Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog – Page 6

Good channel here.

The future of human longevity just got a $500billion booste thanks to Trump’s bold new AI vision! In this video, we explore the recently announced Stargate AI Infrastructure Project—a staggering $500 billion initiative unveiled by President Donald Trump on January 21, 2025, alongside tech titans OpenAI, Oracle, and SoftBank. Designed to build colossal data centers and supercharge AI development, could this ambitious plan hold the key to curing aging? We dive into the cutting-edge science, the potential of AI to revolutionize healthcare, and how Stargate might reshape humanity’s fight against time. Buckle up for a wild ride into the future!

🔍 What You’ll Discover:
The Stargate Project: Trump’s massive AI infrastructure gamble.
How AI could unlock breakthroughs in aging research.
The players: OpenAI, Oracle, SoftBank, and their bold vision.
The big question: Can this tech triumph over mortality?

JOIN LSN Patreon for exclusive access to news, tips and a community of like minded longevity enthusiasts: https://www.patreon.com/user?u=29506604

🔔 Like, subscribe, and hit the bell for more groundbreaking insights every week! Tell us in the comments: Do you think Stargate could be the key to curing aging? Let’s debate it!

Continue reading “How The Stargate Project Plans To Cure Aging” | >

An AI approach developed by researchers from the University of Sheffield and AstraZeneca, could make it easier to design proteins needed for new treatments.

In their study published in the journal Nature Machine Intelligence, Sheffield computer scientists in collaboration with AstraZeneca and the University of Southampton have developed a new machine learning framework that has shown the potential to be more accurate at inverse than existing state-of-the-art methods.

Inverse protein folding is a critical process for creating novel proteins. It is the process of identifying , the building blocks of proteins, that fold into a desired 3D protein structure and enable the protein to perform specific functions.

Read more | >

Scientists are looking at ways to tackle Alzheimer’s and dementia from all kinds of angles, and a new study has identified the molecule hevin (or SPARCL-1) as a potential way of preventing cognitive decline.

Hevin is a protein naturally produced in the brain by cells called astrocytes. These support-worker cells look after the connections or synapses between neurons, and it’s thought that hevin plays a role in this essential work.

In this new study, researchers from the Federal University of Rio de Janeiro (UFRJ) and the University of São Paulo in Brazil boosted hevin production in the brains of both healthy mice and those with an Alzheimer’s-like disease.

Read more | >

You stayed up too late scrolling through your phone, answering emails or watching just one more episode. The next morning, you feel groggy and irritable. That sugary pastry or greasy breakfast sandwich suddenly looks more appealing than your usual yogurt and berries. By the afternoon, chips or candy from the break room call your name. This isn’t just about willpower. Your brain, short on rest, is nudging you toward quick, high-calorie fixes.

There is a reason why this cycle repeats itself so predictably. Research shows that insufficient sleep disrupts hunger signals, weakens self-control, impairs glucose metabolism and increases your risk of weight gain. These changes can occur rapidly, even after a single night of poor sleep, and can become more harmful over time if left unaddressed.

I am a neurologist specializing in sleep science and its impact on health.

Read more | >

Cancer plasticity allows tumor cells to change their identity, evade therapies, and adapt to environmental pressures, contributing to treatment resistance and metastasis. New research is targeting this adaptability through epigenetic drugs, immune checkpoint inhibitors, and strategies to limit phenotypic switching.

Read more | >

Cells are constantly subjected to DNA damage from a range of internal and environmental sources. It is estimated that cells can experience as many as 100,000 DNA lesions per day. One of the most deleterious types of DNA lesions is the DNA double-strand break (DSB). Just one unrepaired DNA DSB may be enough to cause mutations or cell death leading to a wide range of pathologies including cancer, immune deficiency, premature aging and neurodegeneration.

To respond to the array of DNA lesions that occur, cells have developed a complex and coordinated series of steps involving DNA damage recognition, cell cycle arrest and signaling-induced activation of the DNA repair machinery—processes collectively referred to as the DNA damage response (DDR). In recent years, progress has been made in understanding how this process is initiated. However, the later stages of this process, including long range DNA end-resection, are not well understood.

In a new study published in Nature Cell Biology, researchers from Boston University Chobanian & Avedisian School of Medicine, Massachusetts General Hospital (MGH) and Harvard Medical School, identified several uncharacterized chromatin factors (proteins that regulate ) that are recruited to sites of DNA damage, including the gene ZNF280A. Importantly, this gene is hemizygously deleted—meaning one of the two copies of alleles is missing—in a subset of patients with a human developmental syndrome called 22q11.2 distal deletion syndrome.

Read more | >