Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 77

I’m excited to share my latest Opinion article on AI at The Hill, a top political site/paper read by the White House and Congress:

Regardless what politicians promise, this age of AI and robots will also affect the size and growth rates of the U.S. government. Federal and state government may not immediately take up with automation and AI to the extent the private sector does, but eventually the stark rationality of lower overhead expenses—and thus lower taxes for citizens—will prevail.

This is a good thing. A smaller, nimble, more efficient government will benefit the majority of people.

Zoltan Istvan writes and speaks on transhumanism, artificial intelligence, and the future. He is the author of “The Transhumanist Wager,” and is the subject of the forthcoming biography by Dr. Ben Murnane and Changemakers Books titled, “Transhuman Citizen: Zoltan Istvan’s Hunt for Immortality.”

Continue reading “AI can stop government from growing, and that’s a good thing” | >

A study at the University of Cologne’s CECAD Cluster of Excellence in Aging Research has identified a protein complex that is activated by defects in the spliceosome, the molecular scissors that process genetic information. Future research could lead to new therapeutic approaches to treat diseases caused by faulty splicing.

The genetic material, in the form of DNA, contains the information that is crucial for the correct functioning of every human and animal cell. From this information repository, RNA, an intermediate between DNA and protein, the functional unit of the cell, is generated. During this process, the must be tailored for specific cell functions. Information that is not needed (introns) is cut out of the RNA and the important components for proteins (exons) are preserved.

A team of researchers led by Professor Dr. Mirka Uhlirova at the University of Cologne’s CECAD Cluster of Excellence in Aging Research has now discovered that if the processing of this information no longer works properly, a (C/EBP heterodimer) is activated and directs the cell towards a dormant state, known as . The results appear under the title “Xrp1 governs the stress response program to spliceosome dysfunction” in Nucleic Acids Research.

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A preventative anti-aging therapy seems like wishful thinking.

Yet a new study led by Dr. Corina Amor Vegas at Cold Spring Harbor Laboratory describes a treatment that brings the dream to life—at least for mice. Given a single injection in young adulthood, they aged more slowly compared to their peers.

By the equivalent of roughly 65 years of age in humans, the mice were slimmer, could better regulate blood sugar and insulin levels, and had lower inflammation and a more youthful metabolic profile. They even kept up their love for running, whereas untreated seniors turned into couch potatoes.

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Ageing, as you might expect, had a big impact on participants’ feelings of loneliness. The deaths of partners and loved ones was particularly difficult, while participants also commented on how loss of mobility restricted their social activities. Social skills were also identified as a risk factor: one participant noted that those without strong social skills may be more likely to suffer.

Emotionally, loneliness was (unsurprisingly) connected to feelings of emptiness, sadness and lack of meaning. One participant described herself as feeling “lost… and not having control, and sometimes it can lead you to not be able to make decisions and then it just gets worse”, whilst another described loneliness as “the feeling of nothing”

But many participants also commented on strategies they used to protect against loneliness. Though ageing was a risk factor, acceptance of ageing had more positive outcomes. As one participant put it: “I used to mountain climb… If I can’t walk anymore, I’ll crawl. You have to learn how to be realistic and not brood about it. I know I’m getting older, but I consider life a transition.” Compassion was also useful: being proactive about helping others, for example, helped some participants prevent being lonely.

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More deathism from Mr Tyson. Really I’m a big fan but I dislike this sort of thinking. I commented on the vid.

What if we could live forever? Neil deGrasse Tyson takes us through life and death: if we could live forever what would life really mean? We explore why fresh flowers have meaning and why dogs make every day count. Learn about the Cretaceous-Tertiary Event, The Permian-Triassic Extinction, The Holocene Epoc, and how Earth is one killing machine.

Get the NEW StarTalk book, ‘To Infinity and Beyond: A Journey of Cosmic Discovery’ on Amazon: https://amzn.to/3PL0NFn.

Continue reading “Would We Want to Live Forever?” | >

Scientists have discovered a mechanism that lets senescent tumor cells undermine chemotherapy. With this mechanism blocked, standard chemotherapy led to complete regression of mammary tumors in mice [1].

Senescent yet still dangerous

Chemotherapy and radiation therapy, still the two most common treatments for solid tumors, subject cells to powerful stress as they are designed to do. This stress drives cellular senescence. Since senescent cells stop proliferating, inducing senescence in cancer cells is considered a desirable outcome. However, this is not the end of the story.

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Acetamiprid-induced oxidative stress can harm DNA and tRNA, leading to health problems. A study conducted by Huixia Zhang at Macau University of Science and Technology in 2023 introduced a comprehensive approach to assessing acetamiprid-induced oxidative damage to tRNA in human cells through oxidized nucleotide and tRNA profiling. Acetamiprid, a modern insecticide, is known for causing oxidative stress and related toxicity. Despite its impact on oxidative stress, the effects of acetamiprid-induced oxidative stress on RNA, especially tRNA, remained unexplored until this study.

Acetamiprid was found to elevate reactive oxygen species (ROS) production in HepG2 and LO2 cells, contributing to mitochondrial damage, free radical generation, and antioxidant status depletion. Oxidative damage to DNA and RNA can harm organisms, with prior research addressing RNA damage in aging, neurodegenerative diseases, and mental illnesses. However, its role in acetamiprid-induced toxicities has not been investigated.

The study employed TMSD labeling-based LC-MS/MS to measure oxidized nucleotide levels in HepG2 and LO2 cells treated with two mM acetamiprid. It also examined the impact of acetamiprid on the 8-oxo-G content of tRNAs and created volcano plots to compare RNase T1 digestion products of tRNAs from untreated and acetamiprid-treated cells.

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