Lifeboat Foundation

A miniature review of.

The risk of morbidity and mortality increases exponentially with age. Chronic inflammation, accumulation of DNA damage, dysfunctional mitochondria, and increased senescent cell load are factors contributing to this. Mechanistic investigations have revealed specific pathways and processes which, proposedly, cause age-related phenotypes such as frailty, reduced physical resilience, and multi-morbidity. Among promising treatments alleviating the consequences of aging are caloric restriction and pharmacologically targeting longevity pathways such as the mechanistic target of rapamycin (mTOR), sirtuins, and anti-apoptotic pathways in senescent cells. Regulation of these pathways and processes has revealed significant health-and lifespan extending results in animal models. Nevertheless, it remains unclear if similar results translate to humans. A requirement of translation are the development of age-and morbidity associated biomarkers as longitudinal trials are difficult and not feasible, practical, nor ethical when human life span is the endpoint. Current biomarkers and the results of anti-aging intervention studies in humans will be covered within this paper. The future of clinical trials targeting aging may be phase 2 and 3 studies with larger populations if safety and tolerability of investigated medication continues not to be a hurdle for further investigations.

As age increases, so does the susceptibility to a series of chronic diseases which ultimately result in fatal endings. This is such a basic part of life that we rarely consider if there is anything we can do to postpone it. So far, the principal of “one-disease-one-treatment” has brought medical sciences far but this line of thought may soon be outdated when it comes to aging related conditions. It is like fighting a many-headed monster: If one condition is treated successfully, another emerges shortly after. This point is illustrated as eradicating the two leading causes of death (cancer and cardiovascular disease) extends mean life span by 3.3 and 4 years, respectively (Arias et al., 2013). Interestingly, the gain of treating multiple diseases combined exceeds the sum of these numbers.

Continue reading “Clinical Trials Targeting Aging” »

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Levine’s Biological age calculator is embedded as an Excel file in this link from my website:
https://michaellustgarten.com/2019/09/09/quantifying-biological-age/

NOTE FROM TED: Research around aging discussed in this talk remains an ongoing field of study. Please do not look to this talk for health advice. TEDx events are independently organized by volunteers. The guidelines we give TEDx organizers are described in more detail here: http://storage.ted.com/tedx/manuals/tedx_content_guidelines.pdf.

Have you ever wondered how long you will live? And if so, how could you change that number to live drastically longer? The science might be in your favor: follow David Sinclair, Australian biologist and professor of genetics at Harvard University, as he shares his research on slowing and reversing the process of aging in mice, and how the same technology may someday be transferable to humans. David Sinclair, Australian biologist and professor of genetics at Harvard Universityhis insightful research into the science of age reversal and anti-aging medicine.

Continue reading “Is Aging Reversible? A Scientific Look with David Sinclair | David Sinclair | TEDxBoston” »

AI will completely take over game development by the early 2030s. To a point where there will be almost no human developers. Just people telling AI what they want to play and it builds it in real time.

Over the past few years we’ve seen massive improvements in AI technology, from GPT-3, AI picture generation to self-driving cars and drug discovery. But can machine learning progress change games?

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In the new field of quantum computing, magnetic interactions could play a role in relaying quantum information.

In new research, Argonne scientists achieved efficient quantum coupling between two distant magnetic devices, which which may be useful for creating new quantum information technology devices — https://bit.ly/3uk88Q3

They come in many colors: golden, solid onyx, or striped dandelion and cinnamon. Their eyes can be beady black, slate gray, or even bluish-green. Their bodies may be as small as lentils or big as wine grapes. But the most amazing thing about stingless bees are the honeys they produce, which are increasingly being sought after for food and medicine.

In the Peruvian Amazon, people are just beginning to raise a few of the area’s 175 different species of stingless bees, which promise to help beekeepers and their communities. Historically, such honey has typically been harvested from the wild, which destroys the hives.

But in the last few years, scientists including Cesar Delgado, with the Instituto de Investigaciones de la Amazonía Peruana (IIAP), are teaching people to raise and keep the insects in sustainable ways.

Current DNA computation techniques are slow in generating chemical outputs in response to chemical inputs and rely heavily on fluorescence readouts. Here, the authors introduce a new paradigm for DNA computation where the chemical input is processed and transduced into a mechanical output in the form of macroscopic locomotion using dynamic DNA-based motors.

There’s still a long way to go, but it’s an important milestone.

Ten years ago, solar and wind didn’t even make up 1% of our global energy mix. Now, in just a decade, they’ve reached 10%. It may not seem like much, but becoming such a significant part of the global energy mix in such a short time is remarkable — though there’s still a long way to go.

The past couple of years have been horrendous in more ways than one, but that doesn’t mean all is bad in the world. In fact, renewable energy continued its impressive growth, according to research from Ember, a climate and energy think tank.

Continue reading “Wind and solar energy amounted to 10% of the global energy consumption in 2021” »

a cardiac arrhythmia disorder associated with sudden death in young adults.

The findings expand possibilities for predictive risk scoring and provide new targets for therapeutic study, according to Alfred George, Jr., MD, chair and the Alfred Newton Richards Professor of Pharmacology and a co-author of the study.

“Prior to this work, there were only two genomic regions associated with Brugada syndrome risk that were identified by genome-wide studies. Data from the new study greatly expands this to 12 regions with a total of 21 genetic signals to better explain risk for Brugada syndrome,” George said. “The results also provide the basis for a polygenic risk score that can be used to assess risk in individuals.”