The rheological (deformation and flow) properties of biological tissues  are important in processes such as embryo development, wound healing and 
tumour invasion. Indeed, processes such as these spontaneously generate  stresses within living tissue via active process at the single cell level. 
Tissues are also continually subject to external stresses and deformations  from surrounding tissues and organs. The success of numerous physiological 
functions relies on the ability of cells to withstand stress under some conditions, yet to flow collectively under others. Biological tissue is 
furthermore inherently viscoelastic, with a slow time-dependent mechanics.  Despite this rich phenomenology, the mechanisms that govern the 
transmission of stress within biological tissue, and its response to bulk deformation, remain poorly understood to date.

This talk will describe three recent research projects in modelling the rheology of biological tissue. The first predicts a strain-induced 
stiffening transition in a sheared tissue [1]. The second elucidates the interplay of external deformations applied to a tissue as a whole with 
internal active stresses that arise locally at the cellular level, and shows how this interplay leads to a host of fascinating rheological 
phenomena such as yielding, shear thinning, and continuous or discontinuous shear thickening [2]. The third concerns the formulation of 
a continuum constitutive model that captures several of these linear and nonlinear rheological phenomena [3].

[1] J. Huang, J. O. Cochran, S. M. Fielding, M. C. Marchetti and D. Bi, 
Physical Review Letters 128 (2022) 178001

[2] M. J. Hertaeg, S. M. Fielding and D. Bi, Physical Review X 14 (2024) 
011017.

[3] S. M. Fielding, J. O. Cochran, J. Huang, D. Bi, M. C. Marchetti, 
Physical Review E (Letter) 108 (2023) L042602.

During the talk I will describe my research on host-pathogen interactions during lung infections. Various modelling approaches have been used, including a hybrid multiscale individual-based model that we have developed, which simulates pulmonary infection spread, immune response and treatment within in a section of human lung. The model contains discrete agents which model the spatio-temporal interactions (migration, binding, killing etc.) of the pathogen and immune cells. Cytokine and oxygen dynamics are also included, as well as Pharmacokinetic/Pharmacodynamic models, which are incorporated via PDEs. I will also describe ongoing work to develop a continuum model, comparing the spatial dynamics resulting from these different modelling approaches.  I will focus in the most part on two infectious diseases: Tuberculosis and COVID-19.

Circadian clocks generate autonomous daily rhythms of gene expression in anticipation of daily sunlight and temperature cycles in a variety of organisms. The simples and best characterised of all circadian clocks in nature is the cyanobacterial clock, the core of which consists of just 3 proteins - KaiA, KaiB and KaiC - locked in a 24-h phosphorylation-dephosphorylation loop. Substantial progress has been made in understanding how cells generate and sustain this rhythm, but important questions remain: how does the clock maintain resilience in the face of internal and external fluctuations, how is the clock coupled to other cellular processes and what dynamics arise from this coupling? We address these questions using an interdisciplinary approach combining time-lapse microscopy and modelling. In this talk, I will first characterise the clock's free-running robustness and explore how the clock buffers environmental noise and genetic mutations. Our stochastic model predicts how the clock filters out such noise, including fast light fluctuations, to keep time while remaining responsive to environmental shifts, revealing also that the wild-type operates at a noise optimum. Next, I will focus on how the clock interacts with the other major cellular cycle, the cell division cycle. Our single-cell data shows that the clock couples to the division rate and expression of cell cycle-dependent factors using both frequency modulation and amplitude modulation strategies, with implications for cell growth and cell size control. Our findings illustrate how simple systems can exhibit complex dynamics, advancing our understanding of the interdependency between gene circuits and cellular physiology.