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Established in 2020, POSTECH Mathematical Institute for Data Science (MINDS) is the community of researchers in the areas of fundamental data science, machine learning, artificial intelligence, scientific computing, and humanitarian data science. MINDS mission is to provide a platform for collaboration among researchers and to provide various opportunities for students in data science. MINDS also aims to use our data science research to serve our local and global communities pursuing humanitarian data science.

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3nd POSTECH&Peking SIAM Student Chapter Joint Conference 2023.11.01

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[POSTECH(포항공과대학교) 수리 데이터과학 연구소 연구계약직 공고]-상시모집 2023.07.25

[POSTECH(포항공과대학교) 수리 데이터과학 연구소 연구계약직 공고] 2023.07.14

[POSTECH(포항공과대학교) 수리 데이터과학 연구소 연구교수 채용 공고] 2023.06.12

Seminar | Joint seminar for probability and mathematical biology 2023.05.02

[POSTECH(포항공과대학교) 수리 데이터과학 연구소 연구계약직 공고] 2023.02.15

Upcoming Events

Schedule

MINDS SEMINAR

MINDS Seminar Series | Ha, Joon (Howard University) - A Mathematical Structure of Type 2 Diabetes on a Slow Manifold

MINDS SEMINAR

period : 2024-06-19 ~ 2024-06-19

time : 11:00:00 ~ 12:00:00

개최 장소 : Math Bldg 404 & Online streaming (Zoom)

Topic : A Mathematical Structure of Type 2 Diabetes on a Slow Manifold

개요

Date	2024-06-19 ~ 2024-06-19	Time	11:00:00 ~ 12:00:00
Speaker	Ha, Joon	Affiliation	Howard University
Place	Math Bldg 404 & Online streaming (Zoom)	Streaming link	ID : 688 896 1076 / PW : 54321
Topic	A Mathematical Structure of Type 2 Diabetes on a Slow Manifold
Contents	Type 2 diabetes (T2D) is a progressive disease of glucose homeostasis caused by various genetic and environmental factors. The pathophysiology of T2D is a failure of insulin-secreting pancreatic beta-cells to increase levels of insulin demanded by the body as a result of aging and weight gain to maintain normal blood glucose concentration. Clinical studies have shown that glucose concentration gradually increases before frank diabetes and then sharply rises at the onset of the disease, supporting the hypothesis that there exists a threshold for diabetes progression in terms of glucose concentration. Glucose concentration per se, however, cannot be used as the threshold for progression to diabetes: For example, when glucose concentration transiently rises as a result of daily meals, transient insulin resistance due to heavy meals for a short period of time, or sudden changes in medical status, glucose concentration rises beyond the normal range but returns to baseline within a few hours or days. A better way to capture the dynamics of the sharp rise of glucose is to track the two major causative metabolic components, insulin-secretion capacity of the beta-cells (genetic factor) and insulin requirement due to obesity (environmental factor). In this talk, we aim to understand the mechanism underlying the sharp rise of glucose at the onset of diabetes and investigate the threshold behavior of diabetes and its dependence on genetic and environmental factors. Mathematical models recently developed are used for the analyses (Topp et al. 2000 JTB, Ha et al. 2016 Endo., Ha and Sherman 2020 AJP). These models incorporate secretory capacity of beta-cells to regulate beta-cell function and beta-cell mass, and insulin sensitivity to reflect body weight gain. Using these models, the following specific works will be addressed. The first part is to construct a theoretical threshold that is identified by a slow manifold that plays a role of separatrix between diabetes and non-diabetes in the physiological model. The second part is to validate the first part with a longitudinal clinical data from studies of Southwest Native Americans provided by Dr. Clifton Bogardus, NIH. Indeed, the second part is to build a data-derived slow manifold that will be used for personalized therapy.