Stretchable Technology: Revolutionizing Next-Generation Electronics through Freeform Deformation

Flexible and deformable electronics have advanced beyond bendable, foldable, rollable, and slidable designs to fully stretchable systems that allow freeform deformation. Stretchable technology is gaining traction in diverse fields, such as displays, sensors, semiconductors, electronic skin, biomimetic robots, and smart clothing.

Stretchable technology largely relies on two approaches: creating elastic materials similar to rubber and designing stretchable structures that integrate seamlessly with existing semiconductor, display, electrode, and sensor technologies. In structural stretchable technology, the serpentine interconnect — a wavy, elastic connection — plays a crucial role in providing elasticity to non-stretchable electronic components. Advancing this technology requires a thorough understanding of the structural characteristics and deformation processes during all stages of stretching.

Visualizing Deformation of Serpentine Structures in Real Time

Until now, analyzing deformation in serpentine structures was only possible after physical damage, such as breaks, had occurred. This meant researchers had to rely on theoretical simulations or limited observational data from previous stretching cycles, hindering real-time insights into structural behavior.

The POSTECH team tackled this challenge by leveraging changes in structural color — color shifts that occur at the nanoscale during deformation. Using Chiral Liquid Crystal Elastomer (CLCE), a mechanochromic material that changes color when stretched, they developed a system that enables precise, real-time visualization of deformation in serpentine structures. Furthermore, the team validated the results through theoretical finite element analysis, confirming the technology’s potential for optimized design applications.

Technological and Industrial Significance

This innovative approach eliminates the need for complex nanofabrication processes and provides a clear, real-time understanding of how serpentine structures deform. By offering actionable design guidelines for optimizing these structures in diverse stretching environments, this technology is poised to fast-track the commercialization of stretchable devices.

Professor Su Seok Choi remarked, “This research opens the door to precise evaluation and design of the connection structures central to stretchable technology.” He added that the findings are expected to broaden applications and accelerate commercialization in fields such as displays, semiconductors, sensors, electronic skin, smart clothing, and soft robotics.

Acknowledgments

This research was supported by the Samsung Future Technology Development Program and the Stretchable Display Development and Demonstration Initiative under the Korea Planning & Evaluation Institute of Industrial Technology.

This could enable medics to identify sooner any decline in lung function.

The scan method has enabled the team, led by researchers at Newcastle University, UK, to see how air moves in and out of the lungs as people take a breath in patients with asthma, chronic obstructive pulmonary disease (COPD), and patients who have received a lung transplant.

Publishing two complementary papers in Radiology and JHLT Open, the team explain how they use a special gas, called perfluoropropane, that can be seen on an MRI scanner. The gas can be safely breathed in and out by patients, and then scans taken to look at where in the lungs the gas has reached.

The project lead, Professor Pete Thelwallis Professor of Magnetic Resonance Physics and Director of the Centre for In Vivo Imaging at Newcastle University. He said; “Our scans show where there is patchy ventilation in patients with lung disease, and show us which parts of the lung improve with treatment. For example, when we scan a patient as they use their asthma medication, we can see how much of their lungs and which parts of their lung are better able to move air in and out with each breath.”

Using the new scanning method, the team are able to reveal the parts of the lung that air doesn’t reach properly during breathing. By measuring how much of the lung is well-ventilated and how much is poorly ventilated, experts can make an assessment of the effects of a patient’s respiratory disease, and they can locate and visualise the lung regions with ventilation defects.

Demonstrating that the scans work in patients with asthma or COPD, the team comprising experts from across Universities and NHS Trusts in Newcastle and Sheffield publish the first paper in Radiology.

The new scanning technique allows the team to quantify the degree of improvement in ventilation when patients have a treatment, in this case a widely used inhaler, the bronchodilator, salbutamol. This shows that the imaging methods could be valuable in clinical trials of new treatments of lung disease.

Use in lung transplants

A further study, published in JHLT Open, examined patients who had previously received a lung transplant for very severe lung disease at the Newcastle upon Tyne Hospitals NHS Foundation Trust. It demonstrates how the team further developed the imaging method to provide lung function measurements which could be used to better support lung transplant recipients in the future. The sensitivity of the measurement means medics can spot early changes in lung function allowing them to identify lung problems earlier and so provide better care for patients.

In research studies, the team scanned transplant recipients’ lungs over multiple breaths in and out, collecting MRI pictures that show how the air containing the gas reached different areas of the lung. The team scanned those who either had normal lung function or who were experiencing chronic rejection after lung transplant, which is a common issue in lung transplant recipients as their immune system attacks the donor lungs. In those with chronic rejection, the scans showed poorer movement of air to the edges of the lungs, most likely due to damage in the very small breathing tubes (airways) in the lung, a feature typical of chronic rejection also known as chronic lung allograft dysfunction.

Professor Andrew Fisher, Professor of Respiratory Transplant Medicine at Newcastle Hospitals NHS Foundation Trust and Newcastle University, UK, co-author of the study said; “We hope this new type of scan might allow us to see changes in the transplant lungs earlier and before signs of damage are present in the usual blowing tests. This would allow any treatment to be started earlier and help protect the transplanted lungs from further damage.”

The team say there is potential for this scan method to be used in the clinical management of lung transplant recipients and other lung diseases in the future, bringing a sensitive measurement that may spot early changes in lung function that enable better management of these conditions.

This work on lung imaging has been funded by the Medical Research Council and by The Rosetrees Trust.

PolyP and magnesium are involved in many biological processes. Thus, the findings could lead to new methods for tuning cellular responses, which could have impactful applications in translational medicine.

The ensuing study, published in Nature Communications on October 26, 2024, reveals a delicate “Goldilocks” zone — a specific magnesium concentration range — where DNA wraps around polyP-magnesium ion condensates. Similar to a thin eggshell covering a liquid-like interior, this seemingly simple structure may help cells organize and protect their genetic material.

This work began as a collaboration between co-senior authors Associate Professor Lisa Racki, PhD, and Professor Ashok Deniz, PhD, both in the Department of Integrative Structural and Computational Biology at Scripps Research. Racki had been studying these structures in bacterial cells, while Deniz’s next-door lab was exploring the physical chemistry of biomolecular condensates for the past decade. Collaboration, they realized, was the only way to unlock these ancient interactions.

“We knew that DNA was in close proximity to the magnesium-rich polyP condensates in cells, but we were totally surprised by the beautiful spheres of DNA that lit up under the microscope,” says Racki.

“Being molecular detectives, seeing these structures raised exciting questions for us about the physics and mathematics of the DNA shells and whether they influenced the polyP condensates,” adds Deniz.

Their microscopy images revealed that DNA wraps itself around a condensate, creating a thin eggshell-like barrier. This shell could affect molecule transportation and also slow down fusion: the process where two condensates merge into one. Without DNA shells, polyP-magnesium ion condensates readily fused — like how oil drops and vinegar fuse in a salad dressing bottle when shook.

However, careful examination showed that fusion overall slowed to varying extents, depending on DNA length. Longer DNA, the researchers suspected, caused greater entanglement on condensate surfaces — similar to how long hair tangles more than short hair.

DNA is more than 1,000 times thinner in diameter than condensates, making molecular details hard to visualize. Fortunately, infrastructure to capture such imaging has been developed by two other faculty members at Scripps Research: Assistant Professor Danielle Grotjahn, PhD, and Scripps Fellow Donghyun Raphael Park, PhD.

Teaming with Park, with help from Grotjahn, the researchers used cryo-electron tomography to closely examine the condensate surfaces. Using electrons instead of light, this technique captures three-dimensional, high-resolution images of samples that were rapidly frozen to preserve their structures. The new images revealed that DNA forms filaments protruding from condensate surfaces, resembling tangled hairs.

Another crucial discovery: DNA shell formation only occurred within a specific magnesium concentration range — too much or too little, and the shell wouldn’t materialize. This “Goldilocks” effect highlights how cells can regulate condensate structure, size and function simply by tuning control parameters.

“Although we think of cellular interfaces as boundaries, they also create a new landscape by providing a surface for molecules to organize,” notes Racki. “DNA may not actually be a tangled mess at the surface and is instead organized by these condensates.”

In this context, Deniz and Racki are particularly interested in understanding DNA supercoiling — how DNA twists like a spring to fit inside cells.

“Cells have to manage their DNA curls,” explains Racki. “Interestingly, the mathematics of DNA supercoiling results in ‘action-at-a-distance’ effects — like how twisting a rope can create coils far from where you’re holding it.”

The researchers suspect that DNA interactions with polyP condensates in cells might propagate local changes in DNA supercoiling over long distances, resulting in broader changes in gene expression and cell function. Investigating this effect is one of the team’s next goals.

“We’re excited by the prospects of leveraging these discoveries to develop new tools for cellular control — potentially simpler, more cost-effective approaches to manage biomatter for biomedicine,” says Deniz.

In addition to Deniz, Racki, Grotjahn and Park, authors of the study, “Reentrant DNA shells tune polyphosphate condensate size,” include co-first authors Ravi Chawla and Jenna K. A. Tom, and Tumara Boyd, Nicholas H. Tu and Tanxi Bai of Scripps Research.

This work was supported by funding from the National Institutes of Health (NIGMS Grant R35 GM130375, Grant DP2-GM-739-140918 and S10OD032467), Scripps Research start-up funds, a Postdoctoral Fellowship from the American Heart Association (Award #903967) and the Pew Scholars Program.

But sometimes, as in the corporate world, outright theft can be a quicker way to achieve dominance.

University of California, Berkeley biologists have shown that several species of fruit fly have stolen a successful defense from bacteria to survive predation by parasitic wasps, which in some flies can turn half of all fly larvae into surrogate wombs for baby wasps — a gruesome fate that inspired the creature in the 1979 movie “Alien.”

Bacteria and other microbes are famous for stealing genes from other microbes or viruses; this so-called horizontal gene transfer is the source of troublesome antibiotic resistance among disease-causing microbes. But it’s thought to be less common in multicellular organisms, such as insects and humans. Understanding how common it is in animals and how these genes are co-opted and shared can help scientists understand the evolution of animal immune defenses and could point the way to human therapies to fight parasitic or infectious diseases or cancer, itself a kind of parasite.

“It’s a model for understanding how immune systems evolve, including our immune system, which also contains horizontally transferred genes,” said Noah Whiteman, UC Berkeley professor of molecular and cell biology and of integrative biology and director of the campus’s Essig Museum of Entomology.

Last year, the researchers and their colleagues in Hungary used CRISPR genome editing to knock out the gene responsible for the defense in one widespread fly species, Drosophila ananassae, and found that nearly all the genetically modified flies died from predation by parasitic wasps.

In a new study published Dec. 20 in the journal Current Biology, the biologists demonstrated that this defense — a gene that encodes a toxin — can be edited into the genome of the common laboratory fruit fly, Drosophila melanogaster, to make them resistant to parasitoid wasps as well. The gene essentially becomes part of the fly’s immune system, one weapon in its armamentarium to fend off parasites.

The results demonstrate how crucial the stolen defense is to fly survival and highlights a strategy that may be more common in animals that scientists suspect.

“This shows that horizontal gene transfer is an underappreciated way that rapid evolution happens in animals,” said UC Berkeley doctoral student Rebecca Tarnopol, first author of the Current Biology paper. “People appreciate horizontal gene transfer as one of the major drivers of rapid adaptation in microbes, but these events were thought to be super uncommon in animals. But at least in insects, it seems like they’re fairly frequent.”

According to Whiteman, senior author of the paper, “The study shows that in order to keep up with the barrage of parasites that are continually evolving new ways to overcome host defenses, a good strategy for animals is to borrow genes from even more rapidly evolving viruses and bacteria, and that’s just what these flies have done.”

Gene flow from virus to bacteria to fly

Whiteman studies how insects evolve to resist the toxins that plants produce to prevent being eaten. In 2023, he published a book, “Most Delicious Poison,” about the plant toxins that humans have come to enjoy, such as caffeine and nicotine.

One plant-herbivore interaction he focuses on is that between the common fruit fly Scaptomyza flava and sour-tasting mustard plants, like the cresses that grow in streams throughout the world.

“The larvae, the immature stages of the fly, live in the leaves of the plant. They’re leaf miners, they leave little trails in the leaves,” Whiteman said. “They’re true parasites of the plant and the plant’s trying to kill them with its specialized chemicals. We study that arms race.”

What he’s learned, however, likely applies to many other insects, among the most successful herbivores on Earth.

“These are obscure little flies, but if you think about the fact that half of all living insect species are herbivores, it’s a very popular life history. Understanding the evolution of that is really important for understanding evolution in general in terms of how successful herbivores are,” he said.

Several years ago, after sequencing the fly’s genome in search of genes that allow it to resist mustard toxins, he discovered an unusual gene that he learned was widespread in bacteria. A search through earlier published genome sequences turned up the same gene in a related fly, Drosophila ananassae, as well as in a bacteria that lives inside an aphid. Researchers studying the aphid uncovered a complicated story: The gene actually comes from a bacterial virus, or bacteriophage, that infects the bacteria that live inside the aphid. The bacteriophage gene, expressed by the bacteria, makes the aphid resistant to a parasitic wasp that plagues it.

These wasps lay their eggs inside the larvae, or maggots, and remain there until the larvae turn into immobile pupae, at which point the wasp eggs mature into wasp larvae that consume the fly pupa, eventually emerging as adults.

When Tarnopol first used gene editing to express the toxin gene in all cells of D. melanogaster, all the flies died. But when Tarnopol expressed the gene only in certain immune cells, the fly became as resistant to parasites as its cousin, D. ananassae.

Whiteman, Tarnopol, and their colleagues subsequently discovered that the gene found in the genome of D. ananassae — a fusion between two toxin genes, cytolethal distending toxin B (cdtB) and apoptosis inducing protein of 56kDa (aip56), that the researchers called fusionB — codes for an enzyme that cuts up DNA.

To discover how this nuclease is able to kill a wasp egg, the UC Berkeley researchers reached out to István Andó at the Institute of Genetics of the HUN-REN Biological Research Centre in Szeged, Hungary, which had previously shown that these same flies have a cellular defense against wasp eggs that essentially walls off the eggs from the fly’s body and kills them. Andó and his lab colleagues created antibodies to the toxin that allowed them to track it through the fly’s body and found that the nuclease essentially floods the fly’s body to surround and kill the egg.

“We’ve been finding this huge untapped world of humoral immune factors that might be at play in the immune system of invertebrates,” Tarnopol said. “Our paper is one of the first ones to show, at least in Drosophila, that this type of immune response might be a common mechanism by which natural enemies like wasps and nematodes are dealt with. They are way more lethal in nature than some of the microbial infections that most people work with.”

Whiteman and his colleagues are still exploring the complexities of these interactions between fly and wasp, and the cellular and genetic changes that allowed the flies to synthesize a toxin without killing itself.

“If the gene is expressed in the wrong tissue, the fly is going to die. That gene is never going to sweep through populations through natural selection,” Whiteman said. “But if it lands in a place in the genome that’s near some enhancer or some regulatory component that expresses it a little bit in fat body tissue, then you can see how it can get this leg up really quickly, you get this amazing advantage.”

Horizontal gene transfer in any organism would pose similar problems, he said, but in the arms race between predator and prey, it may be worth it.

“When you’re a poor little fruit fly, how do you deal with these pathogens and parasites that are rapidly evolving to take advantage of you?” he said. “One way is to borrow genes from bacteria and viruses because they’re rapidly evolving. It’s an ingenious strategy — instead of waiting around for your own genes to help you, take them from other organisms that are more rapidly evolving than themselves. And that seems to have happened many times independently in insects, given that so many different ones have taken up this gene. It gives us a picture of a new kind of dynamism that is occurring even in animals that have just innate immune systems and don’t have adaptive immunity.”

Whiteman’s work was funded by the National Institute of General Medical Sciences of the National Institutes of Health (R35GM119816). Other co-authors of the paper are Josephine Tamsil, Ji Heon Ha, Kirsten Verster and Susan Bernstein of UC Berkeley, Gyöngyi Cinege, Edit Ábrahám, Lilla B. Magyar and Zoltán Lipinszki of Hungary and Bernard Kim of Stanford University.

Viruses are uniquely designed to encapsulate genetic material within spherical protein shells, enabling them to replicate and invade host cells, often causing disease. Inspired by these complex structures, researchers have been exploring artificial proteins modeled after viruses. These “nanocages” mimic viral behavior, effectively delivering therapeutic genes to target cells. However, existing nanocages face significant challenges: their small size restricts the amount of genetic material they can carry, and their simple designs fall short of replicating the multifunctionality of natural viral proteins.

To address these limitations, the research team used AI-driven computational design. While most viruses display symmetrical structures, they also feature subtle asymmetries. Leveraging AI, the team recreated these nuanced characteristics and successfully designed nanocages in tetrahedral, octahedral, and icosahedral shapes for the first time.

The resulting nanostructures are composed of four types of artificial proteins, forming intricate architectures with six distinct protein-protein interfaces. Among these, the icosahedral structure, measuring up to 75 nanometers in diameter, stands out for its ability to hold three times more genetic material than conventional gene delivery vectors, such as adeno-associated viruses (AAV), marking a significant advancement in gene therapy.

Electron microscopy confirmed the AI-designed nanocages achieved precise symmetrical structures as intended. Functional experiments further demonstrated their ability to effectively deliver therapeutic payloads to target cells, paving the way for practical medical applications.

“Advancements in AI have opened the door to a new era where we can design and assemble artificial proteins to meet humanity’s needs,” said Professor Sangmin Lee. “We hope this research not only accelerates the development of gene therapies but also drives breakthroughs in next-generation vaccines and other biomedical innovations.”

Professor Lee previously worked as a postdoctoral researcher in Professor Baker’s laboratory at the University of Washington for nearly three years, from February 2021 to late 2023, before joining POSTECH in January 2024.

This study was supported by the Republic of Korea’s Ministry of Science and ICT under the Outstanding Young Scientist Program, the Nano and Material Technology Development Program, and the Global Frontier Research Program, with additional funding provided by the Howard Hughes Medical Institute (HHMI) in the United States.

Lithium-ion batteries are indispensable in applications such as electric vehicles and energy storage systems (ESS). The lithium-rich layered oxide (LLO) material offers up to 20% higher energy density than conventional nickel-based cathodes by reducing the nickel and cobalt content while increasing the lithium and manganese composition. As a more economical and sustainable alternative, LLO has garnered significant attention. However, challenges such as capacity fading and voltage decay during charge-discharge cycles have hindered its commercial viability.

While previous studies have identified structural changes in the cathode during cycling as the cause of these issues, the exact reasons behind the instability have remained largely unclear. Additionally, existing strategies aimed at enhancing the structural stability of LLO have failed to resolve the root cause, hindering commercialization.

The POSTECH team focused on the pivotal role of oxygen release in destabilizing the LLO structure during the charge-discharge process. They hypothesized that improving the chemical stability of the interface between the cathode and the electrolyte could prevent oxygen from being released. Building on this idea, they reinforced the cathode-electrolyte interface by improving the electrolyte composition, which resulted in a significant reduction in oxygen emissions.

The research team’s enhanced electrolyte maintained an impressive energy retention rate of 84.3% even after 700 charge-discharge cycles, a significant improvement over conventional electrolytes, which only achieved an average of 37.1% energy retention after 300 cycles.

The research also revealed that structural changes on the surface of the LLO material had a significant impact on the overall stability of the material. By addressing these changes, the team was able to dramatically improve the lifespan and performance of the cathode while also minimizing unwanted reactions like electrolyte decomposition inside the battery.

Professor Jihyun Hong commented, “Using synchrotron radiation, we were able to analyze the chemical and structural differences between the surface and interior of the cathode particles. This revealed that the stability of the cathode surface is crucial for the overall structural integrity of the material and its performance. We believe this research will provide new directions for developing next-generation cathode materials.”

This research was supported by the Ministry of Trade, Industry and Energy through the Korea Institute for Advancement of Technology, and the Ministry of Science and ICT through the National Research Foundation of Korea, with funding for 2024.