Speaking to packed house of journalists, scientists and members of The Planetary Society, Bill Nye the Science Guy, along with some very, very smart people, discussed how human beings might survive for long periods of time on Mars.
Researchers have discovered breaks in nerve cells tied to varous genetically related neurological disorders.
There’s still much that we don’t understand about obesity and its underlying causes, but scientists in Germany say they’ve discovered a genetic ‘switch’ that could effectively turn obesity on or off.
The new report is based on epigenetics research — that is, the way the genes in our bodies change based on chemical and environmental factors, rather than modifications in the fundamental DNA genetic code itself. We’re all born with a certain set of genes, but these can be turned on or off, or dialled up or down, though processes inside the body (it’s part of the reason why identical twins don’t always look identical).
It’s one of these epigenetic tags that the scientists have identified, and it works like a light switch rather than a dimmer. “Once the switch is triggered, it is a lifelong, epigenetically-driven decision that ends in a stable, either a lean or obese phenotype,” lead author Andrew Pospisilik from the Max Planck Institute of Immunobiology and Epigenetics. “The effect is akin to a light switch — on or off, lean or obese. Typically, we usually consider epigenetic control of disease to act much more like a dimmer, shifting phenotypes like body weight up or down gradually.”
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?
Continue reading “Tinkering with Life : Genetics in the 21st Century” »
Could researchers found the magic bullet for cancer? NIH thinks possibly that they have.
Epigenetic marks seen across multiple cancers may serve as a biomarker for identifying solid tumor DNA in blood samples.
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.
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?
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.
