Lifeboat Foundation

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Can the aging process be reversed — or even halted, altogether? If we manage to decode this final mystery of our human biology, we might soon be able to eradicate age-related illnesses like cancer, dementia and heart problems.

Continue reading “More life — Decoding the secret of aging | DW Documentary” »

Epigenetic clocks can measure biological aging, but the relationship between epigenetic age and other hallmarks of aging is incompletely understood. Here the authors show that epigenetic age is associated with nutrient sensing, mitochondria activity and stem cell depletion but distinct from cellular senescence, telomere attrition and genomic instability.

Scientists have long known that touching plants can set off a stress reaction in them – but until now it hasn’t been exactly clear how that worked at a molecular level, something that a new study hopes to shed light on.

The researchers behind the study have identified certain genetic keys inside plants that lead to two separate signaling pathways, explaining why plants react so strongly to being touched.

Understanding more about how this process works at a fundamental level could help researchers in a variety of different areas, from improving plant health to getting higher harvest yields from the same crop.

Can quantum science supercharge genetics? | Jim Al-Khalili for Big Think.

This interview is an episode from The Well, our new publication about ideas that inspire a life well-lived, created with the John Templeton Foundation.

Continue reading “What if quantum physics could eradicate illness? | Jim Al-Khalili for Big Think” »

Stuart Firestein Science is a fundamentally optimistic enterprise. More than a cheery disposition, it is the source of a philosophical outlook that we might call ‘optimistical’. It reliably produces fundamental and actionable knowledge about the world. We are able to take for granted, in a way even our recent ancestors never imagined, the idea of progress. The engines behind science, surprisingly, are ignorance, the unknown, failure, and, perhaps most vexingly, uncertainty. In recent decades, science has undergone a change in perspective and practice — from viewing the universe like a clockwork regimented by laws and formulas to recognizing it as irreducibly complex and uncertain. Perhaps counter intuitively this has freed science to exploit previously unimaginable possibilities and opportunities. It has led to a deeper understanding of the nature of things and to the production of technologies such as lasers, microchips, the internet, genetics, and many more. And yet socially and societally we remain mired in a 19th century view of deterministic science. We might instead learn to revel in the adventure of navigable uncertainty and take advantage of the creative opportunities of a world where we can confidently say ‘it could be otherwise’. Possibility of this sort is the rarest and purest form of optimism. Stuart Firestein is a neuroscientist and the former Chair of Columbia University’s Department of Biological Sciences, where he researches the vertebrate olfactory system. He is also a member of SFI’s Fractal Faculty.

Most people carry the fungus Candida albicans on their bodies without it causing many problems. However, a systemic infection with this fungus is dangerous and difficult to treat. Few antimicrobials are effective, and drug resistance is increasing. An international group of scientists, including Albert Guskov, associate professor at the University of Groningen, have used single-particle cryogenic electron microscopy to determine the structure of the fungal ribosome. Their results, which were published in Science Advances on 25 May, reveal a potential target for new drugs.

Candida albicans usually causes no problems, or just an itchy skin infection that is easily treated. However, in rare cases, it may cause systemic infections that can be fatal. Existing antifungal drugs cause a lot of side effects and are expensive. Furthermore, C. albicans is becoming more drug-resistant, so there is a real need for new drug targets. “We noted that no antifungal drugs are targeting protein synthesis, while half of the antibacterial drugs interfere with this system,” says Guskov. A reason for this is that fungal ribosomes, the cellular machineries that translate the genetic code into proteins, are very similar in humans and fungi. “So, you would need a very selective drug to avoid killing our own cells.”

An experimental cancer-killing virus has been administered to a human patient for the first time, with hopes the testing will ultimately reveal evidence of a new means of successfully fighting cancer tumors in people’s bodies.

The drug candidate, called CF33-hNIS (aka Vaxinia), is what’s called an oncolytic virus, a genetically modified virus designed to selectively infect and kill cancer cells while sparing healthy ones.

In the case of CF33-hNIS, the modified pox virus works by entering cells and duplicating itself. Eventually, the infected cell bursts, releasing thousands of new virus particles that act as antigens, stimulating the immune system to attack nearby cancer cells.

Staphylococcus aureus infections can be highly unpredictable – some cause a slight rash, whereas others can lead to deadly complications – and researchers have identified a genetic mutation that could be the cause of these differences.

A mechanism that causes autism, schizophrenia, Alzheimer’s and other conditions and is shared by mutations in the genes ADNP and SHANK3 has been unraveled by Tel Aviv University researchers who developed an experimental drug they found to be effective in animal models.

The drug could also be suitable for treating a range of rare syndromes that impair brain functions, said the scientists. The researchers were led by Prof. Illana Gozes from the Department of Human Molecular Genetics and Biochemistry at TAU’s Sackler Faculty of Medicine and the Sagol School of Neuroscience. The experimental drug, called Davunetide, had previously been developed in her lab.

The paper, which the team called a “scientific breakthrough,” was published in the scientific journal Molecular Psychiatry under the title “SH3-and actin-binding domains connect ADNP and SHANK3, revealing a fundamental shared mechanism underlying autism.”