Lifeboat Foundation: Safeguarding Humanity
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NaNotics, in another breakthrough, is promising a new kind of medication, and suggests to have found a way to combat age related diseases; boldly going where no nanotech has gone before.

Lou Hawthorne of NaNotics, LLC opened his presentation at a recent longevity investor event using a clip from Star Trek that shows captain Kirk being giving a shot that restores him to his younger years.

“It’s tempting to assume it’s a drug, but what if the content of that syringe was something new?” NaNotics’ CEO Hawthorne asked. “NaNots are a new class of medicine. They are engineered to do just one thing and that’s the holy grail of medicine design, because most drugs do two things: something you want them to do, and something you don’t. In other words, side effects.”

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The relationship between health and the microorganisms living in the gut has increasingly reached the spotlight in the last few years, and a new study led by researchers at Nanyang Technological University, Singapore (NTU Singapore) sheds more light on the gut microbiome and how it can influence aging.

The gut microbiome

The gut microbiome is a complex ecosystem that includes a varied community of bacteria, archaea, eukarya, and viruses that inhabit our guts. The four bacterial phyla of Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria comprise 98% of the intestinal microbiome.

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ERCC1 (excision repair cross complementing‐group 1) is a mammalian endonuclease that incises the damaged strand of DNA during nucleotide excision repair and interstrand cross‐link repair. Ercc1−/Δ mice, carrying one null and one hypomorphic Ercc1 allele, have been widely used to study aging due to accelerated aging phenotypes in numerous organs and their shortened lifespan. Ercc1−/Δ mice display combined features of human progeroid and cancer‐prone syndromes. Although several studies report cellular senescence and apoptosis associated with the premature aging of Ercc1−/Δ mice, the link between these two processes and their physiological relevance in the phenotypes of Ercc1−/Δ mice are incompletely understood. Here, we show that ERCC1 depletion, both in cultured human fibroblasts and the skin of Ercc1−/Δ mice, initially induces cellular senescence and, importantly, increased expression of several SASP (senescence‐associated secretory phenotype) factors. Cellular senescence induced by ERCC1 deficiency was dependent on activity of the p53 tumor‐suppressor protein. In turn, TNFα secreted by senescent cells induced apoptosis, not only in neighboring ERCC1‐deficient nonsenescent cells, but also cell autonomously in the senescent cells themselves. In addition, expression of the stem cell markers p63 and Lgr6 was significantly decreased in Ercc1−/Δ mouse skin, where the apoptotic cells are localized, compared to age‐matched wild‐type skin, possibly due to the apoptosis of stem cells. These data suggest that ERCC1‐depleted cells become susceptible to apoptosis via TNFα secreted from neighboring senescent cells. We speculate that parts of the premature aging phenotypes and shortened health‐ or lifespan may be due to stem cell depletion through apoptosis promoted by senescent cells.

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Last week, the transhumanist activist Zoltan Istvan announced his candidacy for President of the United States in next year’s elections. The writer, humanitarian and outspoken advocate of radical science is no stranger to the issues surrounding Longevity, and has spoken widely on subjects including AI, genetic editing, technology policy, and futurism.

In 2016, Istvan ran as an independent presidential candidate and travelled across the United States, spreading his message from a coffin-shaped bus, known as the “Immortality Bus.” This time he’s on the ballot, running against Donald Trump as a candidate for the Republican party in next year’s primaries. Things are a bit more serious this time.

Among his key policies, Istvan includes transhumanism, universal basic income and the need to beat China in the global innovation race – an issue we addressed in our Jamie Metzl interview. We spoke to him to find out more about his views on the Longevity sector.

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A team from Cincinnati Children’s Hospital tracked stem cells injected into the hearts of mice, and what they found could explain why clinical trials testing stem cell therapies in people with heart disease have been unsuccessful. They believe a smarter approach could be to harness the power of macrophages that provide healing in response to inflammation.

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Doctors at Duke University Medical Center this month “reanimated” a heart for a first-of-its-kind transplant performed on an adult in the United States.

Heart transplants typically come from donations after brain death, in which the still-beating heart of a person who has been declared brain dead is transplanted into a recipient. The approach used at Duke is known as a donation after circulatory death (DCD), and it relies on hearts that have stopped beating and are essentially reanimated and begin beating again.

The TransMedics Organ Care System, a warm perfusion pump, allows doctors to resuscitate and preserve hearts for transplantation. The system was used for the adult donation after circulatory death transplant at Duke University Medical Center, one of five centers in the United States approved by the US Food and Drug Administration for clinical trials of the TransMedics system.

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Drugs that tamp down inflammation in the brain could slow or even reverse the cognitive decline that comes with age.

University of California, Berkeley, and Ben-Gurion University scientists report that senile mice given one such drug had fewer signs of brain inflammation and were better able to learn new tasks, becoming almost as adept as mice half their age.

“We tend to think about the aged brain in the same way we think about neurodegeneration: Age involves loss of function and dead cells. But our new data tell a different story about why the aged brain is not functioning well: It is because of this “fog” of inflammatory load,” said Daniela Kaufer, a UC Berkeley professor of integrative biology and a senior author, along with Alon Friedman of Ben-Gurion University of the Negev in Israel and Dalhousie University in Canada. “But when you remove that inflammatory fog, within days the aged brain acts like a young brain. It is a really, really optimistic finding, in terms of the capacity for plasticity that exists in the brain. We can reverse brain aging.”

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