Lifeboat Foundation: Safeguarding Humanity
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Category: bioengineering

The universe is filled with uncountable amounts of mystery, discovery, opportunity, experiences, marvels and more. So, let’s not die if we don’t have to.

It’s much harder to make the case that radical longevity cannot be engineered into our biology than that it can. Humanity engineers cells in countless ways all the time now, and our knowledge, capability and tools keep growing exponentially.

Now, a mainstream amount of demand to create a bustling global industry of life extension R&D is the only thing standing between you and the ability to live indefinitely.” — Eric Schulke

Fifteen thousand years worth of Netflix are watched every day. Fifteen billion dollars are spent on the Super Bowl and fifteen billion dollars are spent on Valentine’s day. Those aren’t bad things but we need some perspective. Survival is humanity’s main and oldest occupation. We have what it takes to survive if we pay attention and get with the program.

“Yes, the future is transhumanism. Who would ask ‘Is the future being alive and prosperous?’ As if anyone should expect humanity to work for a future of hardship and death.” — Ray Keyes

People suffer in great existential voids these decades, not only do they need life, they need deep meaning and purpose. The movement for indefinite life extension is giving them both.

To rapidly detect the presence of E. coli in drinking water, Cornell University food scientists now can employ a bacteriophage — a genetically engineered virus — in a test used in hard-to-reach areas around the world.

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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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Highly specialized cartilage is characteristically avascular and non-neural in composition with low cell numbers in an aliphatic environment. Despite its apparent simplicity, bioengineering regenerative hyaline cartilage in a form effective for implantation remains challenging in musculoskeletal tissue engineering. Existing surgical techniques including autologous chondrocyte implantation (ACI) and matrix-induced autologous chondrocyte implantation (MACI) are considered superior to self-repair induction techniques. However, both MACI and ACI are complex, multistage procedures that require a double operation; first for surgical excision of native cartilage, followed by expansion of adult chondrocytes in vitro prior to implantation by a second operation.

Regenerating robust articular hyaline-like cartilage is a key priority in musculoskeletal tissue engineering to prevent cost-intensive degenerative osteoarthritis that limits the quality of life in global healthcare. Integrating mesenchymal stem cells and 3D printing technologies has shown significant promise in bone tissue engineering– although the key challenge remains in transferring the bench-based technology to the operating room for real-time applications. To tackle this, a team of Australian orthopedic surgeons and bioengineers collaboratively proposed an in situ additive manufacturing technique for effective cartilage regeneration. The handheld engineered extrusion device known as the BioPen offers an advanced, co-axial extrusion strategy to deposit cells embedded in a hydrogel material within a surgical setting.

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Researchers have used gene editing to completely eliminate populations of mosquitoes in the lab.

The team tested their technique on the mosquito Anopheles gambiae, which transmits malaria.

They altered part of a gene called doublesex, which determines whether an individual mosquito develops as a male or as a female.

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Only time will tell what new forms life will take.

Joyce seeks to understand life by trying to generate simple living systems in the lab. In doing so, he and other synthetic biologists bring new kinds of life into being. Every attempt to synthesize novel life forms points to the fact that there are still more, perhaps infinite, possibilities for how life could be. Synthetic biologists could change the way life evolves, or its capacity to evolve at all. Their work raises new questions about a definition of life based on evolution. How to categorize life that is redesigned, the product of a break in the chain of evolutionary descent?

An origin story for synthetic biology goes like this: in 1997, Drew Endy, one of the founders of synthetic biology and now a professor of bioengineering at Stanford University in California, was trying to create a computational model of the simplest life form he could find: the bacteriophage T7, a virus that infects E coli bacteria. A crystalline head atop spindly legs, it looks like a landing capsule touching down on the Moon as it grabs onto its bacterial host. The bacteriophage is so simple that by some definitions it is not even alive. (Like all viruses, it depends on the molecular machinery of its host cell to replicate.) Bacteriophage T7 has only 56 genes, and Endy thought it might be possible to create a model that accounted for every part of the phage and how those parts worked together: a perfect representation that would predict how the phage would change if any one of its genes were moved or deleted.

Endy built a series of bacteriophage T7 mutants, systematically knocking out genes or scrambling their location in the tiny T7 genome. But the mutant phages conformed to the model only some of the time. A change that should have caused them to weaken would instead have their progeny bursting open E coli cells twice as fast as before. It wasn’t working. Eventually, Endy had a realization: “If we want to model the natural world, we have to rewrite [the natural world] to be modellable.” Instead of trying to make a better map, change the territory. Thus was born the field of synthetic biology. Borrowing techniques from software engineering, Endy began to “refactor” bacteriophage T7’s genome. He made bacteriophage T7.1, a life form designed for ease of interpretation to the human mind.

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