Cells often spread and migrate on curved surfaces inside the body, such as curved tissues, blood vessels, fibers of the extracellular matrix or cylindrical protrusions of other cells. Recent in-vitro experiments provide clear evidence that the dynamics and spreading of cells are affected by the curvature of the substrate on which they spread or migrate. Cellular protrusions at the leading edge are found to wrap (coil) around the extra-cellular fibers, rather than extending axially. The migrating cells are found to prefer certain curvatures to others, such as, when migrating on sinusoidal substrate, the cells move along the grooves (minima), while avoiding motion along the ridges. Our aim is to develop a qualitative understanding of the above-mentioned phenomena using a simple physics-based model. We employ a "minimal cell" model which is composed of a vesicle that contains curved membrane protein complexes, that exert protrusive forces on the membrane (representing the pressure due to actin polymerization). This minimal-cell model gives rise to spontaneous emergence of a motile phenotype, driven by a lamellipodia-like leading edge. Our model could capture the qualitative features observed in real cells, and allows us to make further new predictions that are verified using different cell types.
https://zoom.us/j/97239618248
Meeting ID: 972 3961 8248
Passcode: 588184
In this talk, first, we will describe the construction of the mixed $q$-deformed Araki-Woods $C^*$-algebras. Then, we will discuss
the simplicity of mixed $q$-deformed Araki-Woods $C^*$-algebras under some constraints.
Mathematics Colloquium | Alladi Ramakrishnan Hall
Apr 18 15:30-16:30
Kalyan Chakrabarti | Department of Biological Science and Chemistry, Krea University, Sri City
A complex interplay between various processes underlies neuropathology of Alzheimer's disease (AD) and its progressive course. Several lines of evidence point to the coupling between A$\beta$ aggregation and neuroinflammation and its role in maintaining brain homeostasis during the long prodromal phase of AD. Little is, however, known about how this protective mechanism fails, and as a result, an irreversible and progressive transition to clinical AD occurs. Here, we introduce a minimal model of a coupled system of A$\beta$ aggregation and inflammation, numerically simulate its dynamical behavior, and analyze its bifurcation properties. The introduced model represents the following events: generation of A$\beta$ monomers, aggregation of A$\beta$ monomers into oligomers and fibrils, induction of inflammation by A$\beta$ aggregates, and clearance of various A$\beta$ species. Crucially, the A$\beta$ generation and clearance rates are modulated by inflammation level following a Hill-type response function. Despite its relative simplicity, the model exhibits enormously rich dynamics ranging from overdamped kinetics to sustained oscillations. We then specify the region of inflammation- and coupling-related parameters space where a transition to oscillatory dynamics occurs and demonstrate how changes in A$\beta$ aggregation parameters could shift this oscillatory region in parameter space. Our results reveal the propensity of coupled A$\beta$ aggregation-inflammation systems to oscillatory dynamics. We propose prolonged sustained oscillations and their consequent immune system exhaustion as a potential mechanism underlying the transition to a more progressive phase of amyloid pathology in AD. The implications of our results in regard to early diagnosis of AD and anti-AD drug development are discussed.
Biology Seminar | Alladi Ramakrishnan Hall
Apr 20 16:00-18:00
Dr Srinivas Chakravarthy | Computational Neuroscience Lab at IIT, Madras