Cracking Eggshell Nanostructure: New Discovery Could Have Important Implications For Food Safety

Researchers develop ‘self-healing’ robotics material

Image: Victor Habbick Visions/Science Photo Library

Traditional electronics are made from rigid and brittle materials. However, a new ‘self-healing’ electronic material allows a soft robot to recover its circuits after it is punctured, torn or even slashed with a razor blade.

Made from liquid metal droplets suspended in a flexible silicone elastomer, it is softer than skin and can stretch about twice its length before springing back to its original size.

Soft Robotics & Biologically Inspired Robotics at Carnegie Mellon University. Video: Mouser Electronics 

‘The material around the damaged area automatically creates new conductive pathways, which bypass the damage and restore connectivity in the circuit,’ explains first author Carmel Majidi at Carnegie Mellon University in Pittsburgh, Pennsylvania. The rubbery material could be used for wearable computing, electronic textiles, soft field robots or inflatable extra-terrestrial housing.

‘There is a sweet spot for the size of the droplets,’ says Majidi. ‘We had to get the size not so small that they never rupture and form electronic connections, but not so big they would rupture even under light pressure.’

To read the full article, by Anthony King, in C&I, the members’ magazine for SCI, click here. 

Vacuum printer. Fill up the empty space.

Meet The First-Ever 3D Printer That Can Do Construction in The Vacuum of Space

This will change how we explore space.

One manufacturing company just made history by successfully using a special 3D printer in extreme, space-like conditions.

The team printed polymer alloy parts in a super-high vacuum, and hope their new tech will allow the design and manufacture of much more ambitious spacecraft and space-based telescopes.

“This is an important milestone, because it means that we can now adaptively and on demand manufacture things in space,” Andrew Rush, CEO of Made in Space, told Scientific American.

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@neysastudies

Toxic ‘zombie’ cells seen for 1st time in Alzheimer’s

A type of cellular stress known to be involved in cancer and aging has now been implicated, for the first time, in Alzheimer’s disease. UT Health San Antonio faculty researchers reported the discovery in the journal Aging Cell.

The team found that the stress, called cellular senescence, is associated with harmful tau protein tangles that are a hallmark of 20 human brain diseases, including Alzheimer’s and traumatic brain injury. The researchers identified senescent cells in postmortem brain tissue from Alzheimer’s patients and then found them in postmortem tissue from another brain disease, progressive supranuclear palsy.

Cellular senescence allows the stressed cell to survive, but the cell may become like a zombie, functioning abnormally and secreting substances that kill cells around it. “When cells enter this stage, they change their genetic programming and become pro-inflammatory and toxic,” said study senior author Miranda E. Orr, Ph.D., VA research health scientist at the South Texas Veterans Health Care System, faculty member of the Sam and Ann Barshop Institute for Longevity and Aging Studies, and instructor of pharmacology at UT Health San Antonio. “Their existence means the death of surrounding tissue.”

Improvements in brain structure and function

The team confirmed the discovery in four types of mice that model Alzheimer’s disease. The researchers then used a combination of drugs to clear senescent cells from the brains of middle-aged Alzheimer’s mice. Such drugs are called senolytics. The drugs used by the San Antonio researchers are dasatinib, a chemotherapy medication that is U.S. Food and Drug Administration-approved to treat leukemia, and quercetin, a natural flavonoid compound found in fruits, vegetables and some beverages such as tea.

After three months of treatment, the findings were exciting. “The mice were 20 months old and had advanced brain disease when we started the therapy,” Dr. Orr said. “After clearing the senescent cells, we saw improvements in brain structure and function. This was observed on brain MRI studies (magnetic resonance imaging) and postmortem histology studies of cell structure. The treatment seems to have stopped the disease in its tracks.”

“The fact we were able to treat very old mice and see improvement gives us hope that this treatment might work in human patients even after they exhibit symptoms of a brain disease,” said Nicolas Musi, M.D., study first author, who is Professor of Medicine and Director of the Sam and Ann Barshop Institute at UT Health San Antonio. He also directs the VA-sponsored Geriatric Research, Education and Clinical Center (GRECC) in the South Texas Veterans Health Care System.

Typically, in testing an intervention in Alzheimer’s mice, the therapy only works if mice are treated before the disease starts, Dr. Musi said.

Tau protein accumulation is responsible

In Alzheimer’s disease, patient brain tissue accumulates tau protein tangles as well as another protein deposit called amyloid beta plaques. The team found that tau accumulation was responsible for cell senescence. Researchers compared Alzheimer’s mice that had only tau tangles with mice that had only amyloid beta plaques. Senescence was identified only in the mice with tau tangles.

In other studies to confirm this, reducing tau genetically also reduced senescence. The reverse also held true. Increasing tau genetically increased senescence.

Importantly, the drug combination reduced not only cell senescence but also tau tangles in the Alzheimer’s mice. This is a drug treatment that does not specifically target tau, but it effectively reduced the tangle pathology, Dr. Orr said.

“When we looked at their brains three months later, we found that the brains had deteriorated less than mice that received placebo control treatment,” she said. “We don’t think brain cells actually grew back, but there was less loss of neurons, less brain ventricle enlargement, improved cerebral blood flow and a decrease in the tau tangles. These drugs were able to clear the tau pathology.”

Potentially a therapy to be tested in humans

“This is the first of what we anticipate will be many studies to better understand this process,” Dr. Musi said. “Because these drugs are approved for other uses in humans, we think a logical next step would be to start pilot studies in people.”

The drugs specifically target—and therefore only kill—the senescent cells. Because the drugs have a short half-life, they are cleared quickly by the body and no side effects were observed.

Dasatinib is an oral medication. The mice were treated with the combination every other week. “So in the three months of treatment, they only received the drug six times,” Dr. Orr said. “The drug goes in, does its job and is cleared. Senescent cells come back with time, but we expect that it would be possible to take the drug again and be cleared out again. That’s a huge benefit—it wouldn’t be a drug that people would have to take every day.”

Dosage and frequency in humans would need to be determined in clinical trials, she said.

Next, the researchers will study whether cell senescence is present in traumatic brain injury. TBI is a brain injury that develops tau protein accumulation and is a significant cause of disability in both military and non-military settings, Dr. Orr said.

Researchers Find New DNA Structure in Living Human Cells

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According to Breaking Science News

A team of scientists from the Garvan Institute of Medical Research and the Universities of New South Wales and Sydney has identified a new DNA structure — called the intercalated motif (i-motif) — inside living human cells.

Deep inside the cells in our body lies our DNA. The information in the DNA code — all 6 billion A, C, G and T letters — provides precise instructions for how our bodies are built, and how they work.

The iconic ‘double helix’ shape of DNA has captured the public imagination since 1953, when James Watson and Francis Crick famously uncovered the structure of DNA.

However, it’s now known that short stretches of DNA can exist in other shapes, in the laboratory at least — and scientists suspect that these different shapes might play an important role in how and when the DNA code is ‘read.’

“When most of us think of DNA, we think of the double helix. This research reminds us that totally different DNA structures exist — and could well be important for our cells,” said co-lead author Dr. Daniel Christ, from the Kinghorn Centre for Clinical Genomics at the Garvan Institute of Medical Research and St Vincent’s Clinical School at the University of New South Wales.

“The i-motif is a four-stranded ‘knot’ of DNA,” added co-lead author Dr. Marcel Dinger, also from the Garvan Institute of Medical Research and the University of New South Wales.

“In the knot structure, C letters on the same strand of DNA bind to each other — so this is very different from a double helix, where ‘letters’ on opposite strands recognize each other, and where Cs bind to Gs [guanines].”

Although researchers have seen the i-motif before and have studied it in detail, it has only been witnessed in vitro — that is, under artificial conditions in the laboratory, and not inside cells. In fact, they have debated whether i-motif DNA structures would exist at all inside living things — a question that is resolved by the new findings.

To detect the i-motifs inside cells, Dr. Christ, Dr. Dinger and their colleagues developed a precise new tool — a fragment of an antibody molecule — that could specifically recognize and attach to i-motifs with a very high affinity.

Until now, the lack of an antibody that is specific for i-motifs has severely hampered the understanding of their role.

Crucially, the antibody fragment didn’t detect DNA in helical form, nor did it recognize ‘G-quadruplex structures’ (a structurally similar four-stranded DNA arrangement).

With the new tool, the team uncovered the location of ‘i-motifs’ in a range of human cell lines.

Using fluorescence techniques to pinpoint where the i-motifs were located, the study authors identified numerous spots of green within the nucleus, which indicate the position of i-motifs.

The scientists showed that i-motifs mostly form at a particular point in the cell’s ‘life cycle’ — the late G1 phase, when DNA is being actively ‘read.’

They also showed that i-motifs appear in some promoter regions — areas of DNA that control whether genes are switched on or off — and in telomeres, ‘end sections’ of chromosomes that are important in the aging process.

“We think the coming and going of the i-motifs is a clue to what they do. It seems likely that they are there to help switch genes on or off, and to affect whether a gene is actively read or not,” said study first author Dr. Mahdi Zeraati, also from the Garvan Institute of Medical Research and the University of New South Wales.

“We also think the transient nature of the i-motifs explains why they have been so very difficult to track down in cells until now,” Dr. Christ added.

“It’s exciting to uncover a whole new form of DNA in cells — and these findings will set the stage for a whole new push to understand what this new DNA shape is really for, and whether it will impact on health and disease,” Dr. Dinger said.

The team’s results appear in the journal Nature Chemistry.

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This article and images were originally posted on [Breaking Science News] April 24, 2018 at 03:11PM. Credit to Author and Breaking Science News | ESIST.T>G>S Recommended Articles Of The Day

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Studying DNA Breaks to Protect Future Space Travelers

Genes in Space logo. May 9, 2019 Earth’s atmosphere shields life on the ground from cosmic radiation that can damage DNA.  Astronauts in space have no such protection, and that puts them at risk. An investigation on the International Space Station examines DNA damage and repair in space in order to help protect the long-term health of space travelers. An organism carries all of its genetic information in its deoxyribonucleic acid or DNA. This blueprint for life takes the form of specific sequences of nitrogen bases: adenine, cytosine, guanine, and thymine, represented by the letters A, C, G and T.

Image above: The miniPCR device, used to make multiple copies of a particular strand of DNA in space. Image Credit: NASA. One type of DNA damage is double strand breaks, essentially a cut across both strands of DNA. Cells repair these breaks almost immediately, but can make errors, inserting or deleting DNA bases and creating mutations. These mutations may result in diseases such as cancer. Genes in Space-6 looks at the specific mechanism cells use to repair double strand breaks in space. The investigation takes cells of the yeast Saccharomyces cerevisiae to the space station, where astronauts cause a specific type of damage to its DNA using a genome editing tool known as CRISPR-Cas9. The astronauts allow the cells to repair this damage, then make many copies of the repaired section using a process called polymerase chain reaction (PCR) with an onboard device, the miniPCR. Another device, MinION, is then used to sequence the repaired section of DNA in those copies. Sequencing shows the exact order of the bases, revealing whether the repair restored the DNA to its original order or made errors. The investigation represents a number of firsts, including the first use of CRISPR-Cas9 genetic editing on the space station and the first time scientists evaluate the entire damage and repair process in space.

Image above: The student team that developed the Genes in Space 6 experiment. From left to right: David Li, Aarthi Vijayakumar, Michelle Sung, and Rebecca Li. Image Credit: Boeing. “The damage actually happens on the space station and the analysis also happens in space,” said one of the investigators from miniPCR Bio, Emily Gleason. “We want to understand if DNA repair methods are different in space than on Earth.” This investigation is part of the Genes in Space program. Founded by miniPCR and Boeing, the program challenges students to come up with DNA experiments in space that involve using the PCR technique and the miniPCR device on the station. Students submit ideas online, and the program chooses five finalists. These finalists are paired with a mentor scientist who helps them turn their idea into a presentation for the ISS Research and Development Conference. A panel of judges selects one proposed experiment to fly to the space station. “We want to inspire students to think like scientists and give them the opportunity for an authentic science experience that doesn’t cost them anything,” says Gleason. More than 550 student teams submitted ideas last year. The Genes in Space-6 investigation student team includes Michelle Sung, Rebecca Li, and Aarthi Vijayakumar at Mounds View High School in Arden Hills, Minnesota, and David Li, now a freshman at the Massachusetts Institute of Technology (MIT) in Cambridge, Massachusetts. Their mentor is Kutay Deniz Atabay at MIT.

Image above: The Genes in Space 6 student team. Image Credit: GENES IN SPACE. Other investigators include Sarah E. Stahl and Sarah Wallace with NASA’s Johnson Space Center Microbiology group in Houston; G. Guy Bushkin, Whitehead Institute for Biomedical Research, Cambridge; Melissa L. Boyer, Teresa K. Tan, Kevin D. Foley, and D. Scott Copeland at Boeing; and Ezequiel Alvarez Saavedra, Gleason, and Sebastian Kraves at Amplyus LLC, in Cambridge. Amplyus is the parent company of miniPCR Bio. “One thing the investigation will tell us is yes, we can do these things in space,” said Gleason. “We expect to see the yeast use the error-free method of repair more frequently, which is what we see on Earth; but we don’t know for sure whether it will be the same or not. Ultimately, we can use this knowledge to help protect astronauts from DNA damage caused by cosmic radiation on long voyages and to enable genome editing in space.” The procedures used in this investigation may have applications for protecting people from radiation and other hazards in remote and harsh locations on Earth as well. Related links: Genes in Space-6: https://www.nasa.gov/mission_pages/station/research/experiments/explorer/Investigation.html?#id=7893 miniPCR: https://www.minipcr.com/ MinION: https://www.nasa.gov/mission_pages/station/research/news/biomolecule_sequencer Genes in Space program: https://www.genesinspace.org/ Space Station Research and Technology: https://www.nasa.gov/mission_pages/station/research/index.html International Space Station (ISS): https://www.nasa.gov/mission_pages/station/main/index.html Images (mentioned), Text, Credits: NASA/Michael Johnson/JSC/International Space Station Program Science Office/Melissa Gaskill. Greetings, Orbiter.ch Full article

Hunt for Huntington!

Possible Biomarker for Huntington’s Identified

A new discovery of a potential biomarker for Huntington’s disease (HD) could mean a more effective way of evaluating the effectiveness of treatments for this neurological disease. The findings may provide insight into treatments that could postpone the death of neurons in people who carry the HD gene mutation, but who do not yet show symptoms of the disease.

Chemis-tree

Chem: Crystallization Tree

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Eye o' Sofia

Chasing the Shadow of Neptune’s Moon Triton

Our Flying Observatory

Our flying observatory, called SOFIA, carries a 100-inch telescope inside a Boeing 747SP aircraft. Scientists onboard study the life cycle of stars, planets (including the atmosphere of Mars and Jupiter), nearby planetary systems, galaxies, black holes and complex molecules in space.

AND on Oct. 5, SOFIA is going on a special flight to chase the shadow of Neptune’s moon Triton as it crosses Earth’s surface!

In case you’re wondering, SOFIA stands for: Stratospheric Observatory for Infrared Astronomy.

Triton

Triton is 1,680 miles (2,700 km) across, making it the largest of the 13 moons orbiting Neptune. Unlike most large moons in our solar system, Triton orbits in the opposite direction of Neptune, called a retrograde orbit. This backward orbit leads scientists to believe that Triton formed in an area past Neptune, called the Kuiper Belt, and was pulled into its orbit around Neptune by gravity. 

The Voyager 2 spacecraft flew past Neptune and Triton in 1989 and found that Triton’s atmosphere is made up of mostly nitrogen…but it has not been studied in nearly 16 years!

Occultations are Eclipse-Like Events

An occultation occurs when an object, like a planet or a moon, passes in front of a star and completely blocks the light from that star. As the object blocks the star’s light, it casts a faint shadow on Earth’s surface. 

But unlike an eclipse, these shadows are not usually visible to the naked eye because the star and object are much smaller and not nearly as bright as our sun. Telescopes with special instruments can actually see these shadows and study the star’s light as it passes near and around the object – if they can be in the right place on Earth to catch the shadow.

Chasing Shadows

Scientists have been making advanced observations of Triton and a background star. They’ve calculated exactly where Triton’s faint shadow will fall on Earth! Our SOFIA team has designed a flight path that will put SOFIA (the telescope and aircraft) exactly in the center of the shadow at the precise moment that Triton and the star will align. 

This is no easy feat because the shadow is moving at more than 53,000 mph while SOFIA flies at Mach 0.85 (652 mph), so we only have about two minutes to catch the shadow!! But our SOFIA team has previously harnessed the aircraft’s mobility to study Pluto from inside the center of its occultation shadow, and is ready to do it again to study Triton!

What We Learn From Inside the Shadow

From inside the shadow, our team on SOFIA will study the star’s light as it passes around and through Triton’s atmosphere. This allows us to learn more about Triton’s atmosphere, including its temperature, pressure, density and composition! 

Our team will use this information to examine if Triton’s atmosphere has changed since our Voyager 2 spacecraft flew past it in 1989. That’s a lot of information from a bit of light inside a shadow! Similar observations of Uranus in 1977, from our previous flying observatory, led to the discovery of rings around that planet!

International Ground-Based Support

Ground-based telescopes across the United States and Europe – from Scotland to the Canary Islands – will also be studying Triton’s occultation. Even though most of these telescopes will not be in the center of the shadow, the simultaneous observations, from different locations on Earth, will give us information about how Triton’s atmosphere varies across its latitudes. 

This data from across the Earth and from onboard SOFIA will help researchers understand how Triton’s atmosphere is distorted at different locations by its high winds and its strong tides!

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