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KAIST Develops Wearable Carbon Dioxide Sensor to Enable Real-time Apnea Diagnosis
- Professor Seunghyup Yoo’s research team of the School of Electrical Engineering developed an ultralow-power carbon dioxide (CO2) sensor using a flexible and thin organic photodiode, and succeeded in real-time breathing monitoring by attaching it to a commercial mask - Wearable devices with features such as low power, high stability, and flexibility can be utilized for early diagnosis of various diseases such as chronic obstructive pulmonary disease and sleep apnea < Photo 1. From the left, School of Electrical Engineering, Ph.D. candidate DongHo Choi, Professor Seunghyup Yoo, and Department of Materials Science and Engineering, Bachelor’s candidate MinJae Kim > Carbon dioxide (CO2) is a major respiratory metabolite, and continuous monitoring of CO2 concentration in exhaled breath is not only an important indicator for early detection and diagnosis of respiratory and circulatory system diseases, but can also be widely used for monitoring personal exercise status. KAIST researchers succeeded in accurately measuring CO2 concentration by attaching it to the inside of a mask. KAIST (President Kwang-Hyung Lee) announced on February 10th that Professor Seunghyup Yoo's research team in the Department of Electrical and Electronic Engineering developed a low-power, high-speed wearable CO2 sensor capable of stable breathing monitoring in real time. Existing non-invasive CO2 sensors had limitations in that they were large in size and consumed high power. In particular, optochemical CO2 sensors using fluorescent molecules have the advantage of being miniaturized and lightweight, but due to the photodegradation phenomenon of dye molecules, they are difficult to use stably for a long time, which limits their use as wearable healthcare sensors. Optochemical CO2 sensors utilize the fact that the intensity of fluorescence emitted from fluorescent molecules decreases depending on the concentration of CO2, and it is important to effectively detect changes in fluorescence light. To this end, the research team developed a low-power CO2 sensor consisting of an LED and an organic photodiode surrounding it. Based on high light collection efficiency, the sensor, which minimizes the amount of excitation light irradiated on fluorescent molecules, achieved a device power consumption of 171 μW, which is tens of times lower than existing sensors that consume several mW. < Figure 1. Structure and operating principle of the developed optochemical carbon dioxide (CO2) sensor. Light emitted from the LED is converted into fluorescence through the fluorescent film, reflected from the light scattering layer, and incident on the organic photodiode. CO2 reacts with a small amount of water inside the fluorescent film to form carbonic acid (H2CO3), which increases the concentration of hydrogen ions (H+), and the fluorescence intensity due to 470 nm excitation light decreases. The circular organic photodiode with high light collection efficiency effectively detects changes in fluorescence intensity, lowers the power required light up the LED, and reduces light-induced deterioration. > The research team also elucidated the photodegradation path of fluorescent molecules used in CO2 sensors, revealed the cause of the increase in error over time in photochemical sensors, and suggested an optical design method to suppress the occurrence of errors. Based on this, the research team developed a sensor that effectively reduces errors caused by photodegradation, which was a chronic problem of existing photochemical sensors, and can be used continuously for up to 9 hours while existing technologies based on the same material can be used for less than 20 minutes, and can be used multiple times when replacing the CO2 detection fluorescent film. < Figure 2. Wearable smart mask and real-time breathing monitoring. The fabricated sensor module consists of four elements (①: gas-permeable light-scattering layer, ②: color filter and organic photodiode, ③: light-emitting diode, ④: CO2-detecting fluorescent film). The thin and light sensor (D1: 400 nm, D2: 470 nm) is attached to the inside of the mask to monitor the wearer's breathing in real time. > The developed sensor accurately measured CO2 concentration by being attached to the inside of a mask based on the advantages of being light (0.12 g), thin (0.7 mm), and flexible. In addition, it showed fast speed and high resolution that can monitor respiratory rate by distinguishing between inhalation and exhalation in real time. < Photo 2. The developed sensor attached to the inside of the mask > Professor Seunghyup Yoo said, "The developed sensor has excellent characteristics such as low power, high stability, and flexibility, so it can be widely applied to wearable devices, and can be used for the early diagnosis of various diseases such as hypercapnia, chronic obstructive pulmonary disease, and sleep apnea." He added, "In particular, it is expected to be used to improve side effects caused by rebreathing in environments where dust is generated or where masks are worn for long periods of time, such as during seasonal changes." This study, in which KAIST's Department of Materials Science and Engineering's undergraduate student Minjae Kim and School of Electrical Engineering's doctoral student Dongho Choi participated as joint first authors, was published in the online version of Cell's sister journal, Device, on the 22nd of last month. (Paper title: Ultralow-power carbon dioxide sensor for real-time breath monitoring) DOI: https://doi.org/10.1016/j.device.2024.100681 < Photo 3. From the left, Professor Seunghyup Yoo of the School of Electrical Engineering, MinJae Kim, an undergraduate student in the Department of Materials Science and Engineering, and Dongho Choi, a doctoral student in the School of Electrical Engineering > This study was supported by the Ministry of Trade, Industry and Energy's Materials and Components Technology Development Project, the National Research Foundation of Korea's Original Technology Development Project, and the KAIST Undergraduate Research Participation Project. This work was supported by the (URP) program.
2025.02.13
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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 ysyoosik@kaist.ac.kr 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 borris@kaist.ac.kr Undergraduate Student Department of Biological Sciences Korea Advanced Institute of Science and Technology (KAIST) http://kaist.ac.kr Daejeon, Republic of Korea (END)
2020.02.10
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