CDEV-MS03

Diverse quantitative approaches integrating data and modelling in development and medicine

Monday, June 14 at 5:45pm (PDT)
Tuesday, June 15 at 01:45am (BST)
Tuesday, June 15 09:45am (KST)

SMB2021 Follow Monday (Tuesday) during the "MS03" time block.

Note: this minisymposia has multiple sessions. The second session is MS04-CDEV (click here).

Adriana Dawes (Ohio State University, USA), Sungrim Seirin-Lee (Hiroshima University, Japan)

Description:

Mathematical sciences are making significant contributions to our understanding of developmental biology and its application to medicine using a diversity of approaches. One such approach integrates data with quantitative models under both normal and pathological conditions to uncover hidden rules and relationships underlying biological phenomena. By identifying these basic rules of life, mathematical models can further explore the consequences of these regulatory mechanisms, how they can be exploited by disease processes, and provide testable predictions for unresolved questions that may be difficult to address experimentally. In this minisymposium, we bring together research from a variety of perspectives to share recent developments in techniques and insights for understanding complex, medically relevant, dynamics that are associated with development.

Sungrim Seirin-Lee

(Hiroshima University, Japan)

"A one-line mathematical model that solved the mystery of urticaria"

Urticaria is a common skin disease characterized by the rapid appearance and disappearance of local skin edema and flares with itching. It affects about one in 5 people at some point in their lives and globally about 56/100000 population suffer from urticaria daily. It is characterized by various macroscopic skin eruptions unique to patients with respect to shape, size, and/or duration of eruptions. Nevertheless, the mechanism underlying multifarious eruptions in urticaria is largely unknown in medicine. The eruptions are believed to be evoked by histamine release from mast cells in the skin. However, the majority of visible characteristics of urticaria cannot be explained by a simple injection of histamine to the skin. In this study, we succeeded in developing a mathematical model that can explain various geometrical shapes of eruptions typically observed in patients. Our mathematical model suggests that simultaneous self-regulation of positive and negative feedback of histamine through mast cells plays a critical role in generating the wide-spread wheal patterns. The study findings increase the understanding of the pathogenesis of urticaria and may aid decision-making for appropriate treatments.

Yoichiro Mori

(University of Pennsylvania, USA)

"Mathematical Justification of Slender Body Theory"

Systems in which thin filaments interact with the surrounding fluid abound in science and engineering. The computational and analytical difficulties associated with treating thin filaments as 3D objects has led to the development of slender body theory, in which filaments are approximated as 1D curves in a 3D fluid. In the 70-80s, Keller, Rubinow, Johnson and others derived an expression for the Stokesian flow field around a thin filament given a one-dimensional force density along the center-line curve. Through the work of Shelley, Tornberg and others, this slender body approximation has become firmly established as an important computational tool for the study of filament dynamics in Stokes flow. An issue with slender body approximation has been that it is unclear what it is an approximation to. As is well-known, it is not possible to specify some value along a 1D curve to solve the 3D exterior Stokes problem. What is the PDE problem that slender body approximation is approximating? Here, we answer this question by formulating a physically natural PDE problem with non-conventional boundary conditions on the filament surface, which incorporates the idea that the filament must maintain its integrity (velocity along filament cross sections must be constant). We prove that this PDE problem is well-posed, and show furthermore that the slender body approximation does indeed provide an approximation to this PDE problem by proving error estimates. This is joint work with Laurel Ohm, Will Mitchell and Dan Spirn.

Benjamin Walker

(University of Oxford, UK)

"Hypothesis generation and hypothesis testing in spermatozoa"

Spermatozoa are perhaps the canonical microscopic swimmer, propelled along the path to fertilisation via the wavelike motion of a long slender flagellum. Owing not least to their key role in fertility, they have long been the subject of significant study, driving both experimental and theoretical developments. In this talk, I hope to survey a number of recent advances in the way in which we are able to study and investigate the microscale world of sperm, with applications beyond these cellular swimmers. These new methodologies promise to enable the next generation of quantitative analysis of flagellated swimmers, with the potential to both enhance clinical diagnostics in the future and investigate fundamental and widely conserved cellular biology. In particular, I will begin by recounting recent step changes in data acquisition, with fully automated schemes now replacing tiresome by-hand analysis. Further, I will then highlight how these developments can be coupled to population-level statistical analyses that incorporate the fine details of the flagellar beat, which have classically been absent from quantitative study. Finally, I will touch upon another exciting area of rapid development with broad applicability, that of flagellar simulation, which is enabling sophisticated data-driven modelling and hypothesis generation in spermatozoa, in addition to newly realising exploratory in silico study of these complex microscale organisms.

Kang-Ling Liao

(University of Manitoba, Canada)

"The role of CD200-CD200R in cancer immunotherapy"

CD200 is a cell membrane protein that interacts with CD200 receptor (CD200R) of myeloid lineage cells. CD200-positive tumor cells can interact with M1 and M2 macrophages through CD200–CD200R-compex and downregulate IL-10 and IL-12 productions secreted primarily by M2 and M1 macrophages, respectively. In this talk, I will introduce a PDEs model to determine the combined effect of CD200–CD200R interaction on tumor proliferation. We demonstrate that blocking CD200 on tumor cells may have opposite effects on tumor proliferation depending on the “affinity” of the macrophages to form the CD200–CD200R-complex with tumor cells. We also extend these results to an ODEs model to study how the populations of M1 and M2 macrophages affect the tumor growth.

Hosted by SMB2021 Follow

Virtual conference of the Society for Mathematical Biology, 2021.