Lifeboat Foundation

Nicola Bagalà and Michael Nuschke take a look at the future of pensions and how the possible defeat of age-related diseases will affect them.

If you work in social security, it’s possible that your nightmares are full of undying elderly people who keep knocking on your door for pensions that you have no way of paying out. Tossing and turning in your bed, you beg for mercy, explaining that there’s just too many old people who need pensions and not enough young people who could cover for it with their contributions; the money’s just not there to sustain a social security system that, when it was conceived in the mid-1930s, didn’t expect that many people would ever make it into their 80s and 90s. Your oneiric persecutors won’t listen: they gave the country the best years of their lives, and now it’s time for the country to pay them their due.

When you wake up, you’re relieved to realize that there can’t be any such thing as people who have ever-worsening degenerative diseases yet never die from them, but that doesn’t make your problem all that better; you still have quite a few old people, living longer than the pension system had anticipated, to pay pensions to, and the bad news is that in as little as about 30 years, the number of 65+ people worldwide will skyrocket to around 2.1 billion, growing faster than all younger groups put together [1]. Where in the world is your institution going to find the budget?

Continue reading “The Future of Pensions” »

But they don’t. Instead, they are less likely to develop or die of this enigmatic disease. The same is true of elephants and dinosaurs’ living relatives, birds. Marc Tollis, an assistant professor in the School of Informatics, Computing, and Cyber Systems at Northern Arizona University, wants to know why.

Tollis led a team of scientists from Arizona State University, the University of Groningen in the Netherlands, the Center for Coastal Studies in Massachusetts and nine other institutions worldwide to study potential cancer suppression mechanisms in cetaceans, the mammalian group that includes whales, dolphins and porpoises. Their findings, which picked apart the genome of the humpback whale, as well as the genomes of nine other cetaceans, in order to determine how their cancer defenses are so effective, were published today in Molecular Biology and Evolution.

The study is the first major contribution from the newly formed Arizona Cancer and Evolution Center or ACE, directed by Carlo Maley under an $8.5 million award from the National Cancer Institute. Maley, an evolutionary biologist, is a researcher at ASU’s Biodesign Virginia G. Piper Center for Personalized Diagnostics and professor in the School of Life Sciences. He is a senior co-author of the new study.

Continue reading “How whales defy the cancer odds: Good genes” »

In a medical first, the children were treated with genetically engineered T-cells from another person.

There’s no doubt that genetic therapy won’t be cheap.

Entrepreneurs are taking genetic-editing technology from the lab to the clinic with grand ambitions. But who owns the patents?

Center Stage in the current issue of ACS Central Science: A Conversation with Prof. Jackie Ying, founding director of the A*STAR Institute NanoBio lab in Singapore. Using #nanomaterials to develop inexpensive medical technologies:

The consortium, called LifeTime, aims to use three emerging technologies—machine learning, the study of single cells, and lab-grown organlike tissues called organoids—to map how human cells change over time and develop diseases. It is one of six candidates in the latest round of ambitious proposals for European flagships, billion-euro research projects intended to run for 10 years. There is just one snag: The European Commission has decided that it won’t launch any of them.

Six candidate research proposals lost in limbo.

On senescent cells, mechanism of interaction and (potential?!) side effects of NAD+ supplements. “… Those people self-experimenting with NAD+ precursor supplementation should consider keeping a close eye on markers of inflammation…”

Enhancing levels of NAD+ in mitochondria via delivery of various precursor compounds as supplements is growing in popularity as an approach to boost faltering mitochondrial function and thus modestly slow the progression of aging. A human trial demonstrated improved vascular function as a result of nicotinamide riboside supplementation, for example. Researchers here show that increased NAD+ will likely make worse the inflammatory signaling of senescent cells, however. Senescent cells accumulate with age, and are an important cause of the chronic inflammation of aging that drives the progression of many age-related diseases.

The results here suggest that efficient senolytic treatments to selectively destroy senescent cells should proceed any of the current approaches to raising levels of NAD+ in older individuals — and it is an open question as to whether any of the existing available options are efficient enough to make NAD+ enhancement safe in the longer term. Those people self-experimenting with NAD+ precursor supplementation should consider keeping a close eye on markers of inflammation.

May have posted this, but this is very cool. “We can now generate insulin-producing cells that look and act a lot like the pancreatic beta cells you and I have in our bodies,” explains one of the team, microphysiologist Matthias Hebrok from the University of California San Francisco (UCSF).

Although treatment of type 1 diabetes has come a long way since it was first described in Ancient Egypt, insulin injections and finger pricks are a daily part of life for many diabetics.

But researchers have just made a breakthrough that might one day make these technologies obsolete, by transforming human stem cells into functional insulin-producing cells (also known as beta cells) – at least in mice.

Continue reading “For The First Time, Scientists Turn Human Stem Cells Into Insulin-Producing Cells” »