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A new technique for electrospinning sponges has allowed scientists from the University of Surrey to directly produce 3D scaffolds—on which skin grafts could be grown from the patient’s own skin.

Electrospinning is a technique that electrifies droplets of liquid to form fibers from plastics. Previously, scientists had only been able to make 2D films. This is the first time anybody has electro-spun a 3D structure directly and on-demand so that it can be produced to scale. The research is published in the journal Nanomaterials.

Chloe Howard, from Surrey’s School of Computer Science and Electronic Engineering, said, After spinning these scaffolds, we grew skin cells on them. Seven days later, they were twice as viable as cells grown on 2D films or mats. They even did better than cells grown on plasma-treated polystyrene—previously, the gold standard. They were very happy cells on our 3D scaffolds.

Networks can represent changing systems, like the spread of an epidemic or the growth of groups in a population of people. But the structure of these networks can change, too, as links appear or vanish over time. To better understand these changes, researchers often study a series of static “snapshots” that capture the structure of the network during a short duration.

Network theorists have sought ways to combine these snapshots. In a new paper in Physical Review Letters, a trio of SFI-affiliated researchers describe a novel way to aggregate static snapshots into smaller clusters of networks while still preserving the dynamic nature of the system. Their method, inspired by an idea from quantum mechanics, involves testing successive pairs of network snapshots to find those for which a combination would result in the smallest effect on the dynamics of the system—and then combining them.

Importantly, it can determine how to simplify the history of the network’s structure as much as possible while maintaining accuracy. The math behind the method is fairly simple, says lead author Andrea Allen, now a data scientist at Children’s Hospital of Philadelphia.

Researchers report in the journal Cell that ancient viruses may be to thank for myelin—and, by extension, our large, complex brains.

The team found that a retrovirus-derived genetic element or “retrotransposon” is essential for myelin production in mammals, amphibians, and fish. The gene sequence, which they dubbed “RetroMyelin,” is likely a result of ancient viral infection, and comparisons of RetroMyelin in mammals, amphibians, and fish suggest that retroviral infection and genome-invasion events occurred separately in each of these groups.

“Retroviruses were required for vertebrate evolution to take off,” says senior author and neuroscientist Robin Franklin of Altos Labs-Cambridge Institute of Science. “If we didn’t have retroviruses sticking their sequences into the vertebrate genome, then myelination wouldn’t have happened, and without myelination, the whole diversity of vertebrates as we know it would never have happened.”

A 3D printed ‘metamaterial’ boasting levels of strength for weight not normally seen in nature or manufacturing could change how we make everything from medical implants to aircraft or rocket parts.

RMIT University researchers created the new metamaterial—a term used to describe an artificial material with unique properties not observed in nature—from common titanium alloy.

But it’s the material’s unique lattice structure design, recently revealed in the journal Advanced Materials, that makes it anything but common: tests show it’s 50% stronger than the next strongest alloy of similar density used in aerospace applications.

On Wednesday, February 21st, at 01:40 p.m. PST (04:40 p.m. EST), an interesting package returned to Earth from space.

This was the capsule from the W-1 mission, an orbital platform manufactured by California-based Varda Space Industries, which landed at the Utah Test and Training Range (UTTR). Even more interesting was the payload, which consisted of antiviral drugs grown in the microgravity environment of Low Earth Orbit (LEO).

The mission is part of the company’s goal to develop the infrastructure to make LEO more accessible to commercial industries.

Investigators identified 15 factors that affect risk for young-onset dementia.

Limited data are available on risk factors for young-onset dementia. In this study, researchers assessed 39 potential risk factors for young-onset dementia from data in the UK Biobank. Participants 65 years of age or older without a dementia diagnosis were included in the analysis. Potential risk factors were grouped into sociodemographic factors, genetic factors, lifestyle factors, environmental factors, blood marker factors, cardiometabolic factors, psychiatric factors, and other risk factors.

Among 359,052 participants, the mean age at baseline was 55 years and 55% were women. There were 485 incident all-cause young-onset dementia cases after a mean follow-up of 8 years. Incident young-onset dementia increased with age and was more common in men. Fewer years of formal education, lower socioeconomic status, the presence of two apolipoprotein E ℇ4 alleles, no alcohol use, alcohol use disorder, social isolation, vitamin D deficiency (1 mg/dL), lower handgrip strength, hearing impairment, orthostatic hypotension, stroke, diabetes, heart disease, and depression were associated with higher risk for young-onset dementia in fully adjusted models. Men with diabetes were more likely to have young-onset dementia than men without diabetes, and women with high C-reactive protein were more likely to have young-onset dementia than women with low C-reactive protein levels.

Continue reading “Risk Factors for Young-Onset Dementia” »

DNA and Information combined with science and biotechnology. Can we resurrect the dead?

We don’t exactly know why we age; we know what aging looks like —the “symptoms”, so to speak— but the root causes remain foggy. One leading hypothesis is that the changes associated with old age, both external and internal, are a result of accumulating DNA damage. As this damage builds, cellular functions begin to break down and important pathways start going haywire.

One of the most extreme forms of DNA damage is the double-strand break, which happens when a strand of DNA snaps in half, leaving two separate slivers floating around. Left unfixed, these strands can snag at and break chromosomes, leading to diseases like cancer and other disorders. But how the body repairs this kind of wreckage has been a source of mystery. Now, scientists at the Dresden University of Technology have managed to shine a light on the process. Published in Cell, their work offers important new insights that may eventually help treat, and possibly reverse, DNA damage.

In November last year, UK approved a therapy that uses the CRISPR gene editing tool to treat sickle cell disease and β-thalassaemia.