Lifeboat Foundation

Two eggs fertilized by two sperm coincided in a uterus and, instead of giving rise to two sisters, they fused to form a single person: Karen Keegan. When she was 52 years old, this woman from Boston suffered very serious kidney failure, but luckily she had three children willing to donate a kidney to her. The doctors did genetic tests to see which offspring was most compatible and they got a major surprise: the test said that two of them were not her children. The reality was even more astonishing: Karen Keegan had two different DNA sequences, two genomes, depending on the cell you looked at. Biologist Alfonso Martínez Arias maintains that this chimeric woman is conclusive proof that DNA does not define a person’s identity.

The most inspiring science book of all time is The Selfish Gene, according to a survey carried out by the Royal Society of the United Kingdom. In this famous work from 1976, British biologist Richard Dawkins defended that the DNA molecule uses the human being as a mere envelope in order to be transmitted to the next generation and become immortal. “We are survival machines, robot vehicles blindly programmed to preserve the selfish molecules known as genes,” Dawkins stated. Almost half a century later, Martínez Arias refutes this perspective of the selfish gene and proposes a much more romantic alternative: the altruistic cell. “An organism is the work of cells. Genes merely provide materials for their work,” he says in The Master Builder, a fascinating and provocative book from the London publisher Basic Books that will also be published in Spanish this year.

Martínez Arias, 68, argues that the DNA sequence of an individual is not an instruction manual or a construction plan for their body, but a box of tools and materials for the true architect of life: the cell. The Madrid-born biologist argues that there is nothing in the DNA molecule that explains why the heart is located on the left, why there are five fingers on the hand or why twin brothers have different fingerprints. Cells are what “control time and space,” he proclaims. They are the ones who know where right and left are, and where exactly a person’s foot or an elephant’s trunk should end.

Futurists, including some medical doctors, are signing up to be decapitated—and then have their brains frozen. But without a body, what will their minds become?

Not a happy vid for E5. It appears to be something to make one healthy and as a result get extra time which is a good thing. But its testing standards could have been better and its off to some kind of skin care target.

A new study led by University of Pittsburgh and UPMC Hillman Cancer Center researchers shows that an enzyme called PARP1 is involved in repair of telomeres, the lengths of DNA that protect the tips of chromosomes, and that impairing this process can lead to telomere shortening and genomic instability that can cause cancer.

Researchers have discovered that individuals who live to be 100 years old and remain cognitively healthy possess genetic variations that may protect against Alzheimer’s disease. These “protective alleles” are significantly more prevalent among centenarians compared to Alzheimer’s patients and even middle-aged individuals without the disease. This finding could pave the way for new approaches in preventing and treating Alzheimer’s, particularly by focusing on enhancing these protective genetic mechanisms.

The new findings have been published in the journal Alzheimer’s & Dementia.

Alzheimer’s disease is a progressive neurological disorder that predominantly affects older adults, leading to a decline in cognitive functions such as memory and reasoning. Over time, this can result in a complete loss of independence and eventually death. The risk of developing Alzheimer’s increases significantly with age, and while it is not an inevitable part of aging, it is one of the most common causes of dementia among seniors.

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhDDiscount Links: At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgartenUse Code: C…

Achieving Longevity Escape Velocity is likely within the next 10–20 years—why is this happening, and what are the implications?

In Limitless, the film’s protagonist is a struggling writer desperate for success. As luck would have it, he is introduced to an experimental drug that unlocks his full potential.

The film was a box office success, and it is easy to see why.

Nootropics, drugs, and various supplements for memory, focus, and mental agility have been used for millennia. The desire to elevate ourselves is universal, much like the quest for longevity–and, unsurprisingly, the two are intertwined.

The following is a summary of “Emerging therapeutic frontiers in cancer: insights into posttranslational modifications of PD-1/PD-L1 and regulatory pathways,” published in the April 2024 issue of Hematology by Wang et al.

The intricate interplay between programmed cell death ligand 1 (PD-L1), expressed on the surface of tumor cells, and programmed cell death 1 (PD-1), expressed on T cells, constitutes a pivotal mechanism fostering immune evasion by tumor cells through the thwarting of effective tumor antigen-specific T cell activation. The advent of PD-1/PD-L1 blockade has emerged as a transformative strategy in combating tumor immune evasion, garnering substantial interest within the oncology landscape. Clinical investigations have underscored the remarkable efficacy and safety profile of PD-1/PD-L1 blocking antibodies across a spectrum of malignancies, offering a beacon of hope for patients.

Nonetheless, the therapeutic landscape of anti-PD-1/PD-L1 interventions is fraught with challenges, including limited indications and the emergence of drug resistance, necessitating a nuanced approach to therapeutic intervention. Accordingly, unraveling additional regulatory pathways and molecular players associated with PD-1/PD-L1 signaling assumes paramount importance, alongside the strategic implementation of combinational therapeutic modalities, to address the multifaceted dynamics of tumor immune evasion.