Lifeboat Foundation

USC Dornsife’s CReATiNG technique revolutionizes synthetic biology by facilitating the cost-effective construction of synthetic chromosomes, promising significant advancements in various scientific and medical fields.

A groundbreaking new technique invented by researchers at the USC Dornsife College of Letters, Arts and Science may revolutionize the field of synthetic biology. Known as CReATiNG (Cloning Reprogramming and Assembling Tiled Natural Genomic DNA), the method offers a simpler and more cost-effective approach to constructing synthetic chromosomes. It could significantly advance genetic engineering and enable a wide range of advances in medicine, biotechnology, biofuel production, and even space exploration.

Simplifying Chromosome Construction

In a new paper, Sinclair and his co-authors outline a theory arguing that epigenetic changes are the underlying cause of aging [1].

It is not every day that one of the most prominent geroscientists presents a new theory of aging. David Sinclair of Harvard, along with two co-authors, Yuancheng Ryan Lu and Xiao Tian, have just published “The Information Theory of Aging” in Nature Aging. This theory was proposed by Sinclair years ago [2], and this new paper is an attempt to summarize it based on the most recent research.

The ability to store and retrieve information is central to life, which relies on the constant reproduction of complex organisms using DNA blueprints. However, on top of that digital genetic code, there is a much messier realm of epigenetics, which regulates how genetic information is translated into proteins.

DNA is the building block of life, and the genetic alphabet comprises just four letters or nucleotides. These biochemical building blocks comprise all types of DNA, and scientists have long wondered whether creating working artificial DNA would be possible. Now, a breakthrough may finally provide the answer.

The main goal of a new study, the findings of which were published in Nature Communications this month, shows that scientists may finally be able to create new medicines for certain diseases by creating DNA with new nucleotides that can create custom proteins.

Being able to create artificial DNA could open the door for several important uses. Being able to expand the genetic code could very well diversify the “range of molecules we can synthesize in the lab,” the study’s senior author Dong Wang, Ph.D., explained (via Phys.org).

In this episode, I am joined by Dr. David Sinclair, tenured Professor of Genetics at Harvard Medical School and an expert researcher in the field of longevity. Dr. Sinclair is also the author of the book Lifespan: Why We Age & Why We Don’t Have To, and the host of the Lifespan Podcast, which launches January 5, 2022. In this interview, we discuss the cellular and molecular mechanisms of aging and what we all can do to slow or reverse the aging process. We discuss fasting and supplementation with resveratrol, NAD, metformin, and NMN. We also discuss the use of caffeine, exercise, cold exposure, and why excessive iron load is bad for us. We discuss food choices for offsetting aging and promoting autophagy (clearance of dead cells). And we discuss the key blood markers everyone should monitor to determine your biological versus chronological age. We also discuss the future of longevity research and technology. This episode includes lots of basic science and specific, actionable protocols, right down to the details of what to do and when. By the end, you will have in-depth knowledge of the biology of aging and how to offset it. #HubermanLab #DavidSinclair #Longevity

Nearly two in five U.S. adults have high cholesterol, according to the Centers for Disease Control and Prevention (CDC). Untreated, high cholesterol can lead to heart disease and stroke, which are two of the top causes of death in the U.S. Worldwide; cardiovascular diseases claim nearly 18 million lives every year, according to the World Health Organization.

A new vaccine developed by researchers at The University of New Mexico School of Medicine could be a game-changer, providing an inexpensive method to lower “bad” LDL cholesterol, which creates dangerous plaques that can block blood vessels.

In a recent study published in npj Vaccines, a team led by Bryce Chackerian, Ph.D., Regents’ Professor in the Department of Molecular Genetics & Microbiology, reported the vaccines lowered LDL cholesterol almost as effectively as an expensive class of drugs known as PCSK9 inhibitors.

Two geneticists explain the groundbreaking CRISPR-based therapies approved for sickle-cell disease and β-thalassaemia, and other genetic therapeutics in development, including base-editing and prime-editing.

In 2007, Luciano Marraffini struck out on what was then a scientifically lonely path: to understand CRISPR, which had been discovered in bacteria only about a decade before.

Seventeen years later, we all know what CRISPR is: a revolution in medicine. A once-in-a-lifetime scientific breakthrough. The most promising tool for gene therapy ever discovered. But back then, “clustered regularly interspaced short palindromic repeats” were merely curious genetic fragments with no known purpose.

“When I started, there was nothing that indicated that it was going to one day help people to cure genetic diseases,” Marraffini recalls.

Summary: A new study illuminated a part of the “dark genome,” specifically focusing on LINE-1, a genetic element linked to various diseases and aging.

Researchers have provided the first high-resolution images and structural details of LINE-1, an “ancient genetic parasite” with about 100 active copies in each person. This research, involving international collaboration, reveals LINE-1’s mechanism of integrating DNA into the human genome and its correlation with diseases like cancer and neurodegeneration.

The study’s findings offer a foundation for potential treatments targeting this retrotransposon.

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhDDiscount Links: Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7x…