Lifeboat Foundation

The development of gene therapy, in particular gene editing using the CRISPR-Cas9 method, has prompted a lively discussion around the world about how deeply you can interfere with the human genome. The creators of this method have turned to the world community, including lawyers, to undertake a public discussion of the implications that it can create (The National Academies of Sciences Engineering Medicine, 2015). The most important problem to be resolved in the future, in my opinion, will be the issue of establishing very clear legal principles of liability for damages resulting from the editing of genes in human embryos and reproductive cells. However, before this happens, it is necessary to show the possible legal problems that may arise and that will certainly appear in future legislative work in the world. Questions must be asked to which world legal experts will need to seek answers. The goal of this paper is to show the possible legal problems and ask questions related to the liability for damages resulting from the editing of genes in human embryos and reproductive cells that will be answered in the future.

Private law considerations will be based on Polish law, although it should be pointed out that the conclusions derived from them appear to be of universal nature for different legal systems. Despite the fact that legal considerations will refer to the regulation of Polish law, the subject of the analysis will also be the differences in the legal qualification of reproductive cells and embryos in other European legislations. It seems that nowhere in the world are there special regulations regarding the liability for damage related to the genetic editing of reproductive cells or embryos. Therefore, there is a need to present new challenges for classic private law institutions, such as legal abilities, torts, or liability for damages. Due to the lack of uniform European regulations and different conflicts of rights the subject of analysis will not be wrongful life and wrongful birth actions, but only claims of prenatal damage to a child.

The first major legal problem facing the international community is, of course, the question of the legal acceptability of the editing of genes of human reproductive cells and embryos (van Dijke et al., 2018). In this regard, it should be pointed out that despite the initial demand to ban such editing, over time, increasingly more scientists have pointed to the fact that it is not possible to maintain such a moratorium (Doudna and Sternberg, 2017). Jiankui’s presentation at the Second International Summit on Human Genome Editing on November 272018, showed that the introduction of a moratorium on genetic modifications of embryos in Europe, the condemnation of such research by a group of 120 of the greatest geneticists, even the Chinese regulations (Zhang and Lie, 2018) will not limit its conduct (Cyranoski and Ledford, 2018). Globalization of the medical market means that if any procedures are allowed on other continents, they will also become available to Europeans (Lunshof, 2016).

“The furin cleavage site consists of four amino acids PRRA, which are encoded by 12 inserted nucleotides in the S gene. A characteristic feature of this site is an arginine doublet. This insertion could have occurred by random insertion mutation, recombination or by laboratory insertion. The researchers say the possibility of random insertion is too low to explain the origin of this motif. Surprisingly, the CGGCGG codons encoding the two arginines of the doublet in SARS-CoV-2 are not found in any of the furin sites in other viral proteins expressed by a wide range of viruses. Even within the SARS-CoV-2, where arginine is encoded by six codons, only a minority of arginine residues are encoded by the CGG codon. Again, only two of the 42 arginines in the SARS-CoV-2 spike are encoded by this codon — and these are in the PRRA motif. For recombination to occur, there must be a donor, from another furin site and probably from another virus. In the absence of a known virus containing this arginine doublet encoded by the CGGCGG codons, the researchers discount the recombination theory as the mechanism underlying the emergence of PRRA in SARS-CoV-2.”

The ongoing pandemic of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has largely defied attempts to contain its spread by non-pharmaceutical interventions (NPIs). With the massive loss of life and economic damage, the only way out, in the absence of specific antiviral therapeutics, has been the development of vaccines to achieve population immunity.

A new study on the Preprints server discusses the origin of the furin cleavage site on the SARS-CoV-2 spike protein, which is responsible for the virus’s relatively high infectivity compared to relatives in the betacoronavirus subgenus.

Continue reading “The origin of SARS-CoV-2 furin cleavage site remains a mystery” »

Substantial transmission of SARS-CoV-2 infection occurred in the population of Wuhan in December 2019 with most cases reported in the second half of that month. Many early reported cases were associated with Huanan Market, indicating that it was one of the focus of the transmission. Nevertheless, transmission was also occurring elsewhere in Wuhan at the same time.

It is not possible on the basis of the current epidemiological information to determine how the SARS-CoV-2 was introduced into the Huanan Market. Substantial transmission of SARS-CoV-2 infection occurred among the population of Wuhan in December 2019.

While some of the early cases had an association with the Huanan Seafood Market, others were associated with other markets and other cases have no market association at all. It is likely that Huanan Seafood Market acted as a focus for transmission of the virus, but there are also transmissions appearing to have the occurrence elsewhere in Wuhan at the same time. This is our basic judgment. It is not possible on the basis of the current information to determine how SARS-CoV-2 was introduced into the Huanan Market.

The third part of my introduction will be the research of the animal environment group, the third group of our joint mission. Coronaviruses that phylogenetically relate to SARS-CoV-2 have been identified in different animals, including horseshoe bats and pangolins. Sampling of bats in Hubei Province, however, has failed to identify evidence of SARS-CoV-2-related viruses and sampling of wildlife in different places in China has so far failed to identify the presence of SARS-CoV-2.

Continue reading “COVID-19 Virtual Press conference transcript” »

Summary: A new technique which involves fusing human and chimpanzee skin cells that have been modified to act like stem cells, allowed researchers to identify two novel genetic differences between humans and chimps.

Source: Stanford University.

One of the best ways to study human evolution is by comparing us with nonhuman species that, evolutionarily speaking, are closely related to us. That closeness can help scientists narrow down precisely what makes us human, but that scope is so narrow it can also be extremely hard to define. To address this complication, researchers from Stanford University have developed a new technique for comparing genetic differences.

Today on the Science Talk podcast, Noam Slonim speaks to Scientific American about an impressive feat of computer engineering: an AI-powered autonomous system that can engage in complex debate with humans over issues ranging from subsidizing preschool and the merit of space exploration to the pros and cons of genetic engineering.

In a new Nature paper, Slonim and colleagues show that across 80 debate topics, Project Debater’s computational argument technology has performed very decently—with a human audience being the judge of that. “However, it is still somewhat inferior on average to the results obtained by expert human debaters,” says Slonim.

Continue reading “AI Can Now Debate with Humans and Sometimes Convince Them, Too” »

Here’s my latest video!

Papers referenced in the video:

Continue reading “Carotenoids Are Associated With A Younger Epigenetic Age And Reduced All-Cause Mortality Risk” »

Check out “How Watson Works here.”

Is it possible to live forever by using narrow AI that can perform faster and smarter than humans? Having a doctor give you the correct diagnosis and treatment plan only happens on average, 54% of the time, as the New England Journal of Medicine has pointed out. Having Watson instantly diagnose you with the correct diagnosis and treatment plan 95% of the time will become the new standard. Our crop of new personal medicine products such as continual internal diagnostics, synthetic immune systems, virtual assistants, and regenerative medicine will diagnose and stop sickness from ever occurring while constantly rebuilding and improving body and mind capabilities.

IBM has made a series of Watson computer systems so that any company can raise their industries products and services far beyond our human capability. IBM’s Watson was first featured to the public with its historic Jeopardy win over Ken Jennings and Brad Rutter the best human Jeopardy players. At the time, Watson contained 200 million pages of structured and unstructured content in a ninety server computing system with an analytical software IBM designed called DeepQA. Now, the financial markets, medicine, insurance companies, government, engineering, and customer service call centers are employing (buying) Watson is an artificial intelligence system, that can be specifically tailored to any digitized industry and quickly evolve their industries potential.

Summary: It’s not only our genetics and environment that play a role in aging and longevity, it’s also the random, tiny changes that arise on the cellular level.

Source: USC

A new model of aging takes into account not only genetics and environmental exposures but also the tiny changes that randomly arise at the cellular level.

Most cancers are driven by continuous cell division, the cause of which is largely a mystery. Scientists at Vanderbilt University have discovered a genetic switch that seems to touch off that abnormal proliferation of cells—and they did it with the gene editing system CRISPR.

Using a genomewide CRISPR screen, the Vanderbilt team discovered that deleting a protein made by the gene TRAF3 causes cells to proliferate without stopping, even after they reach a certain density that would normally signal them to stop dividing. Because TRAF3 has not been linked to cancer before, the finding could offer key insights into the development of some cancers, the researchers reported in the journal eLife.

The team started with 40 million epithelial cells, using CRISPR to select cells that kept dividing uncontrollably. They were surprised to discover that a loss of TRAF3 activates signaling that in turn drives cell proliferation. TRAF3 normally activates immunity and had not been linked to uncontrolled cell growth before, they said.