Congratulations to our winners and thank you to all who participated. Happy DNA Day!
Thank you for making this another successful year! We received many submissions from students in 40 U.S. states, and 30 countries. We would also like to thank the ASHG members who participated in judging the essays.
Continue the celebration: ASHG has even more planned to celebrate DNA Day. See how else you can participate on the celebration page.
In this nearly 4-hour SPECIAL EPISODE, Rob Reid delivers a 100-minute monologue (broken up into 4 segments, and interleaved with discussions with Sam) about the looming danger of a man-made pandemic, caused by an artificially-modified pathogen. The risk of this occurring is far higher and nearer-term than almost anyone realizes.
Rob explains the science and motivations that could produce such a catastrophe and explores the steps that society must start taking today to prevent it. These measures are concrete, affordable, and scientifically fascinating—and almost all of them are applicable to future, natural pandemics as well. So if we take most of them, the odds of a future Covid-like outbreak would plummet—a priceless collateral benefit.
Rob Reid is a podcaster, author, and tech investor, and was a long-time tech entrepreneur. His After On podcast features conversations with world-class thinkers, founders, and scientists on topics including synthetic biology, super-AI risk, Fermi’s paradox, robotics, archaeology, and lone-wolf terrorism. Science fiction novels that Rob has written for Random House include The New York Times bestseller Year Zero, and the AI thriller After On. As an investor, Rob is Managing Director at Resilience Reserve, a multi-phase venture capital fund. He co-founded Resilience with Chris Anderson, who runs the TED Conference and has a long track record as both an entrepreneur and an investor. In his own entrepreneurial career, Rob founded and ran Listen.com, the company that created the Rhapsody music service. Earlier, Rob studied Arabic and geopolitics at both undergraduate and graduate levels at Stanford, and was a Fulbright Fellow in Cairo. You can find him at www.after-on.
Scientists at Osaka University, in cooperation with Joanneum Research (Weiz, Austria), have developed wireless health monitoring patches that use embedded piezoelectric nanogenerators to power themselves with harvested biomechanical energy. This work may lead to new autonomous health sensors as well as battery-free wearable electronic devices.
As wearable technology and smart sensors become increasingly popular, the problem of providing power to all of these devices become more relevant. While the energy requirements of each component may be modest, the need for wires or even batteries become burdensome and inconvenient. That is why new energy harvesting methods are needed. Also, the ability for integrated health monitors to use ambient motion to both power and activate sensors will help accelerate their adoption in doctor’s offices.
Now, an international team of researchers from Japan and Austria has invented new ultraflexible patches with a ferroelectric polymer that can not only sense a patient’s pulse and blood pressure, but also power themselves from normal movements. The key was starting with a substrate just one micron thick. Using a strong electric field, ferroelectric crystalline domains in a copolymer were aligned so that the sample had a large electric dipole moment. Based on the piezoelectric effect, which is very efficient in converting natural motion into small electric voltages, the device responds rapidly to strain or pressure changes. These voltages can be transduced either into signals for the medical sensors or to directly harvest the energy. “Our e-health patches may be employed as part of screening for lifestyle-related diseases such as heart disorders, signs of stress, and sleep apnea,” first-author Andreas Petritz says.
Animals are constantly moving and behaving in response to instructions from the brain. But while there are advanced techniques for measuring these instructions in terms of neural activity, there is a paucity of techniques for quantifying the behavior itself in freely moving animals. This inability to measure the key output of the brain limits our understanding of the nervous system and how it changes in disease.
A new study by researchers at Duke University and Harvard University introduces an automated tool that can readily capture behavior of freely behaving animals and precisely reconstruct their three dimensional (3D) pose from a single video camera and without markers.
The April 19 study in Nature Methods led by Timothy W. Dunn, Assistant Professor, Duke University, and Jesse D. Marshall, postdoctoral researcher, Harvard University, describes a new 3D deep-neural network, DANNCE (3-Dimensional Aligned Neural Network for Computational Ethology). The study follows the team’s 2020 study in Neuron which revealed the groundbreaking behavioral monitoring system, CAPTURE (Continuous Appendicular and Postural Tracking using Retroreflector Embedding), which uses motion capture and deep learning to continuously track the 3D movements of freely behaving animals. CAPTURE yielded an unprecedented detailed description of how animals behave. However, it required using specialized hardware and attaching markers to animals, making it a challenge to use.
Over the last 60 years, scientists have been able to observe how and when genetic information was replicated, determining the existence a “replication timing program,” a process that controls when and in what order segments of DNA replicate. However, scientists still cannot explain why such a specific timing sequence exists. In a study published today in Science, Dr. David Gilbert and his team have answered this 60-year-old question.
“Why would cells care about the order in which they replicate DNA?” asked lead scientist Dr. Gilbert. “After all—all cells need to replicate all their DNA. Our hypothesis has been that it’s not just DNA that replicates, but all of the regulatory molecules that read the DNA replicate as well.” Dr. Gilbert further hypothesized that there might be a purpose behind the replication timing program and process because “mother nature would not squander this opportunity to control how the DNA is read.”
“The time at which you replicate provides an ideal time at which to choose whether to maintain all the regulatory factors and continue with the same functional interpretation of the information in DNA or change it to elicit new functions,” explains Dr. Gilbert.
Early trials show Oxford developers may have finally found an effective jab against the disease.
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European cyberknife center to be among the first providers in the world to offer the latest advance in gyroscopic radiosurgery.
Males may have shorter lifespans than females due to repetitive sections of the Y chromosome that create toxic effects as males get older. These new findings appear in a study by Doris Bachtrog of the University of California, Berkeley published April 22 in PLOS Genetics.
In humans and other species with XY sex chromosomes, females often live longer than males. One possible explanation for this disparity may be repetitive sequences within the genome. While both males and females carry these repeat sequences, scientists have suspected that the large number of repeats on the Y chromosome may create a “toxic y effect” that shortens males’ lives. To test this idea, Bachtrog studied male fruit flies from the species Drosophila miranda, which have about twice as much repetitive DNA as females and a shorter lifespan. They showed that when the DNA is in its tightly packed form inside the cells of young male flies, the repeat sections are turned off. But as the flies age, the DNA assumes a looser form that can activate the repeat sections, resulting in toxic side effects.
The new study demonstrates that Y chromosomes that are rich in repeats are a genomic liability for males. The findings also support a more general link between repeat DNA and aging, which currently, is poorly understood. Previous studies in fruit flies have shown that when repeat sections become active, they impair memory, shorten the lifespan and cause DNA damage. This damage likely contributes to aging’s physiological effects, but more research will be needed to uncover the mechanisms underlying repeat DNA’s toxic effects.
A natural compound previously demonstrated to counteract aspects of aging and improve metabolic health in mice has clinically relevant effects in people, according to new research at Washington University School of Medicine in St. Louis.
A small clinical trial of postmenopausal women with prediabetes shows that the compound NMN (nicotinamide mononucleotide) improved the ability of insulin to increase glucose uptake in skeletal muscle, which often is abnormal in people with obesity, prediabetes or Type 2 diabetes. NMN also improved expression of genes that are involved in muscle structure and remodeling. However, the treatment did not lower blood glucose or blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, reduce fat in the liver or decrease circulating markers of inflammation as seen in mice.
The study, published online April 22 in the journal Science, is the first randomized clinical trial to look at the metabolic effects of NMN administration in people.
The second-generation of their implantable scaffold takes the shape of an ice cube tray, and can hold three times as many photoreceptor cells — 300000 of them in all — and features cylindrical holes on the underside so these cells can connect with the patient’s retinal tissue as they mature. It is made from a biocompatible material called poly(glycerol-sebacate) that offers the necessary mechanical strength, but is safely metabolized by the body after it serves its purpose.
One of the main causes of vision loss in adults is deteriorative disorders of the retina, like macular degeneration, that are characterized by the death of the eye’s photoreceptor cells. Scientists are therefore focusing a lot of attention on coming up with ways to regenerate these cells, and a team at the University of Wisconsin-Madison (UW-Madison) has engineered a novel type of scaffold that could give these efforts a boost, by improving the precision with which replacement photoreceptor cells can be delivered into the eye.
Way back in 2012, we looked at research in which UW-Madison scientists demonstrated how pluripotent stem cells could be used to grow retinal tissue in the lab. This tissue featured many of the hallmarks of real retinal tissue, including photoreceptor cells, and raised the prospect of harnessing this technique to grow replacement tissue in place within a damaged or diseased eye to restore vision.
“While it was a breakthrough to be able to make the spare parts – these photoreceptors – it’s still necessary to get them to the right spot so they can effectively reconstruct the retina,” says professor of ophthalmology and visual sciences David Gamm. “So, we started thinking, ‘How can we deliver these cells in a more intelligent way?’ That’s when we reached out to our world-class engineers at UW–Madison.”