genes that produce these behaviors. Thus — except to those who already assume that evolutionary psychology is true — the evidence is profoundly underwhelming.
Now for the Data
If this were an early arthropod with articulating limbs, that might be something. How clear is that evidence? Barras is not embarrassed to admit:
Exactly which animal lineage Y. spiciformis belonged to is unclear. The researchers suggest it might be a relative of insects and crustaceans such as shrimp and lobsters, because it seems to have leg-like structures. If further analysis shows that those structures are actually an artefact of the fossilization process, the animal might instead be some sort of primitive segmented worm.
Some caution is clearly advised. Many Ediacaran creatures were segmented. Some also showed bilateral symmetry. Controlled movement, however, would imply muscles, nerves, some kind of “skeleton” (not necessarily bone) able to hold its shape. The legs would have to be coordinated. How clear is the data on movement? It doesn’t sound too convincing in the Virginia Tech piece:
Remarkably, the find also marks what may be the first sign of decision making among animals — the trails suggest an effort to move toward or away from something, perhaps under the direction of a sophisticated central nerve system, Xiao said.
Maybe, suggest, perhaps. It would be necessary to rule out all other sources of movement, say, from waves and currents, which could cause a long worm-like thing to shift along the sea floor and even change direction. In a video, lead author Shuhai Xiao relies on animation to show his vision of a bilaterian animal, with head and tail and left and right sides and top and bottom, crawling with legs through the mud. The actual fossil, though, seems less clear. The BBC quotes Wood, “Though it’s not well-preserved, it has the hint that it has a front and a back… so this animal has already got some sense of unidirectional movement.”
New Scientist takes “the hint” and runs with it. “An extinct creature that looked like a cross between a millipede and an earthworm was one of the first animals that could move under its own power.” Yet later the article says that other Ediacarans moved passively with the water current, while perhaps Kimberella could “slither across the sea floor.” None of those organisms had a central nervous system, a gut, or a head with mouth parts. Did Yilingia? It’s not clear.
Room for Doubt
The actual paper in Nature leaves plenty of room to doubt the hype. Motility is inferred, because there is no clear evidence of actual legs or any other organs; no mention of a head, either. How is a motile creature supposed to move without eating? The authors impose wishful thinking on a paucity of data from one spot in China. If this were such a monumental discovery, clear evidence of complex organs at this stage would have been found by now, and would be widespread all over the earth. Watch how the authors’ first sentence — an admission of ignorance — launches a Darwin party cruise.
it's standard in the field of evolutionary philosophy
In some fields, speculation is widely accepted and editors of magazines like Nature have no issue giving their stamp of approval which is then interpreted as "peer reviewed" by others (especially in news articles about it).
originally posted by: TheRedneck
a reply to: whereislogic
... You are confusing publication with peer review.
In the wake of the widely publicized recent series of frauds in prestigious research institutes, the Association of American Medical Colleges issued a report setting out guidelines on how to deal with fraud in research. The report, in essence, maintained that “the overwhelming probability that fraudulent data will be detected soon after their presentation” is a safeguard against unethical practices.
This assessment, however, did not sit well with many others, both inside and outside the scientific community. For example, a New York Times editorial, calling the report “a shallow diagnosis of science fraud,” pointed out that “none of the frauds was originally brought to light through the standard mechanisms by which scientists check each other’s work.”
In fact, a member of the report committee, Dr. Arnold S. Relman, who is also an editor of The New England Journal of Medicine, likewise disagreed with the report’s conclusion. “What kind of protection against fraud does peer review offer?” he asked. “Little or none.” To back up his argument, Relman continued: “Fraudulent work was published in peer-reviewed journals, some with very exacting standards. In the case of the two papers we published, no suggestion of dishonesty was raised by any of the referees or editors.”
As for the effectiveness of replication in spotting fraud, there appears to be a vast gap between theory and practice. In today’s highly competitive field of scientific research, scientists are more concerned with breaking new ground than with repeating what someone else has done. Even if a scientist’s work is based on an experiment done by someone else, the experiment is rarely repeated in exactly the same form.
The problem of replication is further compounded by what is sometimes called salami science. Some researchers deliberately ‘slice up’ their experimental findings into small bits in order to multiply the number of publishable works. This “affords an opportunity for dishonesty,” says a Harvard committee, “because such reports are less likely to be verified by others.” Researchers well know that unless an experiment is really important, it is unlikely that anyone will try to repeat it. It has been estimated that as much as half of all published papers are “unchecked, unreplicated, and maybe even unread.”
My point was about those reading an article in scientific magazines like Nature, and automatically thinking that just because it's in that magazine, it has been peer reviewed or is based on something that was peer reviewed; when often, the main reason why it's in the magazine, is just because an editor gave a stamp of approval.
Alex Jones did a show on this not too long ago. I forget what the paper was, but apex 25-28 or some # like that. This was definitely one of the side effects spoken about. I’m going to sit this vax out and take my chances with the virus and my immune systems natural ability to mount a defense.
originally posted by: MichiganSwampBuck
April 8th, 2021: mRNA vaccines may cause your body to churn out PRIONS that “eat your brain” like Mad Cow Disease
The mRNA vaccine works by hijacking your body’s cells and causing them to churn out proteins modeled after the spike proteins in the SARS-cov-2 coronavirus. Since that structure includes prion-like regions, random errors in mRNA sequences — which may be truncated by the human immune system before they reach the ribosomes in the cells — could cause mRNA vaccine recipients to churn out prions in their own bodies. The risk of this was assessed by Dr. J. Bart Classen, who authored a paper in Microbiology & Infectious Diseases: “Covid-19 RNA Based Vaccines and the Risk of Prion Disease.”
The article starts off with a zombie theme, but we're basically talking mad cow disease here, incurable and deadly. Just thought this needed it's own thread, as I mentioned this in the Canadian mystery disease thread. It has source links to the original material.