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KAIST Research Team Develops Sweat-Resistant Wearable Robot Sensor
New electromyography (EMG) sensor technology that allows the long-term stable control of wearable robots and is not affected by the wearer’s sweat and dead skin has gained attention recently. Wearable robots are devices used across a variety of rehabilitation treatments for the elderly and patients recovering from stroke or trauma. A joint research team led by Professor Jae-Woong Jung from the KAIST School of Electrical Engineering (EE) and Professor Jung Kim from the KAIST Department of Mechanical Engineering (ME) announced on January 23rd that they have successfully developed a stretchable and adhesive microneedle sensor that can electrically sense physiological signals at a high level without being affected by the state of the user’s skin. For wearable robots to recognize the intentions behind human movement for their use in rehabilitation treatment, they require a wearable electrophysiological sensor that gives precise EMG measurements. However, existing sensors often show deteriorating signal quality over time and are greatly affected by the user’s skin conditions. Furthermore, the sensor’s higher mechanical hardness causes noise since the contact surface is unable to keep up with the deformation of the skin. These shortcomings limit the reliable, long-term control of wearable robots. < Figure 1. Design and working concept of the Stretchable microNeedle Adhesive Patch (SNAP). (A) Schematic illustration showing the overall system configuration and application of SNAP. (B) Exploded view schematic diagram of a SNAP, consisting of stretchable serpentine interconnects, Au-coated Si microneedle, and ECA made of Ag flakes–silicone composite. (C) Optical images showing high mechanical compliance of SNAP. > However, the recently developed technology is expected to allow long-term and high-quality EMG measurements as it uses a stretchable and adhesive conducting substrate integrated with microneedle arrays that can easily penetrate the stratum corneum without causing discomfort. Through its excellent performance, the sensor is anticipated to be able to stably control wearable robots over a long period of time regardless of the wearer’s changing skin conditions and without the need for a preparation step that removes sweat and dead cells from the surface of their skin. The research team created a stretchable and adhesive microneedle sensor by integrating microneedles into a soft silicon polymer substrate. The hard microneedles penetrate through the stratum corneum, which has high electrical resistance. As a result, the sensor can effectively lower contact resistance with the skin and obtain high-quality electrophysiological signals regardless of contamination. At the same time, the soft and adhesive conducting substrate can adapt to the skin’s surface that stretches with the wearer’s movement, providing a comfortable fit and minimizing noise caused by movement. < Figure 2. Demonstration of the wireless Stretchable microNeedle Adhesive Patch (SNAP) system as an Human-machine interfaces (HMI) for closed-loop control of an exoskeleton robot. (A) Illustration depicting the system architecture and control strategy of an exoskeleton robot. (B) The hardware configuration of the pneumatic back support exoskeleton system. (C) Comparison of root mean square (RMS) of electromyography (EMG) with and without robotic assistance of pretreated skin and non-pretreated skin. > To verify the usability of the new patch, the research team conducted a motion assistance experiment using a wearable robot. They attached the microneedle patch on a user’s leg, where it could sense the electrical signals generated by the muscle. The sensor then sent the detected intention to a wearable robot, allowing the robot to help the wearer lift a heavy object more easily. Professor Jae-Woong Jung, who led the research, said, “The developed stretchable and adhesive microneedle sensor can stability detect EMG signals without being affected by the state of a user’s skin. Through this, we will be able to control wearable robots with higher precision and stability, which will help the rehabilitation of patients who use robots.” The results of this research, written by co-first authors Heesoo Kim and Juhyun Lee, who are both Ph.D. candidates in the KAIST School of EE, were published in Science Advances on January 17th under the title “Skin-preparation-free, stretchable microneedle adhesive patches for reliable electrophysiological sensing and exoskeleton robot control”. This research was supported by the Bio-signal Sensor Integrated Technology Development Project by the National Research Foundation of Korea, the Electronic Medicinal Technology Development Project, and the Step 4 BK21 Project.
KAIST develops an artificial muscle device that produces force 34 times its weight
- Professor IlKwon Oh’s research team in KAIST’s Department of Mechanical Engineering developed a soft fluidic switch using an ionic polymer artificial muscle that runs with ultra-low power to lift objects 34 times greater than its weight. - Its light weight and small size make it applicable to various industrial fields such as soft electronics, smart textiles, and biomedical devices by controlling fluid flow with high precision, even in narrow spaces. Soft robots, medical devices, and wearable devices have permeated our daily lives. KAIST researchers have developed a fluid switch using ionic polymer artificial muscles that operates at ultra-low power and produces a force 34 times greater than its weight. Fluid switches control fluid flow, causing the fluid to flow in a specific direction to invoke various movements. KAIST (President Kwang-Hyung Lee) announced on the 4th of January that a research team under Professor IlKwon Oh from the Department of Mechanical Engineering has developed a soft fluidic switch that operates at ultra-low voltage and can be used in narrow spaces. Artificial muscles imitate human muscles and provide flexible and natural movements compared to traditional motors, making them one of the basic elements used in soft robots, medical devices, and wearable devices. These artificial muscles create movements in response to external stimuli such as electricity, air pressure, and temperature changes, and in order to utilize artificial muscles, it is important to control these movements precisely. Switches based on existing motors were difficult to use within limited spaces due to their rigidity and large size. In order to address these issues, the research team developed an electro-ionic soft actuator that can control fluid flow while producing large amounts of force, even in a narrow pipe, and used it as a soft fluidic switch. < Figure 1. The separation of fluid droplets using a soft fluid switch at ultra-low voltage. > The ionic polymer artificial muscle developed by the research team is composed of metal electrodes and ionic polymers, and it generates force and movement in response to electricity. A polysulfonated covalent organic framework (pS-COF) made by combining organic molecules on the surface of the artificial muscle electrode was used to generate an impressive amount of force relative to its weight with ultra-low power (~0.01V). As a result, the artificial muscle, which was manufactured to be as thin as a hair with a thickness of 180 µm, produced a force more than 34 times greater than its light weight of 10 mg to initiate smooth movement. Through this, the research team was able to precisely control the direction of fluid flow with low power. < Figure 2. The synthesis and use of pS-COF as a common electrode-electrolyte host for electroactive soft fluid switches. A) The synthesis schematic of pS-COF. B) The schematic diagram of the operating principle of the electrochemical soft switch. C) The schematic diagram of using a pS-COF-based electrochemical soft switch to control fluid flow in dynamic operation. > Professor IlKwon Oh, who led this research, said, “The electrochemical soft fluidic switch that operate at ultra-low power can open up many possibilities in the fields of soft robots, soft electronics, and microfluidics based on fluid control.” He added, “From smart fibers to biomedical devices, this technology has the potential to be immediately put to use in a variety of industrial settings as it can be easily applied to ultra-small electronic systems in our daily lives.” The results of this study, in which Dr. Manmatha Mahato, a research professor in the Department of Mechanical Engineering at KAIST, participated as the first author, were published in the international academic journal Science Advances on December 13, 2023. (Paper title: Polysulfonated Covalent Organic Framework as Active Electrode Host for Mobile Cation Guests in Electrochemical Soft Actuator) This research was conducted with support from the National Research Foundation of Korea's Leader Scientist Support Project (Creative Research Group) and Future Convergence Pioneer Project. * Paper DOI: https://www.science.org/doi/abs/10.1126/sciadv.adk9752
Tinkering with Roundworm Proteins Offers Hope for Anti-aging Drugs
- The somatic nuclear protein kinase VRK-1 increases the worm’s lifespan through AMPK activation, and this mechanism can be applied to promoting human longevity, the study reveals. - KAIST researchers have been able to dial up and down creatures’ lifespans by altering the activity of proteins found in roundworm cells that tell them to convert sugar into energy when their cellular energy is running low. Humans also have these proteins, offering up the intriguing possibilities for developing longevity-promoting drugs. These new findings were published on July 1 in Science Advances. The roundworm Caenorhabditis elegans (C. elegans), a millimeter-long nematode commonly used in lab testing, enjoyed a boost in its lifespan when researchers tinkered with a couple of proteins involved in monitoring the energy use by its cells. The proteins VRK-1 and AMPK work in tandem in roundworm cells, with the former telling the latter to get to work by sticking a phosphate molecule, composed of one phosphorus and four oxygen atoms, on it. In turn, AMPK’s role is to monitor energy levels in cells, when cellular energy is running low. In essence, VRK-1 regulates AMPK, and AMPK regulates the cellular energy status. Using a range of different biological research tools, including introducing foreign genes into the worm, a group of researchers led by Professor Seung-Jae V. Lee from the Department of Biological Sciences at KAIST were able to dial up and down the activity of the gene that tells cells to produce the VRK-1 protein. This gene has remained pretty much unchanged throughout evolution. Most complex organisms have this same gene, including humans. Lead author of the study Sangsoon Park and his colleagues confirmed that the overexpression, or increased production, of the VRK-1 protein boosted the lifespan of the C. elegans, which normally lives just two to three weeks, and the inhibition of VRK-1 production reduced its lifespan. The research team found that the activity of the VRK-1-to-AMPK cellular-energy monitoring process is increased in low cellular energy status by reduced mitochondrial respiration, the set of metabolic chemical reactions that make use of the oxygen the worm breathes to convert macronutrients from food into the energy “currency” that cells spend to do everything they need to do. It is already known that mitochondria, the energy-producing engine rooms in cells, play a crucial role in aging, and declines in the functioning of mitochondria are associated with age-related diseases. At the same time, the mild inhibition of mitochondrial respiration has been shown to promote longevity in a range of species, including flies and mammals. When the research team performed similar tinkering with cultured human cells, they found they could also replicate this ramping up and down of the VRK-1-to-AMPK process that occurs in roundworms. “This raises the intriguing possibility that VRK-1 also functions as a factor in governing human longevity, and so perhaps we can start developing longevity-promoting drugs that alter the activity of VRK-1,” explained Professor Lee. At the very least, the research points us in an interesting direction for investigating new therapeutic strategies to combat metabolic disorders by targeting the modulation of VRK-1. Metabolic disorders involve the disruption of chemical reactions in the body, including diseases of the mitochondria. But before metabolic disorder therapeutics or longevity drugs can be contemplated by scientists, further research still needs to be carried out to better understand how VRK-1 works to activate AMPK, as well as figure out the precise mechanics of how AMPK controls cellular energy. This work was supported by the National Research Foundation (NRF), and the Ministry of Science and ICT (MSIT) of Korea. Image credit: Seung-Jae V. LEE, KAIST. Image usage restrictions: News organizations may use or redistribute this image, with proper attribution, as part of news coverage of this paper only. Publication: Park, S., et al. (2020) ‘VRK-1 extends life span by activation of AMPK via phosphorylation’. Science Advances, Volume 6. No. 27, eaaw7824. Available online at https://doi.org/10.1126/sciadv.aaw7824 Profile: Seung-Jae V. Lee, Ph.D. Professor firstname.lastname@example.org https://sites.google.com/view/mgakaist Molecular Genetics of Aging Laboratory Department of Biological Sciences Korea Advanced Institute of Science and Technology (KAIST) https://www.kaist.ac.krDaejeon 34141, Korea (END)
A Study Finds Neuropeptide Somatostatin Enhances Visual Processing
Researchers have confirmed that neuropeptide somatostatin can improve cognitive function in the brain. A research group of Professor Seung-Hee Lee from the Department of Biological Sciences at KAIST found that the application of neuropeptide somatostatin improves visual processing and cognitive behaviors by reducing excitatory inputs to parvalbumin-positive interneurons in the cortex. This study, reported at Science Advances on April 22nd (EST), sheds a new light on the therapeutics of neurodegenerative diseases. According to a recent study in Korea, one in ten seniors over 65 is experiencing dementia-related symptoms in their daily lives such like memory loss, cognitive decline, and motion function disorders. Professor Lee believes that somatostatin treatment can be directly applied to the recovery of cognitive functions in Alzheimer’s disease patients. Professor Lee started this study noting the fact that the level of somatostatin expression was dramatically decreased in the cerebral cortex and cerebrospinal fluid of Alzheimer’s disease patients Somatostatin-expressing neurons in the cortex are known to exert the dendritic inhibition of pyramidal neurons via GABAergic transmission. Previous studies focused on their inhibitory effects on cortical circuits, but somatostatin-expressing neurons can co-release somatostatin upon activation. Despite the abundant expression of somatostatin and its receptors in the cerebral cortex, it was not known if somatostatin could modulate cognitive processing in the cortex. The research team demonstrated that the somatostatin treatment into the cerebral cortex could enhance visual processing and cognitive behaviors in mice. The research team combined behaviors, in vivo and in vitro electrophysiology, and electron microscopy techniques to reveal how the activation of somatostatin receptors in vivo enhanced the ability of visual recognition in animals. Interestingly, somatostatin release can reduce excitatory synaptic transmission to another subtype of GABAergic interneurons, parvalbumin (PV)-expressing neurons. As somatostatin is a stable and safe neuropeptide expressed naturally in the mammalian brain, it was safe to be injected into the cortex and cerebrospinal fluid, showing a potential application to drug development for curing cognitive disorders in humans. Professor Lee said, “Our research confirmed the key role of the neuropeptide SST in modulating cortical function and enhancing cognitive ability in the mammalian brain. I hope new drugs can be developed based on the function of somatostatin to treat cognitive disabilities in many patients suffering from neurological disorders.” This study was supported by the National Research Foundation of Korea. Publication: Song, Y. H et al. (2020) ‘Somatostatin enhances visual processing and perception by suppressing excitatory inputs to parvalbumin-positive interneurons in V1’, Science Advances, 6(17). Available online at https://doi.org/10.1126/sciadv.aaz0517 Profile: Seung-Hee Lee Associate Professor email@example.com https://sites.google.com/site/leelab2013/ Sensory Processing Lab (SPL) Department of Biological Sciences (BIO) Korea Advanced Institute of Science and Technology (KAIST) Profile: You-Hyang Song Researcher (Ph.D.) firstname.lastname@example.org SPL, KAIST BIO Profile: Yang-Sun Hwang Researcher (M.S.) email@example.com SPL, KAIST BIO (END)
What Fuels a “Domino Effect” in Cancer Drug Resistance?
KAIST researchers have identified mechanisms that relay prior acquired resistance to the first-line chemotherapy to the second-line targeted therapy, fueling a “domino effect” in cancer drug resistance. Their study featured in the February 7 edition of Science Advances suggests a new strategy for improving the second-line setting of cancer treatment for patients who showed resistance to anti-cancer drugs. Resistance to cancer drugs is often managed in the clinic by chemotherapy and targeted therapy. Unlike chemotherapy that works by repressing fast-proliferating cells, targeted therapy blocks a single oncogenic pathway to halt tumor growth. In many cases, targeted therapy is engaged as a maintenance therapy or employed in the second-line after front-line chemotherapy. A team of researchers led by Professor Yoosik Kim from the Department of Chemical and Biomolecular Engineering and the KAIST Institute for Health Science and Technology (KIHST) has discovered an unexpected resistance signature that occurs between chemotherapy and targeted therapy. The team further identified a set of integrated mechanisms that promotes this kind of sequential therapy resistance. “There have been multiple clinical accounts reflecting that targeted therapies tend to be least successful in patients who have exhausted all standard treatments,” said the first author of the paper Mark Borris D. Aldonza. He continued, “These accounts ignited our hypothesis that failed responses to some chemotherapies might speed up the evolution of resistance to other drugs, particularly those with specific targets.” Aldonza and his colleagues extracted large amounts of drug-resistance information from the open-source database the Genomics of Drug Sensitivity in Cancer (GDSC), which contains thousands of drug response data entries from various human cancer cell lines. Their big data analysis revealed that cancer cell lines resistant to chemotherapies classified as anti-mitotic drugs (AMDs), toxins that inhibit overacting cell division, are also resistant to a class of targeted therapies called epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs). In all of the cancer types analyzed, more than 84 percent of those resistant to AMDs, representatively ‘paclitaxel’, were also resistant to at least nine EGFR-TKIs. In lung, pancreatic, and breast cancers where paclitaxel is often used as a first-line, standard-of-care regimen, greater than 92 percent showed resistance to EGFR-TKIs. Professor Kim said, “It is surprising to see that such collateral resistance can occur specifically between two chemically different classes of drugs.” To figure out how failed responses to paclitaxel leads to resistance to EGFR-TKIs, the team validated co-resistance signatures that they found in the database by generating and analyzing a subset of slow-doubling, paclitaxel-resistant cancer models called ‘persisters’. The results demonstrated that paclitaxel-resistant cancers remodel their stress response by first becoming more stem cell-like, evolving the ability to self-renew to adapt to more stressful conditions like drug exposures. More surprisingly, when the researchers characterized the metabolic state of the cells, EGFR-TKI persisters derived from paclitaxel-resistant cancer cells showed high dependencies to energy-producing processes such as glycolysis and glutaminolysis. “We found that, without an energy stimulus like glucose, these cells transform to becoming more senescent, a characteristic of cells that have arrested cell division. However, this senescence is controlled by stem cell factors, which the paclitaxel-resistant cancers use to escape from this arrested state given a favorable condition to re-grow,” said Aldonza. Professor Kim explained, “Before this research, there was no reason to expect that acquiring the cancer stem cell phenotype that dramatically leads to a cascade of changes in cellular states affecting metabolism and cell death is linked with drug-specific sequential resistance between two classes of therapies.” He added, “The expansion of our work to other working models of drug resistance in a much more clinically-relevant setting, perhaps in clinical trials, will take on increasing importance, as sequential treatment strategies will continue to be adapted to various forms of anti-cancer therapy regimens.” This study was supported by the Basic Science Research Program of the National Research Foundation of Korea (NRF-2016R1C1B2009886), and the KAIST Future Systems Healthcare Project (KAISTHEALTHCARE42) funded by the Korean Ministry of Science and ICT (MSIT). Undergraduate student Aldonza participated in this research project and presented the findings as the lead author as part of the Undergraduate Research Participation (URP) Program at KAIST. < Figure 1. Schematic overview of the study. > < Figure 2. Big data analysis revealing co-resistance signatures between classes of anti-cancer drugs. > Publication: Aldonza et al. (2020) Prior acquired resistance to paclitaxel relays diverse EGFR-targeted therapy persistence mechanisms. Science Advances, Vol. 6, No. 6, eaav7416. Available online at http://dx.doi.org/10.1126/sciadv.aav7416 Profile: Prof. Yoosik Kim, MA, PhD firstname.lastname@example.org https://qcbio.kaist.ac.kr/ Assistant Professor Bio Network Analysis Laboratory Department of Chemical and Biomolecular Engineering Korea Advanced Institute of Science and Technology (KAIST) http://kaist.ac.kr Daejeon, Republic of Korea Profile: Mark Borris D. Aldonza email@example.com Undergraduate Student Department of Biological Sciences Korea Advanced Institute of Science and Technology (KAIST) http://kaist.ac.kr Daejeon, Republic of Korea (END)
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