Lifeboat Foundation: Safeguarding Humanity
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Category: genetics – Page 541

I have nothing against the idea of designer babies. Why not better ourselves through science? There will always be a baseline version of humanity kicking around, even if it’s in cold storage,thus ensuring that any mistakes made early on don’t destroy the species. Besides, the same technology that allows us to make ourselves better could just as easily be used to repair us if we do make a mistake of some kind. TOO much red-tape, as always.

Room: B-3245.

Recent discoveries and advances in medicine are setting the bioethical world on fire. Some technologies, such as CRISPR-Cas9 and fast DNA sequencing techniques, have tremendously increased our control over our own genome. GMOs, Gene Therapy and life extension are examples of applications of our new gained knowledge in genetics. For more than a few, the thought of scientists playing with the fundamental building blocks of life brings an uneasy feeling. Yet, what are the scientists really doing?

As technologies keep on advancing, it is crucial to question ourselves on the implications of genetic research, and the first step to do so is to understand what is being done in the laboratories. The goal of this presentation is to convey reliable information on the field of genomics to non-experts so that they can take on a rational stance on the issues at hand. Simultaneously, in the spirit of Philopolis, the presentation revolves around the philosophical question of what is natural and what is not.

Christophe Lachance-Brais and @[601985428:2048:Philippe Castonguay] will give the talk and animate the discussion.

The 1h presentation will be followed by a 30 minute discussion.

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NGS — news flash; gene editing corrects genetically linked liver disease.

For the first time, researchers have treated an animal model of a genetic disorder using a viral vector to deliver genome-editing components in which the disease- causing mutation has been corrected. Delivery of the vector to newborn mice improved their survival while treatment of adult animals, unexpectedly, made them worse, according to a new study by investigators from the Perelman School of Medicine at the University of Pennsylvania The team published their findings in Nature Biotechnology.

“Correcting a disease-causing mutation following birth in this animal model brings us one step closer to realizing the potential of personalized medicine,” said senior author James Wilson, MD, PhD, a professor of Medicine and director of the Orphan Disease Center at Penn. “Nevertheless, my 35-year career in gene therapy has taught me how difficult translating mouse studies to successful human treatments can be. From this study, we are now adjusting the gene-editing system in the next phases of our investigation to address the unforeseen complications seen in adult animals.” Wilson is also director of the Penn Gene Therapy Program.

The Wilson lab focused on liver as a target for gene editing since they had solved the problem of gene delivery in this organ in previous work using traditional gene therapy using vectors based on adeno-associated virus (AAV). However, gene replacement therapy with AAV is not ideal for treating genetic diseases of the liver that manifest as newborns since the non-integrating genome is lost as developing liver cells proliferate.

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Aging, inflammation, cancer, and cellular senescence are all intimately interconnected. Deciphering the nature of each thread is a tremendous task, but must be done if preventative and geriatric medicine ever hope to advance. A one dimensional analysis simply will not suffice. Without a strong understanding of the genetic, epigenetic, intercellular, and intracellular factors at work only an incomplete picture can be formed. However, even with an incomplete picture useful therapeutics can and are being developed. One face is cancer, a number of diseases characterized by uncontrolled cell division. The other is slue of degenerative disorders stemming from deterioration in regenerative capacity.

Geroprotectors are a diverse and growing family of compounds that assist in preventing and reversing the unwanted side-effects of aging. Senolytics, a subset of this broad group, accomplish this feat by encouraging the removal of decrepit cells. A few examples include dasatinib, quercetin, and ABT263. Although more research must be done, there are a precious handful of studies accessible to anyone with the inclination to scroll to the works cited section of this article. Those within the life extension community and a few enlightened souls outside of it already know this, but it bears repeating: in the developed world all major diseases are the direct result of the aging process. Accepting this rather simple premise, and you really ought to, should stoke your enthusiasm for the first generation of anti-aging elixirs. Before diving into the details of this promising new pharmaceuticals we must ask what is cellular senescence? What causes it? What purpose does it serve?

Depending on the context in which they are operating a single gene can have positive or negative effects on an organism’s phenotype. Often the gene is exerting both desirable and undesirable influences at the same time. This is called antagonistic pleiotropy. For example, high levels of testosterone can confer several reproductive advantages in youth, but in elderly men can increase their likelihood of developing prostate cancer. Cellular senescence is a protective measure; it is a response to damage that could potentially turn a healthy cell into a malignant one. Understandably, this becomes considerably more complex when one is examining multiple genes and multiple pathways. Identifying all of the players involved is difficult enough. Conboy’s famous parabiosis experiment shows that alterations in the microenviornment, in this case identified and unidentified factors in the blood of young mice, can have be very beneficial to their elders. Conversely, there is a solid body of evidence that shows senescent cells can have a bad influence their neighbors. How can something similar be achieved in humans without having to surgically attach a senior citizen to a college freshman?

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A few weeks into sixth grade, Colman Chadam had to leave school because of his DNA.

The situation, odd as it may sound, played out like this. Colman has genetic markers for cystic fibrosis, and kids with the inherited lung disease can’t be near each other because they’re vulnerable to contagious infections. Two siblings with cystic fibrosis also attended Colman’s middle school in Palo Alto, California in 2012. So Colman was out, even though he didn’t actually have the disease, according to a lawsuit that his parents filed against the school district. The allegation? Genetic discrimination.

Yes, genetic discrimination. Get used to those two words together, because they’re likely to become a lot more common. With DNA tests now cheap and readily available, the number of people getting tests has gone way up—along with the potential for discrimination based on the results. When Colman’s school tried to transfer him based on his genetic status, the lawsuit alleges, the district violated the Americans With Disabilities Act and Colman’s First Amendment right to privacy. “This is the test case,” says the Chadam’s lawyer, Stephen Jaffe.

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Less than a year after scientists in China became the first to genetically modify human embryos, a research team in Britain has been given the green light to perform similar work. It’s a huge moment in biotech history—one that could eventually lead to “designer babies.”

Last September, scientists at London’s Francis Crick Institute asked the U.K’s Human Fertilisation and Embryology Authority (HEFA) for permission to perform gene editing work on human embryos. Their request has now been granted, potentially paving the way for other similar work. Human germline editing is deemed controversial because any baby born through the technique has the potential to pass those genetically modified traits down to the next generation. Advocates of the practice say it could eliminate a host of genetic diseases, while at the same time introducing the possibility of human enhancement.

“The work carried out at the Crick will be for research purposes and will look at the first seven days of a fertilized egg’s development (from a single cell to around 250 cells),” noted the lab in a statement. “The knowledge acquired from the research will be important for understanding how a healthy human embryo develops.” Geneticist Kathy Niakan will be overseeing the work.

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First, this study is very biased and flawed. Secondly, have the tech companies considered all of the resistance that we’re all going to face with the provider and payer communities plus their lobbyists when we try to promote medical AI, nanobots, etc.

I have seen some resistance mounted by some providers, some pharma, etc. against CRISPR. And, I believe this type of resistance is only going to hurt patients as well as many cancer survivors with a genetic predisposition to cancer, and other genetic mutations.

A study of mobile health apps’ impact on health care costs represents a limited but crucial step for assessing digital medicine.

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