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AI Opens a New Era in Medical Science and Bio < (From left) KAIST Professors Yoonjae Choi, Tae-Kyun Kim, Jong Chul Ye, Hyunwoo Kim, Seunghoon Hong, Sang Yup Lee > KAIST announced on the 14th of November that it has been selected as a major participating institution in the 'Lunit Consortium' for the 'AI Specialized Foundation Model Development Project' supervised by the Ministry of Science and ICT, and has officially started developing an AI foundation model for the medical science and bio fields. Through this project, KAIST plans to develop an 'AI Foundation Model Specialized for Medical Science' that encompasses the entire lifecycle of bio and medical data, and lead the creation of an AI based life science innovation ecosystem. The 'Lunit Consortium' includes 7 companies-Lunit, Trillion Labs, Kakao Healthcare, Igenscience, SK Biopharm, and Rebellion-along with 9 medical and research institutions, including KAIST, Seoul National University, NYU, National Health Insurance Service Ilsan Hospital, and Yonsei Severance Hospital. This consortium will be supported by 256 state of the art B200 GPUs to build and demonstrate a 'Chain of Evidence-Based Full-Cycle Medical Science AI Model', an AI system that connects and analyzes medical data from beginning to end, and a 'Multi-Agent Service', a system where multiple AIs collaborate to perform diagnosis and prediction. KAIST's participation in this project involves a joint research team formed by professors from the School of Computing and the Kim Jaechul Graduate School of AI. Professors Yoonjae Choi, Tae-Kyun Kim, Jong Chul Ye, Hyunwoo Kim, and Seunghoon Hong will serve as the research team, and Vice President for Research Sang Yup Lee will take on an advisory role. The research team is not merely collecting data but they are establishing a strategy (L1~L7 stages) to precisely process and systematically manage medical and life science data so that the AI can actually learn and utilize it. Through this, they plan to develop and verify an AI model that connects and analyzes diverse life science data, including medical information, gene/protein data, and new drug candidates. The data the research team aims to integrate includes a wide range from language to actual patient treatment information. Specifically, L1 represents language data, L2 is the structure of molecules, L3 is proteins and antibodies, L4 is omics data encompassing genetic and protein information, L5 is drug information, L6 is medical science research and clinical data, and L7 is real-world clinical data obtained from actual hospitals. In essence, the data handled by the AI connects everything from speech and text to molecules, proteins, drugs, clinical research, and actual patient treatment information. < The process of training AI by viewing X ray images and doctor's interpretation (text) together (MedViLL from Professor Jae-Yoon Choi' s lab) > Vice President Sang Yup Lee is a world-renowned scholar in the fields of synthetic biology and systems metabolic engineering, leading the establishment of a bio manufacturing platform and policy advice through the convergence of life science, engineering, and AI. He advises on the analysis of life information (omics) such as genes and proteins and designs a feedback system for verifying experimental results, supporting the Korean-developed medical AI model to secure international reliability and competitiveness. Vice President Lee stated, "AI technology is breaking down the boundaries of life science and engineering, creating a new paradigm for knowledge creation," adding, "KAIST will utilize full cycle medical science data to accelerate the era where AI uncovers the causes of diseases and predicts treatments." KAIST President Kwang Hyung Lee said, "KAIST will contribute to creating an AI-based life science innovation ecosystem, lead the innovation of national strategic industries through world-class AI-bio convergence research, and drive the progress of human health and science and technology." The model developed in the Lunit Consortium will be released as an Open License for commercial use, and is expected to expand into various medical and healthcare services such as national health chatbots. With this participation, KAIST plans to strengthen research on AI-based life science data infrastructure establishment, medical AI standardization, and AI ethics and policy advice, leading the AI transition of national bio and medical science research.
2025.11.14 View 1557
KAIST Uncovers the Mechanism Behind Overactive Immune Cells <(From Right) Professor Eui-Cheol Shin, Ph.D candidate So-Young Kim, Professor Su-Hyung Park, Professor Hyuk Soo Eun, Dr. Hoyoung Lee> “Why do immune cells that are supposed to eliminate viruses suddenly turn against our own body?” There are instances where killer T cells—which are meant to precisely remove virus-infected cells—malfunction like overheated engines, attacking even healthy cells and damaging tissues. A KAIST research team has now identified the key mechanism that regulates this excessive activation of killer T cells, offering new insights into controlling immune overreactions and developing therapies for immune-related diseases. KAIST (President Kwang Hyung Lee) announced on November 5 that a research team led by Professors Eui-Cheol Shin and Su-Hyung Park from the Graduate School of Medical Science and Engineering, in collaboration with Professor Hyuk Soo Eun from Chungnam National University College of Medicine, has uncovered the molecular basis of nonspecific activation in killer T cells and proposed a new therapeutic strategy to control it. Killer T cells (CD8⁺ T cells) selectively eliminate infected cells to prevent viral spread. However, when excessively activated, they can attack uninfected cells, causing inflammation and tissue damage. Such overactive immune responses can lead to severe viral infections and autoimmune diseases. In 2018, Professor Shin’s team was the first in the world to discover that killer T cells can be nonspecifically activated by cytokines and randomly attack host cells—a phenomenon they termed “bystander activation of T cells”. The current study builds on that discovery by revealing the molecular mechanism driving this abnormal process. The team focused on a cytokine called interleukin-15 (IL-15). Experiments showed that IL-15 can abnormally excite killer T cells by a bystander activation mechanism, causing them to attack uninfected host cells. However, when there is a concurrent antigen-specific stimulation, IL-15-induced bystander activation is suppressed. The researchers further identified that this suppression occurs through an intracellular signaling process. When the concentration of calcium ions (Ca²⁺) changes, a protein called calcineurin activates, which in turn triggers a regulatory protein known as NFAT, suppressing IL-15-induced bystander activation of killer T cells. In other words, the calcineurin–NFAT pathway activated by antigen stimulation acts as a brake on overactivation by a bystander mechanism. The team also discovered that some immunosuppressants, which are known to block the calcineurin pathway, may not always suppress immune responses—in certain contexts, they can instead promote IL-15-induced bystander activation of killer T cells. This finding underscores that not all immunosuppressants work the same way and that treatments must be carefully tailored to each patient’s immune response. Through gene expression analysis, the researchers identified a gene set that increase only in abnormally activated killer T cells induced by IL-15 as markers. They further confirmed that these same markers were elevated in bystander killer T cells from patients with acute hepatitis A, suggesting that the markers could be used for disease diagnosis. <In a normal immune response, killer T cells are activated by antigen stimulation and selectively eliminate only virus-infected cells, thereby controlling viral replication and promoting the patient’s rapid recovery. However, when killer T cells are nonspecifically overactivated by interleukin-15, they may randomly attack normal cells as well, causing excessive tissue damage and leading to severe disease. Future research may identify diseases in which such nonspecific hyperimmune responses occur, making it possible to develop new drugs to control them> This study provides crucial clues for understanding the pathogenesis of various immune-related diseases, including severe viral infections, chronic inflammatory disorders, autoimmune diseases, and organ transplant rejection. It also paves the way for developing novel immunoregulatory therapies targeting IL-15 signaling. Professor Eui-Cheol Shin explained that, “this study shows that killer T cells are not merely defenders—they can transform into ‘nonspecific attackers’ depending on the inflammatory environment. By precisely regulating this abnormal activation, we may be able to develop new treatments for intractable immune diseases.” This research was published in the journal Immunity on October 31, with Dr. Hoyoung Lee and Ph.D. candidate So-Young Kim as co–first authors. Title: “TCR signaling via NFATc1 constrains IL-15-induced bystander activation of human memory CD8⁺ T cells”, DOI: doi.org/10.1016/j.immuni.2025.10.002 The study was supported by the National Research Foundation of Korea (NRF), the Korea Health Industry Development Institute (KHIDI), and the Institute for Basic Science (IBS).
2025.11.06 View 1908
KAIST Exports Global License for New Drug Candidate for Intractable Epilepsy Worth 750 Billion KRW <(From Left) Professor Jeong Ho Lee, CEO Cheolwon Park, Principal Researcher Sang-min Park> KAIST (President Kwang Hyung Lee) announced on the 9th of October that Sovargen (co-led by CEOs Cheolwon Park and Jeong Ho Lee), a faculty startup led by Professor Jeong Ho Lee of the KAIST Graduate School of Medical Science and Engineering, has successfully achieved a global technology export deal worth a total of 750 billion KRW. The deal involves an innovative RNA-based new drug candidate for the treatment of intractable epilepsy. This achievement is drawing attention as a representative example of how groundbreaking discoveries from KAIST’s fundamental medical science research can evolve into actual drug development and global market expansion. Professor Jeong Ho Lee’s research team was the first in the world to identify that the cause of severe brain diseases such as intractable epilepsy and malignant brain tumors lies in brain somatic mutations—acquired mutations that occur in neural stem cells. Their findings were published in Nature (2015) and Nature Medicine (2018). Later, together with Cheolwon Park of Sovargen, an expert in drug development, they discovered an RNA-based therapeutic—an Antisense Oligonucleotide (ASO)—that directly targets MTOR, a key mutated gene responsible for epilepsy. Through a large-scale technology transfer agreement with a global pharmaceutical company, they also demonstrated the drug’s commercial potential. This achievement is particularly significant in that it was led by Professor Jeong Ho Lee, a physician-scientist (M.D.-Ph.D.) who integrates intensive basic research with translational studies and venture entrepreneurship. An idea that originated in a basic research lab has developed into the world’s first innovative drug (first-in-class) candidate through a startup, creating a virtuous cycle that connects back to the global market. Sovargen’s Principal Researcher Sang Min Park (KAIST Graduate School of Medical Science and Engineering alumnus) stated, “From identifying the disease cause to developing a new drug and exporting the technology globally, this achievement was made possible entirely through the power of Korean science.” Sovargen CEO Cheolwon Park added, “This success was made possible thanks to the strong support of President Kwang Hyung Lee and key KAIST leaders for both the Graduate School of Medical Science and Engineering and faculty-led startups.” Professor Jeong Ho Lee commented, “While traditional medical schools in Korea are centered around clinical practice, KAIST fosters a research culture focused on innovation and industrialization. This enabled us to achieve both groundbreaking basic research and global new drug technology export.” He continued, “This success serves as an excellent example of the future direction of KAIST’s medical science research.” Experts have evaluated this accomplishment as one that opens new therapeutic possibilities for patients suffering from intractable epilepsy—conditions that previously had no treatment options—while also demonstrating that Korean medical science and biotech ventures are capable of competing on the global stage in innovative new drug development. KAIST President Kwang Hyung Lee remarked, “This achievement is a representative example of how KAIST’s research philosophy—‘from fundamentals to industry’—has been realized in the field of medical science.” He added, “KAIST will continue to pursue bold fundamental research to lead innovations that advance human health and the future bioindustry.”
2025.10.10 View 1553
Professor Jinsoo Kim Donates 3.4 Billion Won in Stocks to Pioneer Solutions for Climate and Food Crises through Gene Editing < (From left) Daesoo Kim, Dean of College of Life Sciences and BioEngineering / Kyunmin Lee, Vice President for Academic Affairs/ Professor Jinsoo Kim/ Kwang Hyung Lee, President / Sang Yup Lee, Vice President for Research> KAIST announced that Professor Jinsoo Kim of the Graduate School of Medical Science and Engineering has donated 85,000 shares of ToolGen Inc. stock to help overcome climate disasters and agricultural crises. The shares are valued at approximately 3.438 billion won as of September 15, and KAIST plans to use them to actively promote innovative research in the fields of agriculture and life sciences. The donation will be used to establish the "Center for Plant-based Carbon Capture," which is scheduled to be founded in the second half of this year. Based on this, KAIST aims to contribute to a sustainable future by fully embarking on research to address climate change and global food security issues. The research center will focus on developing technologies that maximize the photosynthetic efficiency of plants and microalgae. The goal is to contribute to carbon neutrality by increasing the absorption rate of atmospheric carbon dioxide, while also significantly improving food productivity to enhance food security. The core technology is the "direct editing technology for organelle DNA (chloroplasts and mitochondria)," which Professor Kim developed for the first time in the world. Chloroplasts, which perform photosynthesis using sunlight, and mitochondria, which act as the cell's energy powerhouse, have their own DNA that could not be edited with existing CRISPR technology. This new technology can precisely edit even this DNA, and it can also be used in the future for research and treatment of intractable genetic diseases. Furthermore, because the crops developed with this technology involve direct editing of the DNA already present in the plant rather than inserting foreign genes, they are not considered GMOs (Genetically Modified Organisms). They are recognized as "Non-GMOs" in countries like the United States and Japan. This lowers regulatory barriers and increases consumer acceptance, greatly expanding the potential for commercialization and market entry. With the establishment of this research center, KAIST anticipates various achievements, including overcoming the food crisis amid climate change, a revolutionary increase in agricultural productivity, the presentation of sustainable carbon reduction methods, and the creation of a next-generation bioenergy industry. Applying Professor Kim's core technology, high-efficiency crops that can absorb a large amount of carbon dioxide and be used as an energy source can be mass-produced. These crops can be used as a raw material for Sustainable Aviation Fuel (SAF), an eco-friendly aviation fuel, which is expected to be an important stepping stone for Korea to emerge as a powerhouse in future aviation fuels. Professor Kim stated, "The climate change and food security crises facing humanity are no longer issues that we can turn a blind eye to. I decided to make this donation with the hope of contributing to a sustainable future through the advancement of gene editing science and technology, talent cultivation, and industry-academia-research collaboration." KAIST President Kwang Hyung Lee emphasized, "Professor Jinsoo Kim's donation is a role model that shows a scientist's dedication and social responsibility. KAIST will lead innovative technologies and take the lead in solving the global climate and food crises through the Center for Plant-based Carbon Capture."
2025.09.16 View 1430
Opening the Door to Personalized Bipolar Disorder Treatment <(From Left) Professor Jinju Han, Dr. Gyu Hyeon Baek, Dr. Dayeon Kim, Dr. Geurim Son, Dr. Hyunsu Do> Bipolar disorder, also known as 'manic-depressive illness,' a brain disorder known to have afflicted the famous painter Vincent van Gogh, is characterized by recurrent episodes of mania and depression. This disease affects about 1-2% of the world's population, and the risk of suicide is 10 to 30 times higher than in the general population. However, because each patient's response to lithium, the main treatment, varies greatly, there is an urgent need to develop personalized treatments. In response, a research team at KAIST has identified the differences in lithium responsiveness and presented the new possibility of developing personalized treatments and a drug discovery platform based on this finding. On September 10th, the research team led by Professor Jinju Han from the KAIST Graduate School of Medical Science and Engineering announced they were the first to identify metabolic differences in astrocytes based on lithium responsiveness, thereby suggesting the potential for personalized treatment develogpment for bipolar disorder. Astrocytes are star-shaped cells in the brain that act as 'helpers to neurons,' providing them with nutrients and maintaining the brain's environment. Breaking away from the existing neuron-centric research paradigm, Professor Jinju Han's team focused on astrocytes, which make up half of the brain's cells, and discovered that they play a key role in regulating the metabolism of bipolar disorder. The research team differentiated induced pluripotent stem cells (iPSCs) from patients' cells into astrocytes (a process in which stem cells grow and specialize into cells with specific functions) and observed them. As a result, it was confirmed that the cells' energy metabolism changed significantly depending on whether they responded to lithium. In cases of no lithium response, distinct metabolic abnormalities were observed, including an excessive accumulation of lipid droplets (tiny fat storage depots) inside the cells, decreased mitochondrial function (the cell's power plant), an over-activation of the glucose breakdown process, and excessive lactate secretion. <The process of astrocyte-neuron interaction in patients with bipolar disorder> Specifically, in the astrocytes of lithium-responsive patients, lipid droplets decreased upon lithium treatment, but there was no improvement in non-responsive patients. Furthermore, significant differences were found in the metabolites produced by astrocytes depending on the patient type. This suggests that the cell's energy factory does not function properly depending on the lithium response, and alternative pathways are overused, leading to a buildup of byproducts. This finding is particularly significant as it proves that astrocytes play a key role in regulating energy metabolism in bipolar disorder, explaining the differences in lithium responsiveness and paving the way for personalized treatment strategies for each patient. Professor Jinju Han stated, "The development of new treatments targeting astrocytes is now possible, which could provide better treatment strategies for patients who do not respond to existing medications." This research was published online on August 22 in Molecular Psychiatry, a leading international journal in the field of neuropsychiatric disorders. ※ Paper Title: Differential effects of lithium on metabolic dysfunctions in astrocytes derived from bipolar disorder patients DOI: https://doi.org/10.1038/s41380-025-03176-w ※ Author Information: Gyu Hyeon Baek, Dayeon Kim, Geurim Son, Hyunsu Do (KAIST, co-first authors) and Jinju Han (KAIST, corresponding author). This research was supported by the National Research Foundation of Korea and the Korea Environmental Industry and Technology Institute, among others.
2025.09.10 View 1846
KAIST reveals for the first time the mechanism by which alcohol triggers liver inflammation <(From left)Dr. Keungmo Yang, Professor Won-Il Jeong, Ph.D candidate Kyurae Kim> Excessive alcohol consumption causes alcoholic liver disease, and about 20% of these cases progress to alcohol-associated steatohepatitis (ASH), which can lead to liver cirrhosis and liver failure. Early diagnosis and treatment are therefore extremely important. A KAIST research team has identified a new molecular mechanism in which alcohol-damaged liver cells increase reactive oxygen species (ROS), leading to cell death and inflammatory responses. In addition, they discovered that Kupffer cells, immune cells residing in the liver, act as a “dual-function regulator” that can either promote or suppress inflammation through interactions with liver cells. KAIST (President Kwang-Hyung Lee) announced on the 17th that a research team led by Professor Won-Il Jeong from the Graduate School of Medical Science and Engineering, in collaboration with Professor Won Kim’s team at Seoul National University Boramae Medical Center, has uncovered the molecular pathway of liver damage and inflammation caused by alcohol consumption. This finding offers new clues for the diagnosis and treatment of alcohol-associated liver disease (ALD). Professor Won-Il Jeong’s research team found that during chronic alcohol intake, expression of the vesicular glutamate transporter VGLUT3 increases, leading to glutamate accumulation in hepatocytes. Subsequent binge drinking causes rapid changes in intracellular calcium levels, which then triggers glutamate* secretion. The secreted glutamate stimulates the glutamate receptor mGluR5 on liver-resident macrophages (Kupffer cells), which induces ROS production and activates a pathological pathway resulting in hepatocyte death and inflammation. *Glutamate: A type of amino acid involved in intercellular signaling, protein synthesis, and energy metabolism in various tissues including the brain and liver. In excess, it can cause overexcitation and death of nerve cells. Glutamate accumulation in perivenous hepatocytes through vesicular glutamate transporter 3 after 2-week EtOH intake and its release by binge drinking> A particularly groundbreaking aspect of this study is that damaged hepatocytes and Kupffer cells can form a "pseudosynapse"—a structure similar to a synapse which is previously thought to occur only in the brain—enabling them to exchange signals. This is the first time such a phenomenon has been identified in the liver. This pseudosynapse forms when hepatocytes expand (ballooning) due to alcohol, becoming physically attached to Kupffer cells. Simply put, the damaged hepatocytes don’t just die—they send distress signals to nearby immune cells, prompting a response. This discovery proposes a new paradigm: even in peripheral organs, direct structural contact between cells can allow signal transmission. It also shows that damaged hepatocytes can actively stimulate macrophages and induce regeneration through cell death, revealing the liver’s “autonomous recovery function.” The team also confirmed in animal models that genetic or pharmacological inhibition of VGLUT3, mGluR5, or the ROS-producing enzyme NOX2 reduces alcohol-induced liver damage. They also confirmed that the same mechanism observed in animal models was present in human patients with ALD by analyzing blood and liver tissue samples. Professor Won-Il Jeong of KAIST said, “These findings may serve as new molecular targets for early diagnosis and treatment of ASH in the future.” This study was jointly led by Dr. Keungmo Yang (now at Yeouido St. Mary’s Hospital) and Kyurae Kim, a doctoral candidate at KAIST, who served as co–first authors. It was conducted in collaboration with Professor Won Kim’s team at Seoul National University Boramae Medical Center and was published in the journal Nature Communications on July 1. ※ Article Title: Binge drinking triggers VGLUT3-mediated glutamate secretion and subsequent hepatic inflammation by activating mGluR5/NOX2 in Kupffer cells ※ DOI: https://doi.org/10.1038/s41467-025-60820-3 This study was supported by the Ministry of Science and ICT through the National Research Foundation of Korea's Global Leader Program, Mid-Career Researcher Program, and the Bio & Medical Technology Development Program.
2025.07.17 View 2788
Scientist Discover How Circadian Rhythm Can Be Both Strong and Flexible Study reveals that master and slave oscillators function via different molecular mechanisms From tiny fruit flies to human beings, all animals on Earth maintain their daily rhythms based on their internal circadian clock. The circadian clock enables organisms to undergo rhythmic changes in behavior and physiology based on a 24-hour circadian cycle. For example, our own biological clock tells our brain to release melatonin, a sleep-inducing hormone, at night time. The discovery of the molecular mechanism of the circadian clock was bestowed the Nobel Prize in Physiology or Medicine 2017. From what we know, no one centralized clock is responsible for our circadian cycles. Instead, it operates in a hierarchical network where there are “master pacemaker” and “slave oscillator”. The master pacemaker receives various input signals from the environment such as light. The master then drives the slave oscillator that regulates various outputs such as sleep, feeding, and metabolism. Despite the different roles of the pacemaker neurons, they are known to share common molecular mechanisms that are well conserved in all lifeforms. For example, interlocked systems of multiple transcriptional-translational feedback loops (TTFLs) composed of core clock proteins have been deeply studied in fruit flies. However, there is still much that we need to learn about our own biological clock. The hierarchically-organized nature of master and slave clock neurons leads to a prevailing belief that they share an identical molecular clockwork. At the same time, the different roles they serve in regulating bodily rhythms also raise the question of whether they might function under different molecular clockworks. Research team led by Professor Kim Jae Kyoung from the Department of Mathematical Sciences, a chief investigator at the Biomedical Mathematics Group at the Institute for Basic Science, used a combination of mathematical and experimental approaches using fruit flies to answer this question. The team found that the master clock and the slave clock operate via different molecular mechanisms. In both master and slave neurons of fruit flies, a circadian rhythm-related protein called PER is produced and degraded at different rates depending on the time of the day. Previously, the team found that the master clock neuron (sLNvs) and the slave clock neuron (DN1ps) have different profiles of PER in wild-type and Clk-Δ mutant Drosophila. This hinted that there might be a potential difference in molecular clockworks between the master and slave clock neurons. However, due to the complexity of the molecular clockwork, it was challenging to identify the source of such differences. Thus, the team developed a mathematical model describing the molecular clockworks of the master and slave clocks. Then, all possible molecular differences between the master and slave clock neurons were systematically investigated by using computer simulations. The model predicted that PER is more efficiently produced and then rapidly degraded in the master clock compared to the slave clock neurons. This prediction was then confirmed by the follow-up experiments using animal. Then, why do the master clock neurons have such different molecular properties from the slave clock neurons? To answer this question, the research team again used the combination of mathematical model simulation and experiments. It was found that the faster rate of synthesis of PER in the master clock neurons allows them to generate synchronized rhythms with a high level of amplitude. Generation of such a strong rhythm with high amplitude is critical to delivering clear signals to slave clock neurons. However, such strong rhythms would typically be unfavorable when it comes to adapting to environmental changes. These include natural causes such as different daylight hours across summer and winter seasons, up to more extreme artificial cases such as jet lag that occurs after international travel. Thanks to the distinct property of the master clock neurons, it is able to undergo phase dispersion when the standard light-dark cycle is disrupted, drastically reducing the level of PER. The master clock neurons can then easily adapt to the new diurnal cycle. Our master pacemaker’s plasticity explains how we can quickly adjust to the new time zones after international flights after just a brief period of jet lag. It is hoped that the findings of this study can have future clinical implications when it comes to treating various disorders that affect our circadian rhythm. Professor Kim notes, “When the circadian clock loses its robustness and flexibility, the circadian rhythms sleep disorders can occur. As this study identifies the molecular mechanism that generates robustness and flexibility of the circadian clock, it can facilitate the identification of the cause of and treatment strategy for the circadian rhythm sleep disorders.” This work was supported by the Human Frontier Science Program. -PublicationEui Min Jeong, Miri Kwon, Eunjoo Cho, Sang Hyuk Lee, Hyun Kim, Eun Young Kim, and Jae Kyoung Kim, “Systematic modeling-driven experiments identify distinct molecularclockworks underlying hierarchically organized pacemaker neurons,” February 22, 2022, Proceedings of the National Academy of Sciences of the United States of America -ProfileProfessor Jae Kyoung KimDepartment of Mathematical SciencesKAIST
2022.02.23 View 16262
President Lee Presents Plans to Nurture Next-Generation Talents President Lee stressed that nurturing medical scientists, semiconductor R&D personnel, startup entrepreneurs, and global innovators are key missions he will continue to pursue during a news conference KAIST President Kwang Hyung Lee said that nurturing medical scientists, semiconductor R&D personnel, startup entrepreneurs, and global innovators are key missions he will continue to pursue during an online news conference marking the 1st anniversary of him becoming the president on February 15. He said that nurturing physician-scientists is the most critical mission for KAIST to help the nation create a new growth engine. He said KAIST will help the nation drive the bio-industry and provide medical science resources for the nation’s health sector. To this end, he said that KAIST will open its Medical Science and Technology School by 2026. “We plan to expand the current Graduate School of Medical Science and Engineering into a new Medical Science and Technology School that will focus entirely on a condensed MD-PhD course converging the fields of AI, bio, and physics,” he said. The school aims to foster medical scientists whose research results will eventually be commercialized. He said that the university is now discussing revisions to related laws and regulations with the government and other universities. To supply human resources to the semiconductor industry, President Lee said the university will add a campus in Pyongtaek City that will serve as an advanced convergence research hub in the field of next generation semiconductors in collaboration with Samsung Electronics and the city of Pyongtaek. The three-stage opening plan projected the final opening of the campus by 2036. During the first stage, which will be completed by 2026, it will construct the campus infrastructure in Pyongtaek city where Samsung Semiconductors runs two massive semiconductor complexes. By 2031, it plans to launch the open research platform including a future cities research center and future vehicles research center. The campus will open the global industrial collaboration cluster hub by 2036. In the global arena, President Lee said he is working to open the New York campus with stakeholders in the United States. He announced the plan last December that was endorsed by New York-based entrepreneur Hee-Nam Bae, the chairman of Big Continent Inc. President Lee and Chairman Lee signed an MOU for the funding to open the campus in New York. “We are discussing how to facilitate the plan and best accommodate the interests and potential of our students. Many ideas and plans are on the table and we think it will take longer than expected to finalize the plan,” explained President Lee. However, he added that the basic idea is to offer art tech and health technology programs as well as an AI-based finance MBA at the New York campus, in addition to it serving as the startup accelerator of KAIST. President Lee stressed the importance of technology commercialization when successfully launching KAIST Holdings last month to help spinoffs of KAIST labs accelerate their end results. He said that KAIST Holdings will build a virtuous supporting system to commercialize the technology startups coming from KAIST. “We plan to list at least 10 KAIST startups on the KOSDAQ and two on the NASDAQ by 2031. KAIST Holdings also aims to nurture companies valued at a total of one billion KRW and earn 100 billion KRW in technology fees by 2031.
2022.02.17 View 18154
'Mini-Lungs' Reveal Early Stages of SARS-CoV-2 Infection Researchers in Korea and the UK have successfully grown miniature models of critical lung structures called alveoli, and used them to study how the coronavirus that causes COVID-19 infects the lungs. To date, there have been more than 40 million cases of COVID-19 and almost 1.13 million deaths worldwide. The main target tissues of SARS-CoV-2, the virus that causes COVID-19, especially in patients that develop pneumonia, appear to be alveoli – tiny air sacs in the lungs that take up the oxygen we breathe and exchange it with carbon dioxide to exhale. To better understand how SARS-CoV-2 infects the lungs and causes disease, a team of Professor Young Seok Ju from the Graduate School of Medical Science and Engineering at KAIST in collaboration with the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge turned to organoids – ‘mini-organs’ grown in three dimensions to mimic the behaviour of tissue and organs. The team used tissue donated to tissue banks at the Royal Papworth Hospital NHS Foundation Trust and Addenbrooke’s Hospital, Cambridge University NHS Foundations Trust, UK, and Seoul National University Hospital to extract a type of lung cell known as human lung alveolar type 2 cells. By reprogramming these cells back to their earlier ‘stem cell’ stage, they were able to grow self-organizing alveolar-like 3D structures that mimic the behaviour of key lung tissue. “The research community now has a powerful new platform to study precisely how the virus infects the lungs, as well as explore possible treatments,” said Professor Ju, co-senior author of the research. Dr. Joo-Hyeon Lee, another co-senior author at the Wellcome-MRC Cambridge Stem Cell Institute, said: “We still know surprisingly little about how SARS-CoV-2 infects the lungs and causes disease. Our approach has allowed us to grow 3D models of key lung tissue – in a sense, ‘mini-lungs’ – in the lab and study what happens when they become infected.” The team infected the organoids with a strain of SARS-CoV-2 taken from a patient in Korea who was diagnosed with COVID-19 on January 26 after traveling to Wuhan, China. Using a combination of fluorescence imaging and single cell genetic analysis, they were able to study how the cells responded to the virus. When the 3D models were exposed to SARS-CoV-2, the virus began to replicate rapidly, reaching full cellular infection just six hours after infection. Replication enables the virus to spread throughout the body, infecting other cells and tissue. Around the same time, the cells began to produce interferons – proteins that act as warning signals to neighbouring cells, telling them to activate their antiviral defences. After 48 hours, the interferons triggered the innate immune response – its first line of defence – and the cells started fighting back against infection. Sixty hours after infection, a subset of alveolar cells began to disintegrate, leading to cell death and damage to the lung tissue. Although the researchers observed changes to the lung cells within three days of infection, clinical symptoms of COVID-19 rarely occur so quickly and can sometimes take more than ten days after exposure to appear. The team say there are several possible reasons for this. It may take several days from the virus first infiltrating the upper respiratory tract to it reaching the alveoli. It may also require a substantial proportion of alveolar cells to be infected or for further interactions with immune cells resulting in inflammation before a patient displays symptoms. “Based on our model we can tackle many unanswered key questions, such as understanding genetic susceptibility to SARS-CoV-2, assessing relative infectivity of viral mutants, and revealing the damage processes of the virus in human alveolar cells,” said Professor Ju. “Most importantly, it provides the opportunity to develop and screen potential therapeutic agents against SARS-CoV-2 infection.” “We hope to use our technique to grow these 3D models from cells of patients who are particularly vulnerable to infection, such as the elderly or people with diseased lungs, and find out what happens to their tissue,” added Dr. Lee. The research was a collaboration involving scientists from KAIST, the University of Cambridge, Korea National Institute of Health, Institute for Basic Science (IBS), Seoul National University Hospital and Genome Insight in Korea. - ProfileProfessor Young Seok JuLaboratory of Cancer Genomics https://julab.kaist.ac.kr the Graduate School of Medical Science and EngineeringKAIST
2020.10.26 View 16230
Professor Won-Ki Cho Selected as the 2020 SUHF Young Investigator Professor Won-Ki Cho from the Department of Biological Sciences was named one of three recipients of the 2020 Suh Kyung-Bae Science Foundation (SUHF) Young Investigator Award. The SUHF is a non-profit organization established in 2016 and funded by a personal donation of 300 billion KRW in shares from Chairman and CEO Kyung-Bae Suh of the Amorepacific Group. The primary purpose of the foundation is to serve as a platform to nurture and provide comprehensive long-term support for creative and passionate young Korean scientists committed to pursuing research in the field of life sciences. The SUHF selects three to five scientists through an open recruiting process every year and grants each scientist a maximum of 2.5 billion KRW over a period of up to five years. Since January this year, the foundation received 67 research proposals from scientists across the nation, especially from those who had less than five years of experience as professors, and selected the three recipients. Professor Cho proposed research on how to observe the interactions between nuclear structures and constantly-changing chromatin monomers in four dimensions through ultra-high-resolution imaging of single living cells. This proposal was recognized as one that could help us better understand the process of transcription regulation, which remains a long-standing question in biology. The other awards were given to Professor Soung-hun Roh of Seoul National University and Professor Joo-Hyeon Lee of the University of Cambridge. With these three new awardees, a total of 17 scientists have been named SUHF Young Investigators to date, and the funding to support these scientists now totals 42.5 billion KRW. Professor Inkyung Jung and Professor Ki-Jun Yoon from the Department of Biological Sciences, and Professor Young Seok Ju and Professor Jeong Ho Lee from the Graduate School of Medical Science and Engineering are the four previous winners from KAIST in the years 2017 through 2019. (END)
2020.10.15 View 20165
Two Professors Recognized for the National R&D Excellence 100 < Professor Haeng-Ki Lee (left) and Professor Jeong-Ho Lee (right) > Two KAIST professors were listed among the 2019 National R&D Excellence 100 announced by the Ministry of Science and ICT and the Korea Institute of S&T Evaluation and Planning. Professor Haeng-Ki Lee from the Department of Civil and Environmental Engineering was recognized in the field of mechanics and materials for his research on developing new construction materials through the convergence of nano- and biotechnologies. In the field of life and marine science, Professor Jeong-Ho Lee from the Graduate School of Medical Science and Engineering was lauded for his research of diagnostic tools and therapies for glioblastoma and pediatric brain tumors. A certificate from the Minister of Ministry of Science and ICT will be conferred to these two professors, and their names will be inscribed on a special 2019 National R&D Excellence 100 plaque to celebrate their achievements. The professors will also be given privileges during the process of new R&D project selection. (END)
2019.10.15 View 18778
KAIST Professors Selected as Y-KAST Members Professor YongKeun Park, Professor Bumjoon Kim, Professor Keon Jae Lee, and Professor Young Seok Ju were selected as the newest members of the Young Korean Academy of Science and Technology (Y-KAST). The Korean Academy of Science and Technology, an academic institution of professional experts, selected 26 promising scientists under the age of 43 to join Y-KAST. and four KAIST professors were included in the list. The newest members were conferred on February 26. Research Field Name Natural Sciences YongKeun Park (Dept. of Physics) Engineering Bumjoon Kim (Dept. of Chemical and Biomolecular Engineering) Agricultural & Fishery Sciences Keon Jae Lee (Dept. of Materials Science and Engineering) Medical Sciences Young Seok Ju (Graduate School of Medical Science and Engineering)
2018.03.05 View 13785