Genetic testing may also apply another scientific strategy to the field of eugenics, or to intervene to promote a social philosophy that improves the genetic characteristics of humans. In the past, eugenics was used to demonstrate practices including involuntary sterilization and euthanasia.
Today, many people are concerned that preimplantation genetic diagnosis may be well established and can be applied technically to select specific non-disease features (rather than eliminating the serious diseases currently used) implanted embryos, thus equivalent to a eugenics Form of study.
In the media, this possibility has been sensational and often referred to as the so-called designer baby creation, which is even included in the Oxford English Dictionary. Although possible, this genetic technology has not yet been implemented; nevertheless, it still brings many intense moral issues.
The selection and enhancement of embryo characteristics can lead to ethical issues involving individuals and society. First, does the choice of specific characteristics poses a health risk, otherwise, these risks do not exist?
The safety of procedures for preimplantation genetic diagnosis is currently under investigation and, as this is a relatively new form of reproductive technology, lacks long-term data and a sufficient number of subjects.
However, a security question often asked about the fact that most genes have multiple effects. For example, in the late 1990s, scientists discovered a gene associated with memory (Tang et al., 1999).
Modification of this gene in mice greatly improved learning and memory, but it also caused an increased sensitivity to pain (Wei et al., 2001), which is clearly not an ideal feature.
In addition to security issues, personal freedom issues arise. For example, when a child cannot express consent by himself, should parents be allowed to manipulate the childs genes to select certain characteristics?
Suppose a mother and father choose an embryo based on their so-called musical sexual predisposition, but the child does not like music when he grows up. Does this change the childs feelings about his or her parents, and vice versa?
Finally, as far as society is concerned, everyone cannot get this expensive technology. Therefore, perhaps only the most privileged members of society can have designer children with more intelligence or physical appeal. This can cause genetic aristocracy and lead to new forms of inequality.
At present, these questions and conjectures are purely hypothetical because the techniques required for feature selection are not yet available. In fact, this technique may not be possible considering that most features are complex and involve many genes. Nevertheless, if you can create genetically enhanced humans, then thinking about these and other issues related to genetic engineering is also important.
After all, the vision of a designer baby may not be that far away. Last year was full of news about genetic engineering most of which was driven by cutting and pasting technique called Crispr. At the top of the list. Crisp can modify human embryos to correct relatively common, often fatal, mutations.
A controversial cell biologist named Shoukhrat Mitalipov, who pioneered work in the US, said his team not only used CRISPR to correct mutations in newly fertilized embryos, but they did it through a mechanism.
If not novel, at least it is unusual. The response of the scientific community is direct and negative. They just didnt buy a bit. So, Wednesday, in Nature Mitafilov published the initial working journal two groups of researchers published a criticism of the Mitalipov 2017 paper and Mitalipovs sharp, acronym and infographic filled with criticism trying to respond. Because morality doesnt matter well, not yet if science doesnt actually work.
You know how the baby is made, right? Ok, Mitalipovs team didnt do that. Scientific research using existing human embryos is contraindicated in most cases in the United States, so scientists fertilize them with normal human eggs and fertilize them with sperm containing the mutant MYBPC3 gene.
This version is a disease called hypertrophic cardiomyopathy, which is the most common cause of sudden death in young athletes. People with two mutants MYBPC3 one from mom, another from dad, or homologous alleles, in genetic language rarely survived childhood. Only one person who replicates heterozygotes often develops heart problems as they age.
To try to correct the mutation, Mitalipovs team used CRISPR to cut the mutant gene from the paternal chromosome and then insert the synthetic corrected version.
But the second step did not happen. In contrast, according to the analysis of Mitalipov, the cells replicated the wild-type gene from the maternal chromosome and inserted it. Results: The embryo has two wild-type alleles. It is called homology-dependent repair or homologous homeopathic repair.
Some of these authors have been studying DNA repair, and somehow they missed the elephant in the room, said Mitalipov, director of the Embryonic Cell and Gene Therapy Center at Oregon Health and Science University. We point out that there is a huge gap in how genes are repaired. We are not sure if it occurs in the somatic lineage, but in the embryonic lineage we have now demonstrated this.
Embryologists and cell biologists dont think they missed the elephant. They dont think so. We think there is another explanation, said Paul Thomas, the editor of the SA genome at the South Australian Institute of Health and Medical Research, a lead author of a review article.
Thomass research shows that in mice, Crispy tends to cut large pieces of DNA from the genome, the so-called large deletions. He suspects that this is also what happened in the Mitalipov embryos they missed a lot of deletion failures. If you create a lot of deletes on a chromosome, you need to specialize in that event, Thomas said. If you use the test method they use, this is a very standard test and cannot be detected.
Its like trying to figure out how many bagels a bakery makes by calculating whats on the shelf at the end of the day. Your statistics will say that the bakery mainly produces blueberries, but thats because the good taste of poppy seeds, garlic, salt and plains is invisible until you arrive. Your number will overestimate the proportion of blueberry production to the overall bagel.
Is this just a problem for mice and men? of course. Of course, more and more people are seeing a large number of mouse embryos missing. It is unclear whether a large number of deletions have occurred in human embryos because in fact we only have this research and a few other studies, Thomas said.
So Mitalipovs team returned to the lab. They took their old samples and re-analyzed them. This technique, called polymerase chain reaction, allows sequencing and analysis of a large enough amount of DNA. This time, they watched a longer chromosome.
We used large-scale PCR for analysis, up to 10,000 base pairs, and we still dont see any missing, Mitalipov said. He did not expect to find anything. The first paper of his group reported a success rate that is, a modified mutation rate about 70%. Mitalipov said it is hard to believe that 70% of his embryos will have a large number of defects caused by Crispr. He said that this made the technology unusable.
However, the case has not yet been closed. We were very surprised that they did not see any evidence of deletion in any of their responses, Thomas said. We dont think they completely rule out this possibility. One of Thomass co-authors, Fatwa Adikusuma, proposed a more accurate method of detection, such as qPCR (quantitative detection of DNA amount hence Q value). Mitalipov has not tried it.
Other teams have other questions. For example, a team led by Dieter Egli of Columbia University and Maria Jasin of the Memorial Sloan Kettering Cancer Center (including the outspoken Georges Biotech expert George Church) wondered how the CRISPR complex could support the maternal wild-type gene because, In the early part of cell division, mother contribution and father contribution are separate.
According to Mitalipov, the parental DNA cluster contained in an envelope called a pronucleus is exposed enough time for the repair process to work. Paul Knoepfler, a cell biologist at the University of California, Davis, said: If this is correct, what puzzles them is that they dont report more mosaics in these embryos.
Refers to a single organism with different genomes in different cells. The fragility is so late, for example in the two-cell embryo stage, which can lead to different genetic results, Knoepfler said and this could lead to later unhealthy embryos.
So is it possible for Mitalipov to do the right thing? As mentioned above, the new data is consistent with the genetic correction, Jasin wrote in an email. However, she said that Mitalipovs own response shows how difficult this research is.
When his team could not detect the parents allele, one of his embryos showed allele dropout. Not sure if there is no genetic correction for gene homologous recombination in all embryos, some embryos, or in the most extreme cases, adds Jasin.
Everyone, including Mitalipov, said that more research is needed to determine. It doesnt matter to him; he knows that people have a lot of concerns about what he said. If his method does work, then it only applies to embryos with a wild-type copy of the gene, on the one hand, there must be a wild-type gene version to replicate the cells.
But more importantly, new ideas require time and work to penetrate into one area. There is dogma, especially in biology, Mitalipov said. We just accepted our findings, calling it an unknown but powerful repair pathway in human embryos.
This dogma definitely takes time to make way for this approach. Mitalipovs team has strengthened their case to some extent, Knoepfler said. Maybe this points to the direction we fundamentally understand the new mechanism in early human embryos, but it is also possible that we will treat this completely differently a year later. Either way, for something going to the clinic, its my performance must exceed 70%. This means its time to do more work in the lab.
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Genetic Engineering in Humans About Its Future Pros and ...
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