Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 169

UC San Diego researchers have identified a new inflammatory mechanism in the heart’s borderzone after a heart attack, driven by stressed cardiomyocytes. This discovery may lead to novel therapies aimed at preventing heart failure by targeting mechanical stress, DNA sensing, and IFN signaling.

Ischemic heart disease is the leading cause of death globally. It typically starts with a heart attack, or myocardial infarction (MI), during which part of the heart muscle dies because it doesn’t receive enough blood from the coronary arteries. This event triggers intense inflammation, changes to the structure of the heart wall, and eventually can lead to heart failure.

Anti-inflammatory drugs have been surprisingly ineffective at preventing heart failure. As a consequence, they are not a routine part of post-MI care. However, it is possible that the most potent molecular and cellular inflammation targets have yet to be discovered.

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It was a career-defining (and perhaps life changing) moment when Dr. Vittorio Sebastiano, a reproductive biologist by training, realized that because we are able to create life, that same body of information could be harnessed to create youth — that is, radically reverse our biological aging process to a younger time point without losing cellular identity.

In 2014, he and his lab began unpacking this epiphany. They made the radical decision to conduct their investigations in human cells and tissue rather than in rodents, with the expectation that such a start would be a better bridge to human clinical trials.

Flash forward a decade and Dr. Sebastiano and his team stand poised to begin trials in humans. Dr. Sebastiano is, in my opinion, one of the most extraordinary scientists in the longevity space today who flies under the radar of most of us in functional medicine.

In this podcast — which is actually two-in-one because I continued the conversation with him on a second date — you’ll hear about the remarkable work they’re undertaking at his lab. For example: They’ve created a biological clock that encompasses the whole genome consisting of millions and millions of CpG sites. They are able to clearly demonstrate the reversal of bioage using their methodology — a cocktail of Yamanaka factors plus, with clear time limits — which changes the epigenome first, and in so doing influences all of the hallmarks of aging. Teaser: they’ve identified one intervention routinely used in clinical practice that influences their bio age clock in the same way that their cocktail does. What is it? I was riveted with this conversation, as I am sure you’ll be. Leave a review if you like it, and — Yes — let me know what you think. I know this will prompt deep questions for you, as it did for me. ~DrKF

Continue reading “Decoding Aging: The Science Of Cellular Rejuvenation With Dr. Vittorio Sebastiano” | >

During aging, the human methylome undergoes both differential and variable shifts, accompanied by increased entropy. The distinction between variably methylated positions (VMPs) and differentially methylated positions (DMPs), their contribution to epigenetic age, and the role of cell type heterogeneity remain unclear.

We conduct a comprehensive analysis of 32,000 human blood methylomes from 56 datasets (age range = 6–101 years). We find a significant proportion of the blood methylome that is differentially methylated with age (48% DMPs; FDR 0.005) and variably methylated with age (37% VMPs; FDR 0.005), with considerable overlap between the two groups (59% of DMPs are VMPs). Bivalent and Polycomb regions become increasingly methylated and divergent between individuals, while quiescent regions lose methylation more uniformly. Both chronological and biological clocks, but not pace-of-aging clocks, show a strong enrichment for CpGs undergoing both mean and variance changes during aging. The accumulation of DMPs shifting towards a methylation fraction of 50% drives the increase in entropy, smoothening the epigenetic landscape. However, approximately a quarter of DMPs exhibit anti-entropic effects, opposing this direction of change.

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Alzheimer’s, Parkinson’s, and other neurological disorders can be seen as “dirty brain” diseases, where the brain struggles to clear out harmful waste. Aging is a key risk factor because, as we grow older, our brain’s ability to remove toxic buildup slows down. However, new research in mice demonstrates that it’s possible to reverse age-related effects and restore the brain’s waste-clearing process.

“This research shows that restoring cervical lymph vessel function can substantially rescue the slower removal of waste from the brain associated with age,” says Douglas Kelley, a professor of mechanical engineering at the University of Rochester. “Moreover, this was accomplished with a drug already being used clinically, offering a potential treatment strategy.”

Kelley is one of the lead authors of the study, which appears in the journal Nature Aging, along with Maiken Nedergaard, codirector the University’s Center for Translational Neuromedicine. The study is one of many collaborations carried out by researchers at Rochester’s Hajim School of Engineering & Applied Sciences and the Medical Center.

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“This selection underscores WFIRM’s commitment to pushing the boundaries of scientific research and finding innovative solutions to some of the world’s most challenging health issues,” said Dr. Anthony Atala.

How can microgravity help advance cancer research? This is what an upcoming grant-awarded project sponsored by the International Space Station (ISS) National Lab hopes to address as a team of researchers from the Wake Forest Institute for Regenerative Medicine (WFIRM) have been selected to send samples to the ISS with the goal of observing how microgravity influences cancer growth and their responses to treatment. This project holds the potential to help scientists and cancer researchers develop new methods for combating cancer here on Earth.

“Being selected for this project is an incredible honor and opportunity for our team at WFIRM,” said Dr. Shay Soker, who is the project lead and a professor in the Wake Forest University School of Medicine. “The microgravity environment of the ISS provides a unique setting to study cancer in ways that are not possible on Earth. This research has the potential to unlock new understandings of cancer behavior and lead to more effective treatments.”

For the project, astronauts onboard the ISS will monitor organoids, which are lab-grown organs produced from colorectal cancer patient cells, and how the cancer cells within these organoids respond to microgravity and the treatment designed to reduce their growth and spread. The ISS has a rich history of promoting scientific innovation and discovery using the unique environment of microgravity, as more than 3,000 scientific experiments have been conducted onboard the ISS since its first module launched into orbit in 1999.

Continue reading “NASA and ISS National Lab Choose WFIRM for Innovative Cancer Study” | >