Lifeboat Foundation

Most nanoelectromechanical systems are formed by etching inorganic materials such as silicon. Kopperger et al. improved the precision of such machines by synthesizing a 25-nm-long arm defined by a DNA six-helix bundle connected to a 55 nm-by-55 nm DNA origami plate via flexible single-stranded scaffold crossovers (see the Perspective by Hogberg). When placed in a cross-shaped electrophoretic chamber, the arms could be driven at angular frequencies of up to 25 Hz and positioned to within 2.5 nm. The arm could be used to transport fluorophores and inorganic nanoparticles.

Science, this issue p. 296; see also p. 279

The use of dynamic, self-assembled DNA nanostructures in the context of nanorobotics requires fast and reliable actuation mechanisms. We therefore created a 55-nanometer–by–55-nanometer DNA-based molecular platform with an integrated robotic arm of length 25 nanometers, which can be extended to more than 400 nanometers and actuated with externally applied electrical fields. Precise, computer-controlled switching of the arm between arbitrary positions on the platform can be achieved within milliseconds, as demonstrated with single-pair Förster resonance energy transfer experiments and fluorescence microscopy. The arm can be used for electrically driven transport of molecules or nanoparticles over tens of nanometers, which is useful for the control of photonic and plasmonic processes. Application of piconewton forces by the robot arm is demonstrated in force-induced DNA duplex melting experiments.

This is where it gets a little weird.

When the team treated human cells in culture with extract of tardigrade, the GFP-tagged proteins stuck to human DNA just like they stick to tardigrade DNA, and cheerfully started doing what they do best: tamping down oxidative stress. When X-rays hit human cells, they do two kinds of damage. X-rays can cause direct DNA strand breaks, which are mostly single-strand. When they strike water molecules, they can also excite them into producing reactive oxygen species, which also cause single-strand breaks. High enough doses of X-rays can cause double-strand breaks. The damage-suppressing protein Dsup went immediately to work on the culture of human cells, suppressing or repairing single-strand and double-strand breaks by about 40%.

Clearly this means we can consume water bears to gain their powers. The study authors remark that the gene portfolio of the tardigrade represents “a treasury of genes” to improve or augment stress tolerance in other cells. Plug-and-play genetics, anyone?

Harvard and Japanese scientists say they’ve made a “landmark” discovery in cancer drug development. In a new study published Monday, they say they have finally found a way to synthesize in bulk a complex class of promising cancer-fighting molecules derived from sea sponges. Their new strategy has already helped speed up research into these molecules, including a planned clinical trial in humans.

Called halichondrins, the molecules were originally discovered by Japanese researchers in the mid-1980s in sea sponges. It became quickly apparent that they were capable of aggressively fighting tumors in both mice and lab dishes containing human cells, and in a way different from other existing treatments.

To understand our brains, scientists need to know their components. This theme underlies a growing effort in neuroscience to define the different building blocks of the brain—its cells.

With the mouse’s 80 million neurons and our 86 billion, sorting through those delicate, microscopic building blocks is no small feat. A new study from the Allen Institute for Brain Science, which was published today in the journal Nature Neuroscience, describes a large profile of mouse neuron types based on two important characteristics of the cells: their 3D shape and their electrical behavior.

The study, which yielded the largest dataset of its kind from the adult laboratory mouse to date, is part of a larger effort at the Allen Institute to discover the brain’s “periodic table” through large-scale explorations of brain cell types. The researchers hope a better understanding of cell types in a healthy mammalian brain will lay the foundation for uncovering the cell types that underlie human brain disorders and diseases.

Geneticists exploring the dark heart of the human genome have discovered big chunks of Neanderthal and other ancient DNA. The results open new ways to study both how chromosomes behave during cell division and how they have changed during human evolution.

Centromeres sit in the middle of chromosomes, the pinched-in “waist” in the image of a chromosome from a biology textbook. The centromere anchors the fibers that pull chromosomes apart when cells divide, which means they are really important for understanding what happens when cell division goes wrong, leading to cancer or genetic defects.

But the DNA of centromeres contains lots of repeating sequences, and scientists have been unable to properly map this region.

Vaccination against rotavirus is associated with a reduced incidence of type 1 diabetes in children, according to an analysis of U.S. insurance data.

“I am committed to the notion that the past predicts the present,” Larsen tells Inverse, “and we need to understand that past to understand the world we live in now.”

Larsen has had a longstanding interest in the health and lifestyle of early farmers — those who were working around the Neolithic transition from hunting and gathering to farming. So when Ian Hodder, Ph.D., an archeologist who leads the Çatalhöyük Research Project, invited him to join the project in 2004, he quickly accepted the opportunity.

This new study is based on 25 years of findings linked to the human remains found in Çatalhöyük. Dating of remains shows that the population there grew to its peak in the period from 6,700 to 6,500 B.C. and then declined rapidly. That decline is likely linked to the evidence of disease and malnutrition Larsen and colleagues found in the remains.

Editor’s Note: The U.S. Transhumanist Party features this article by Nicola Bagalà and Michael Nuschke of the Life Extension Advocacy Foundation (LEAF), originally published on the LEAF site on May 15th, 2019. The article brings attention to and responds to concerns related to the impacts of increased longevity on pension systems, a possible result of our mission of ending age-related diseases, which the U.S. Transhumanist Party supports as part of our policy goals.

~ Brent Reitze, Director of Publication, United States Transhumanist Party, June 15th, 2019

If you work in social security, it’s possible that your nightmares are full of undying elderly people who keep knocking on your door for pensions that you have no way of paying out. Tossing and turning in your bed, you beg for mercy, explaining that there’s just too many old people who need pensions and not enough young people who could cover for it with their contributions; the money’s just not there to sustain a social security system that, when it was conceived in the mid-1930s, didn’t expect that many people would ever make it into their 80s and 90s. Your oneiric persecutors won’t listen: they gave the country the best years of their lives, and now it’s time for the country to pay them their due.

A team of UK scientists have identified the mechanism behind hardening of the arteries, and shown in animal studies that a generic medication normally used to treat acne could be an effective treatment for the condition.

The team, led by the University of Cambridge and King’s College London, found that a molecule once thought only to exist inside cells for the purpose of repairing DNA is also responsible for hardening of the arteries, which is associated with dementia, heart disease, high blood pressure and stroke.

There is no current treatment for hardening of the arteries, which is caused by build-up of bone-like calcium deposits, stiffening the arteries and restricting blood flow to organs and tissues.