Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

Dr. Shigeaki Hinohara had an extraordinary life for many reasons. For starters, the Japanese physician and longevity expert lived until the age of 105.

When he died, in 2017, Hinohara was chairman emeritus of St. Luke’s International University and honorary president of St. Luke’s International Hospital, both in Tokyo.

Perhaps best known for his book, “Living Long, Living Good,” Hinohara offered advice that helped make Japan the world leader in longevity. Some were fairly intuitive points, while others were less obvious:

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The plastic tips attached to the ends of shoelaces keep them from fraying. Telomeres are repetitive DNA (deoxyribonucleic acid) sequences that serve a similar function at the end of chromosomes, protecting its accompanying genetic material against genome instability, preventing cancers and regulating the aging process.

Each time a in our body, the telomeres shorten, thus functioning like a molecular “clock” of the cell as the shortening increases progressively with aging. An accurate measure of the quantity and length of these telomeres, or “clocks,” can provide vital information if a cell is aging normally, or abnormally, as in the case of cancer.

To come up with an innovative way to diagnose telomere abnormalities, a research team led by Assistant Professor Cheow Lih Feng from the NUS Institute for Health Innovation & Technology (iHealthtech) has developed a novel method to measure the absolute telomere length of individual telomeres in less than three hours. This unique telomere profiling method can process up to 48 samples from low amounts (1 ng) of DNA.

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Our muscles start to shrink and weaken when we reach our 50s and 60s in a process called sarcopenia, but new research in mice from the University of Michigan offers new insights into why this loss may occur, and how we might begin to prevent it.

Sarcopenia is the progressive loss of mass in aging, and it’s linked to other age-related pathologies such as osteoarthritis, cardiovascular disease and cancer, as well as an overall reduction in function and independence.

The research, led by Carlos Aguilar, a U-M assistant professor of biomedical engineering, focused on since they are dedicated solely to keeping muscles healthy. And to better understand stem cell function during aging, testing was conducted on two sets of mice, one “young” and one “old,” before and after muscle injury.

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As best we can guess, life started on planet Earth about 3.5 billion years ago. Unfortunately, so did death. And the reaper remains undefeated.

About 99 percent of all species that ever lived are now extinct. There’s almost no scientific reason to believe humans won’t join them in a relatively insignificant amount of time. I say almost because, if we try really hard, we can conceive of a theoretical, science-based intervention for death. Let’s call it a “quantum respawn.”

We’re not the first generation to imagine immortality. But we are the first one to have access to this really cool research paper from physicists working at the University of Rochester in New York, and Purdue University in Indiana.

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Salk Institute scientists have harnessed stem cell technology to generate the first human insulin-producing pancreatic cell clusters that can evade the immune system. Generated from induced pluripotent stem cells (iPSCs), these “immune shielded” human islet-like organoids (HILOs) controlled blood glucose following transplantation into a mouse model of diabetes, without the use of immunosuppressive drugs. The researchers suggest the achievement represents a major advance in the quest for a safe and effective treatment for type 1 diabetes (T1D), which impacts an estimated 1.6 million people in the United States, at a cost of $14.4 billion annually.

“Most type 1 diabetics are children and teenagers,” said Salk professor Ronald Evans, PhD, holder of the March of Dimes chair in molecular and developmental biology. Evans is senior author of the team’s paper, which is published in Nature. “This is a disease that is historically hard to manage with drugs. We hope that regenerative medicine in combination with immune shielding can make a real difference in the field by replacing damaged cells with lab-generated human islet-like cell clusters that produce normal amounts of insulin on demand.”

Evans and colleagues reported on their development in a paper titled, “Immune-evasive human islet-like organoids ameliorate diabetes.”

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We are witnessing the birth of a new faith. It is not a theistic religion. Indeed, unlike Christianity, Judaism, and Islam, it replaces a personal relationship with a transcendent God in the context of a body of believers with a fervent and radically individualistic embrace of naked materialistic personal recreation.

Moreover, in contrast to the orthodox Christian, Judaic, and Islamic certainty that human beings are made up of both material body and immaterial soul – and that both matter – adherents of the new faith understand that we have a body, but what really counts is mind, which is ultimately reducible to mere chemical and electrical exchanges. Indeed, contrary to Christianity’s view of an existing Heaven or, say, Buddhism’s conception of the world as illusion, the new faith insists that the physical is all that has been, is, or ever will be.

Such thinking leads to nihilism. That’s where the new religion leaves past materialistic philosophies behind, by offering adherents hope. Where traditional theism promises personal salvation, the new faith offers the prospect of rescue via radical life-extension attained by technological applications – a postmodern twist, if you will, on faith’s promise of eternal life. This new religion is known as “transhumanism,” and it is all the rage among the Silicon Valley nouveau riche, university philosophers, and among bioethicists and futurists seeking the comforts and benefits of faith without the concomitant responsibilities of following dogma, asking for forgiveness, or atoning for sin – a foreign concept to transhumanists. Truly, transhumanism is a religion for our postmodern times.

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“Using microfluidics, computer modeling and other techniques, they found that about half of the cells age through a gradual decline in the stability of the nucleolus, a region of nuclear DNA where key components of protein-producing “factories” are synthesized,” a press release announcing the research explains. “In contrast, the other half age due to dysfunction of their mitochondria, the energy production units of cells.”

Researchers studying aging have discovered that cells tend to follow one of two aging pathways. The way each individual cell ages is determined early on, and scientists can predict how a cell will age based on early observations.

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If you eschew hyperbole and hang in for the long haul, maintaining a discipline of understatement in the midst of a flashy neon world, you may be offered a modicum of credence when you make an extraordinary announcement. No one is entitled to this courtesy twice. If the news that you trumpet to the moon does not pan out, your readers will be justified in discounting everything you say thereafter.

Here goes.

I believe major rejuvenation has been achieved in a mammal, using a relatively benign intervention that shows promise of scaling up to humans. I’m going to stake my reputation on it.

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How we adapt to aging late in life may be genetically influenced, according to a study led by a psychologist at the University of California, Riverside.

The research, published in Aging Cell, has implications for how relate to aging. Epigenesis is a process in which chemicals attached to DNA control its activity. Epigenetic changes, which can be passed on to offspring, may be critical to accelerated aging as well as declines in cognitive and physical functioning that often accompany aging. Epigenetic modifications resulting in altered may occur due to a number of biological processes, including one the researchers focused on: DNA methylation.

In DNA methylation, groups are added to the DNA molecule. DNA has four different types of nucleotides: A, T, G, and C. DNA methylation occurs at the C bases of eukaryotic DNA. Changes in DNA methylation correlate strongly with aging.

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