Scientists successfully extended the average lifespan of mice by breeding them using embryonic stem cells with extra-long telomeres. The findings are significant because the researchers managed to extend lifespan without genetic modification, and they also shed light on the aging process and techniques that might someday slow it.
The study — published October 17 in Nature Communications — focuses on telomeres, which are stretches of DNA found at the end of chromosomes.
Because telomeres protect the genetic material inside chromosomes, they’ve been likened to the plastic tips on the ends of shoelaces. But telomeres have also been compared to bomb fuses, or “molecular clocks,” because they become shorter each time a cell divides, eventually shrinking so much that the cell dies or stops dividing. This shortening of our telomeres is associated with aging, cancer, and death.
When the first smartphones arrived, few people understood how they would change our reality. Today, our internet-connected mobile device maps our travel, manages our finances, delivers our dinner, and connects us to every corner of human knowledge. In less than a generation, it has become almost an extension of our central nervous system — so indispensable that we can’t imagine leaving home without it to guide us.
We are about to embark on another journey even more important to every individual and to human society. We are entering the age of genomics, an amazing future that will dramatically improve the health outcomes of people across the planet. Soon, we won’t be able to imagine a time when we left home without knowledge of our genome to guide us.
But this future isn’t a generation away. As early as 2020, I believe we will be living in a world where software uses knowledge of our personal genome to guide us, like a health GPS, toward choices that are appropriate for us as individuals. From the foods we choose to eat to the medicines we take to prevent or cure disease, from helping us avoid exposure to environmental risks to eradicating thousands of genetic diseases, genomics will reveal such immense possibilities that it will feel as if we can see and hear for the first time.
Metabesity 2019: Epigenetic resetting of cellular age mediated by nuclear reprogramming – A new paradigm in overcoming aging and aging-associated diseases. Featuring Vittorio Sebastiano, PhD, Assistant Professor of Stanford University; Co-Founder of Turn Biotechnologies, USA
Researchers at the University of Dundee have made a discovery they believe has the potential to put the brakes on the ‘runaway train’ that is Parkinson’s disease.
The team, based at the Medical Research Council Protein Phosphorylation and Ubiquitylation Unit (MRC-PPU) in the School of Life Sciences, have discovered a new enzyme that inhibits the LRRK2 pathway. Mutations of the LRRK2 gene are the most common cause of genetic Parkinson’s.
Enzymes are molecular machines that regulate the biological processes required to maintain healthy functioning life. They can also be targeted by drugs to increase or decrease the level of certain activity –in this instance the LRRK2 pathway.
Unlike chemotherapy or radiation, which attack cancer directly, CAR-T engineers patients’ immune cells so they can do it themselves. T-cells are removed from the blood and given new genes that produce receptors that let the T-cells recognize and bind to leukemia cells with a specific protein, CD19.
The genetically modified T-cells are then multiplied in the lab and infused back into the patient, where they ideally multiply even further and begin to target and kill cancer cells with CD19.
“While researching epilepsy, neuroscientist Itzhak Fried stumbled on a ‘mirth’ center in the brain — given this, what ought we be doing to combat extreme suffering and promote wellbeing?”
David Pearce — The Anatomy of Happiness… While researching epilepsy, neuroscientist Itzhak Fried stumbled on a ‘mirth’ center in the brain — given this, what ought we be doing to combat extreme suffering and promote wellbeing?
If one finds oneself viscerally hostile to the idea of universal happiness, and if by contemporary standards one falls within the statistically normal range in one’s emotional repertoire, then just how seriously should one contemplate the following possibility? Today we are the victims of what our successors will reckon an atavistic mood disorder. This disorder infects all our thoughts as well as all our feelings and volitions. It is a historical condition no less epistemically defective than are dream-psychoses from the perspective of the waking state.
Is the worry one might be locked in such an affective psychosis just the product of idle scepticism? Given the cognitive inaccessibility of most of the generically ecstatic states alluded to here, perhaps one wouldn’t know if one were so afflicted. After all, damaged and disfigured minds may have limited self-insight. Nor would one necessarily have the conceptual resources even to grasp what was at stake if one suffered from such a neural deficit. Pure, “unearned”, genetically-driven bliss of even the mildest flavour detracted from the inclusive fitness of one’s genes in the ancestral environment. Constitutionally happy freaks-of-nature got eaten or outbred. Hence unipolar euphoric mania today is vanishingly rare; unipolar melancholic depression and chronic dysthymia are all too common. Is one’s potential unease, if not revulsion, at the prospect of paradise-on-earth an incidental cultural by-product of natural selection? Or has selection pressure ensured that one is genetically predisposed to be biased against the idea of enduring bliss in the first instance?
This is a clip from a conversation with Michio Kaku from Oct 2019. New full episodes once or twice a week and 1–2 new clips or a new non-podcast video on all other days. You can watch the full conversation here: https://www.youtube.com/watch?v=kD5yc1LQrpQ (more links below)
A pair of new studies report “impressive” benefits from a drug therapy for cystic fibrosis, a deadly and devastating disease that affects tens of thousands of people worldwide, the director of the National Institutes of Health wrote in an editorial published in The New England Journal of Medicine on Thursday.
“These findings indicate that it may soon be possible to offer safe and effective molecularly targeted therapies to 90 percent of persons with cystic fibrosis,” wrote the director, Dr. Francis S. Collins, who led the team that in 1989 identified the gene that causes the genetic disease affecting the lungs and digestive system.
“This should be a cause for major celebration,” he wrote in the Thursday editorial.
Bacteria living in people’s intestines pump out toxins to deter microbial intruders. But each person’s gut comes with its own set of toxins—an individualized “passcode” microbes must solve to survive, scientists report October 30, 2019, in the journal Nature.
The findings suggest that there’s not a one-size-fits-all approach to probiotics or live biotherapeutics, the microbial supplements that promote the growth of healthy bacteria, says study coauthor Joseph Mougous, a Howard Hughes Medical Institute (HHMI) Investigator at the University of Washington (UW). His team’s work is an early step toward figuring out how scientists might instead tailor beneficial microbes to different people.
At the University of Copenhagen, researchers have discovered how some types of proteins stabilize damaged DNA and thereby preserve DNA function and integrity. This new finding also explains why people with inborn or acquired defects in certain proteins cannot keep their DNA stable and develop diseases such as cancer.
Every day, the body’s cells divide millions of times, and the maintenance of their identity requires that a mother cell passes complete genetic information to daughter cells without mistakes.
This is not a small task because our DNA is constantly under attack, both from the environment but also from the cell’s own metabolic activities. As a result, DNA strands can be broken at least once during each cell division cycle and this frequency can increase by certain lifestyles, such as smoking, or in individuals who are born with defects in DNA repair.
