Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 483

Even with an increasing number of articles about aging and rejuvenation technologies in mass media, the general public’s lack of information remains a problem. Pro-longevity organizations try to spread useful information; however, it’s clear that this information is, quite often, only delivered to current members of the community instead of to a new audience. My work at LEAF is partially focused on finding ways to break this border and explore new social territories as often as possible. Last week, this journey brought me to a meeting with a title that speaks for itself: Death Cafe.

What is Death Cafe?

A Death Cafe is not a place. It is a meeting at which people are encouraged to discuss everything related to death over a cup of tea. The official mission of this community is defined as follows: “Our objective is to increase awareness of death with a view to helping people make the most of their (finite) lives.” It is not a form of group therapy, not a support group or a survivors’ group (though only the living can attend…); rather, it’s just a space where people can talk to each other about a topic that is usually excluded from public dialogue.

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A recent open-access mouse study published by Xi’an Institute of Tissue Engineering and Regenerative Medicine scientists in the journal Bone Research describes how the ALPL gene affects bone aging and suggests that metformin might constitute a viable therapeutic option to prevent it [1].

Study abstract

Mutations in the liver/bone/kidney alkaline phosphatase (Alpl) gene cause hypophosphatasia (HPP) and early-onset bone dysplasia, suggesting that this gene is a key factor in human bone development. However, how and where Alpl acts in bone ageing is largely unknown. Here, we determined that ablation of Alpl induces prototypical premature bone ageing characteristics, including bone mass loss and marrow fat gain coupled with elevated expression of p16INK4A (p16) and p53 due to senescence and impaired differentiation in mesenchymal stem cells (MSCs). Mechanistically, Alpl deficiency in MSCs enhances ATP release and reduces ATP hydrolysis. Then, the excessive extracellular ATP is, in turn, internalized by MSCs and causes an elevation in the intracellular ATP level, which consequently inactivates the AMPKα pathway and contributes to the cell fate switch of MSCs.

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The Imagine Science Films Festival is happening on October 12-19th, 2018 in New York, at a variety of venues, and this year, it is featuring a theme close to home: survival.

Crisis. Entropy. Extinction. This year we look at the high stakes for all life on Earth and beyond. Between nuclear proliferation, species loss and dwindling resources, existence itself is not assured. But for every dystopia, a corresponding utopia may be within reach. It may be a struggle, but the record of all life is that of an eon-spanning fight to stay alive. We’ll feature tumultuous natural history and startling feats of adaptation. Apoptosis versus immortal cell lines. Half-lives and radical life extension. The deaths of stars and extraordinary paths to SURVIVAL.

With this year’s theme including life extension, we may well see some interesting and thought-provoking films on the topic. Lifespan.io is also an official event sponsor for the festival, as we strongly feel that the worlds of filmmaking and science can be a perfect match in helping to encourage a wider dialogue about aging and doing something about it.

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Today, we have an interview with Dr. Michael Bonkowski, an expert on NAD+ biology and aging from the David Sinclair Lab, Harvard Medical School.

Michael Bonkowski aims to advance our understanding of the links between metabolism, aging, and age-associated diseases. He has published 35 peer-reviewed journal articles and has conducted multiple successful longevity studies. In Dr. David Sinclair’s lab, his research efforts are focused on the role of nutrient sensors’ regulation of endocrine signaling and aging in the mouse. He is also working on direct and indirect ways to drive the activity of these nutrient sensors by using dietary manipulations, small molecules, and chemical treatments.

Michael is trained as a pharmacologist, physiologist, and animal scientist. Some of his areas of expertise include animal physiology, genetics, glucose, and insulin homeostasis, metabolism, assay development, protein biochemistry, and transmission electron microscopy imaging.

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A duty to die at 75 by law?! No need to cure one disease because anyway you will die from another after 65?! A new article uncovers the dangers of going to ‘healthy’ and not longer lifespan:

2) A duty to die becomes greater as you grow older. As we age, we will be giving up less by giving up our lives, if only because we will sacrifice fewer remaining years of life and a smaller portion of our life plans… To have reached the age of, say, seventy-five or eighty years without being ready to die is itself a moral failing, the sign of a life out of touch with life’s basic realities.

3) A duty to die is more likely when you have already lived a full and rich life. You have already had a full share of the good things life offers.

Most bioethicists who denigrate the equal importance of the lives of the elderly and/or who promote age-based health-care-rationing schemes are not as explicit or impolitic in their advocacy as Hardwig. But changing the “primary goal of medicine” to “healthspan” — if involuntary or based on policy — would come perilously close to justifying that same utilitarian end.

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https://youtu.be/FxmAeh7mIRk

DONATE TO CAMPAIGN ► https://goo.gl/kfGdnh
Original Video ► https://goo.gl/YrjnLa

Website ► https://www.lifespan.io/

“Conquering the negative effects of aging is one of the oldest dreams of humanity, and now through the steady progress of science, we are poised to fulfill that dream.

Whether this occurs in 20 years or 200 is largely a question of funding. The best way to accelerate this process is by mobilizing those who desire the option of a longer and healthier life into a cohesive social force — crowdfunding relevant research and advocating for its benefits to society.

On lifespan.io researchers post projects related to longevity or age related disease, and receive funds from contributors to fulfill their goals. Contributors, in turn, are able to exercise agency in the development of potentially life changing research, as well as receiving rewards specified by the project creators.” “Keith Comito is a computer programmer and mathematician whose work brings together a variety of disciplines to provoke thought and promote social change. He has created video games, bioinformatics programs, musical applications, and biotechnology projects featured in Forbes and NPR. In addition to developing high-profile mobile applications, he explores the intersection of technology and biology at the Brooklyn community lab Genspace, where he helped to create games which allow players to direct the motion of microscopic organisms. He earned a B.S. in Mathematics, B.S. in Computer science, and M.S. in Applied Mathematics at Hofstra University, where his work included analysis of the LMNA protein.”

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Continue reading “David Sinclair — Can NMN Reverse Aging?” | >

Why aging isn’t a way out if you’re tired of living…

Suppose that, at a point, you get completely, irreparably tired of life and want to die. In these circumstances, how willing would you be to bear with around twenty more years of the same life that you can’t stand any more, particularly in a state of declining health? It would seem more reasonable that if you are tired of life right now and you are absolutely certain that you will not change your mind, you would rather end your life at once than wait for two more, increasingly miserable, decades. Yet, there is a certain narrative suggesting that the decay of old age, which inevitably leads to death, is an acceptable option for people who are sure that they are through with life.

Warning: spoilers

In a moment, I will be revealing the ending of a recent podcast titled “The 200-year-old”—an interesting and, all-in-all, rejuvenation-friendly series. It is only four episodes long, and if you haven’t listened to it yet, I would say that it is worth your time. If you wish to do so, stop reading right now to avoid spoilers. (Do come back to finish the article once you’re done with the podcast, though.)

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Today, we would like to share a talk given by Stephen Hilbert, President of Oisin Biotechnologies, in which he discusses treating aging and cancer by removing harmful senescent cells.

On July 12th, we hosted our first conference, Ending Age-Related Diseases: Investment Prospects & Advances in Research, at the Frederick P. Rose Auditorium, which is part of the Cooper Union campus in New York City. The packed event saw a range of people from research, investment, and the wider community coming together for a day of science and biotech business presentations and panels.

One of the companies at the event was Oisin Biotechnologies, a company working on therapies that remove harmful senescent cells, which accumulate as we age and drive aging processes through the senescence-associated secretory phenotype (SASP), which leads to chronic inflammation.

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