Lifeboat Foundation: Safeguarding Humanity
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Agreeing to state-of-the art theory, a warp drive might cut the travel time between stars from tens of thousands of years to only weeks or months. Harold G. White, a physicist and innovative propulsion engineer at NASA and other NASA engineers are working to regulate whether faster-than-light travel — warp drive — might soon be possible. The group is trying to some extent warp the course of a photon, altering the distance it travels in a definite area, and then detecting the change with a device called an interferometer.

In 1994, a Mexican physicist, Miguel Alcubierre, speculated that faster-than-light speeds were conceivable in a technique that did not deny Einstein by binding the growth and reduction of space itself. Under Dr. Alcubierre’s theory, a ship still couldn’t surpass light speed in a native region of space. But a theoretical thrust system he sketched out operated space-time by producing a so-called “warp bubble” that would inflate space on one side of a spacecraft and contract it on another.

Image source: With thanks to Shutterstock.com.

An Alcubierre Warp Drive expanses spacetime in a wave producing the material of space ahead of a spacecraft to contract and the space behind it to enlarge. The ship can ride the wave to go faster to high speeds and time travel. The Alcubierre drive, also famous as the Alcubierre metric or Warp Drive, is a mathematical model of a spacetime showing features suggestive of the fictional “warp drive” from Star Trek, which can move “faster than light”.

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THE genome is written in an alphabet of just four letters. Being able to read, study and compare DNA sequences for humans, and thousands of other species, has become routine. A new technology promises to make it possible to edit genetic information quickly and cheaply. This could correct terrible genetic defects that blight lives. It also heralds the distant prospect of parents building their children to order.

The technology is known as CRISPR-Cas9, or just CRISPR. It involves a piece of RNA, a chemical messenger, designed to target a section of DNA; and an enzyme, called a nuclease, that can snip unwanted genes out and paste new ones in. Other ways of editing DNA exist, but CRISPR holds the promise of doing so with unprecedented simplicity, speed and precision.

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The circadian rhythm is a subject of many studies, yet it remains a mystery in many ways. While scientists have identified many of the cell proteins involved in circadian rhythm and several genes that contribute to a healthy rhythm, the ‘master clock’ gene remained elusive. However, a recent chronobiology study on rats indicates that the Zfhx3, or Zinc Finger Homeobox 3, gene may be the master gene that dictates this important biological rhythm.

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V2V communication is a viable way to mitigate accidents amongst autonomous vehicles.

Engineers have known for some time that if cars could only “talk” to each other, they could avoid a lot of accidents.

Vehicles could be driven more safely with information about another car, obstacle or pedestrian around a blind curve, for example.

But the hurdles to implementing these systems are numerous: they require a and the allocation of to enable vehicle-to-vehicle (V2V) communications.

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Dr DePinho released a paper in 2012, this builds on previous papers and his theory of the “telomere-p53-PGC axis”. This is a big reason along with the work of Dr Michael Fossel I believe telomerase therapy is probably the best chance of radical life extension in the near future. This is one of a number of papers that implicate dysfunctional telomeres in a cascade that causes mitochondrial dysfunction and various other aging consequences.

ABSTRACT Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1α and PGC-1β, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1α expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1α and PGC-1β promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.

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Cancer researchers dream of the day they can force tumor cells to morph back to the normal cells they once were. Now, researchers on Mayo Clinic’s Florida campus have discovered a way to potentially reprogram cancer cells back to normalcy.

The finding, published in Nature Cell Biology, represents “an unexpected new biology that provides the code, the software for turning off cancer,” says the study’s senior investigator, Panos Anastasiadis, Ph.D., chair of the Department of Cancer Biology on Mayo Clinic’s Florida campus.

That code was unraveled by the discovery that adhesion proteins — the glue that keeps cells together — interact with the microprocessor, a key player in the production of molecules called microRNAs (miRNAs). The miRNAs orchestrate whole cellular programs by simultaneously regulating expression of a group of genes. The investigators found that when normal cells come in contact with each other, a specific subset of miRNAs suppresses genes that promote cell growth. However, when adhesion is disrupted in cancer cells, these miRNAs are misregulated and cells grow out of control. The investigators showed, in laboratory experiments, that restoring the normal miRNA levels in cancer cells can reverse that aberrant cell growth.

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A study led by researchers from the U.S. Department of Energy’s (DOE) SLAC National Accelerator Laboratory and the University of California, Los Angeles has demonstrated a new, efficient way to accelerate positrons, the antimatter opposites of electrons. The method may help boost the energy and shrink the size of future linear particle colliders — powerful accelerators that could be used to unravel the properties of nature’s fundamental building blocks.

The scientists had previously shown that boosting the energy of charged particles by having them “surf” a wave of , or plasma, works well for . While this method by itself could lead to smaller accelerators, electrons are only half the equation for future colliders. Now the researchers have hit another milestone by applying the technique to positrons at SLAC’s Facility for Advanced Accelerator Experimental Tests (FACET), a DOE Office of Science User Facility.

“Together with our previous achievement, the new study is a very important step toward making smaller, less expensive next-generation electron-positron colliders,” said SLAC’s Mark Hogan, co-author of the study published today in Nature. “FACET is the only place in the world where we can accelerate positrons and electrons with this method.”

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