BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Biomedical Mathematics Group - ECPv6.15.20//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-WR-CALNAME:Biomedical Mathematics Group
X-ORIGINAL-URL:https://www.ibs.re.kr/bimag
X-WR-CALDESC:Events for Biomedical Mathematics Group
REFRESH-INTERVAL;VALUE=DURATION:PT1H
X-Robots-Tag:noindex
X-PUBLISHED-TTL:PT1H
BEGIN:VTIMEZONE
TZID:Asia/Seoul
BEGIN:STANDARD
TZOFFSETFROM:+0900
TZOFFSETTO:+0900
TZNAME:KST
DTSTART:20200101T000000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Asia/Seoul:20210723T110000
DTEND;TZID=Asia/Seoul:20210723T120000
DTSTAMP:20260502T205228
CREATED:20210707T160416Z
LAST-MODIFIED:20210707T160416Z
UID:4715-1627038000-1627041600@www.ibs.re.kr
SUMMARY:Inference method for a stochastic target-mediated drug disposition model via ABC-MCMC
DESCRIPTION:Abstract: Inference method for a stochastic target-mediated drug disposition model via ABC-MCMC In this study\, we discuss model robustness. Model robustness is consistent performance over variations of parameters. We formulate a stochastic target-mediated drug (TMDD) model\, one of the pharmacokinetic models\, to capture bi-exponential drug decay in plasma. A stochastic process is used to account for system randomness\, and this process is transformed into system of stochastic differential equations. Parameter inference is performed by Approximation Bayesian Computation using the likelihood-free method. Using these collected samples\, global sensitivity of parameters is compared to Uniform and Normal distributions. This approach in the TMDD model may improve model robustness without changing the global sensitivity of parameters and the model.
URL:https://www.ibs.re.kr/bimag/event/inference-method-for-a-stochastic-target-mediated-drug-disposition-model-via-abc-mcmc/
LOCATION:B305 Seminar room\, IBS\, 55 Expo-ro Yuseong-gu\, Daejeon\, 34126\, Korea\, Republic of
CATEGORIES:Biomedical Mathematics Seminar
ORGANIZER;CN="Jae Kyoung Kim":MAILTO:jaekkim@kaist.ac.kr
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Asia/Seoul:20210723T150000
DTEND;TZID=Asia/Seoul:20210723T160000
DTSTAMP:20260502T205228
CREATED:20210629T013222Z
LAST-MODIFIED:20210629T013222Z
UID:4686-1627052400-1627056000@www.ibs.re.kr
SUMMARY:Scalable Modeling Approaches in Systems Immunology
DESCRIPTION:Abstract: \nSystems biology seeks to build quantitative predictive models of biological system behavior. Biological systems\, such as the mammalian immune system\, operate across multiple spatiotemporal scales with a myriad of molecular and cellular players. Thus\, mechanistic\, predictive models describing such systems need to address this multiscale nature. A general outstanding problem is to cope with the high-dimensional parameter space arising when building reasonably detailed models. Another challenge is to devise integrated frameworks incorporating behavioral characteristics manifested at various organizational levels seamlessly. First\, we aimed to understand how cell-to-cell heterogeneities are regulated through gene expression variations and their propagation at the single-cell level. To better understand detailed gene regulatory circuit models with many parameters without analytical solutions\, we developed a framework called MAchine learning of Parameter-Phenotype Analysis (MAPPA). MAPPA combines machine learning approaches and stochastic simulation methods to dissect the mapping between high-dimensional parameters and phenotypes. MAPPA elucidated regulatory features of stochastic gene-gene correlation phenotypes. Next\, we sought to quantitatively dissect immune homeostasis conferring tolerance to self-antigens and responsiveness to foreign antigens. Towards this goal\, we built a series of models spanning from intracellular to organismal levels to describe the recurrent reciprocal relationships between self-reactive T cells and regulatory T cells in collaboration with an experimentalist. This effort elucidated critical immune parameters regulating the circuitry enabling the robust suppression of self-reactive T cells\, followed by experimental validation. Moreover\, by bridging these models across organizational scales\, we derived a framework describing immune homeostasis as a dynamical equilibrium between self-activated T cells and regulatory T cells\, typically operating well below thresholds that could result in clonal expansion and subsequent autoimmune diseases. We propose that our framework and predictions may help guide therapeutic manipulation of immune homeostasis to treat cancer and autoimmune diseases. \n  \nReferences: \nPark\, K.\, Prüstel\, T.\, Lu\, Y.\, and Tsang\, J.S. (2019). Machine learning of stochastic gene network phenotypes. BioRxiv 825943. \nWong\, H.S.\, Park\, K.\, Gola\, A.\, Baptista\, A.P.\, Miller\, C.H.\, Deep\, D.\, Lou\, M.\, Boyd\, L.F.\, Rudensky\, A.Y.\, Savage\, P.A.\, et al. (2021). A local regulatory T cell feedback circuit maintains immune homeostasis by pruning self-activated T cells. Cell S0092867421006589.
URL:https://www.ibs.re.kr/bimag/event/2021-07-23/
LOCATION:B305 Seminar room\, IBS\, 55 Expo-ro Yuseong-gu\, Daejeon\, 34126\, Korea\, Republic of
CATEGORIES:Biomedical Mathematics Seminar
ORGANIZER;CN="Jae Kyoung Kim":MAILTO:jaekkim@kaist.ac.kr
END:VEVENT
END:VCALENDAR