Seminars LMAH 2025


Hours are in French Time. Any questions about the seminars can be addressed to benjamin.ambrosio@univ-lehavre.fr

  • June 5 2025, 03:00 pm H. Rezaei, INRAE

    Title: Intrinsic Dynamics and Deterministic Diversification Drive a New Model of Prion Replication and Dissemination
    Abstract: Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative disorders caused by the accumulation of misfolded conformers (PrPSc ) of the cellular prion protein (PrPC ). These pathogenic assemblies propagate through a self-templating process, resulting in strain- specific patterns of neurodegeneration, yet the mechanisms underlying their tissue tropism and dissemination remain incompletely understood. Using advanced physico-chemical approaches, we revealed that PrP Sc assemblies exhibit an intrinsic capacity for structural diversification and material exchange, independently of templated replication. These findings challenge traditional paradigms by suggesting that prion replication is not solely governed by templating kinetics, but also shaped by inherent assembly dynamics. Building on this foundation, we incorporated these experimental observations into a stochastic reaction-diffusion model—parametrized with the Gillespie algorithm—that accounts for nonlinear tissue responses, particularly the unfolded protein response (UPR), and strain-specific replication kinetics. This integrated framework demonstrates that the interplay between the intrinsic dynamics of prion assemblies and tissue feedback mechanisms can lead to diverse replication regimes, including oscillatory, transient, and abortive behaviors. Notably, the model reveals that structural subpopulations such as PrPSc A and PrPSc Bi can be differentially selected depending on tissue environment and strain properties. Furthermore, strain co-propagation and dominance interference are emergent behaviors resulting from shared substrate competition and UPR coupling, independent of direct kinetic interaction. By simulating prion dissemination across neural networks, the model also underscores the role of the brain’s connectome—not as a passive conduit, but as an active modulator of propagation dynamics through axon-guided diffusion and local replication. Together, these insights offer a comprehensive and mechanistically rich model of prion replication and neuroinvasion, with broader implications for other protein misfolding diseases characterized by strain diversity and tissue tropism.

  • April 29 2025, 03:00 pm Loïc MICHEL, Nantes University and Centrale School of Nantes

    Title: A Connectome-Based Inference of Dynamical Neural Wiring: A Control Approach
    Abstract: This work aims to build a growing neural network in order to explore the concept of learning through a closed-loop control algorithm and additionally propagate statistic information from the synaptic weights. To emphasize the interactions between the connections and the neurons, the connections are activated randomly, like into a « connectome », for which the neurons can be used simultaneously to learn and store several type of information from the learning process and the wiring statistics, depending on the configuration of the connections. The preliminary results highlight the feasibility of the proposed learning concept considering few neurons, for which stabilization of the trained synaptic weights is a priori observed. Joint work with Jean-Pierre BARBOT from Cergy-Pontoise University. Video

  • April 17 2025, 03:00 pm A. Thorel, Le Havre Normandie University

    Title: Exemples concrets.
    Abstract: TBA

  • April 10 2025, 03:00 pm A. Thorel, Le Havre Normandie University

    Title: Introduction à la théorie des sommes d'opérateurs linéaires.
    Abstract: TBA

  • April 3 2025, 03:00 pm A. Thorel, Le Havre Normandie University

    Title: Fermabilité et fermeture d'opérateurs linéaires non bornés dans les espaces de Banach.
    Abstract: TBA

  • March 27 2025, 03:00 pm Zhenkun Wang, University of Science and Technology of China

    Title: Threshold Dynamics of an Impulsive PDE Model with Habitat Shift Driven by Climate Change
    Abstract: Persistence or extinction of moving animal species is a fundamental question in spatial ecology. This paper focuses on the impact of habitat shift driven by climate change on the persistence and propagation of a population with birth pulse. We first present a class of impulsive reaction-diffusion models with heterogeneous nonlinear reaction in high-dimensional space and study their threshold dynamics. We provide the persistence criterion of the system in bounded domains, and prove the existence, uniqueness and global attraction of a positive steady state. Then we extend the results from bounded domains to the whole space. Our results indicate how the speed of the shifting habitat edge and impulsive reproduction (or harvesting) rate determine the persistence and extinction of the population. Numerical simulations are presented to illustrate the theoretical results.

  • March 7 2025, 03:30 pm Sapna Ratan Shah,Jawaharlal Nehru University, New Delhi, India

    Title: Computational and Mathematical Modeling of Biological Systems in Biomechanics
    Abstract: This talk deals with several contributions on mathematical models of bio-fluids with practical medical applications.

  • February 27 2025, 03:30 pm Todd L. Parsons, CNRS and Sorbonne University

    Title: Puzzles in the Persistence of Pathogens
    Abstract: If a new pathogen causes a large epidemic then it might "burn out" before causing a second epidemic. The burnout probability can be estimated from large numbers of computationally intensive simulations, but an easily computable formula for the burnout probability has never been found. Using a conceptually simple approach, we have derived an accurate and easily computable formula for the burnout probability for the stochastic SIR epidemic model with vital dynamics (host births and deaths). With this formula, we have recently shown (https://www.pnas.org/doi/10.1073/pnas.2313708120) that the burnout probability is always smaller for diseases with longer infectious periods, but is bimodal with respect to transmissibility (the basic reproduction number). Our analysis has shown further that the persistence of typical human infectious diseases cannot be explained by births of new susceptibles alone. However, in current work applying our analytical approach to models that include more biological details, we are able to make precise comments on the roles of other mechanisms, substantially improving our understanding of disease persistence. Joint work with Ben Bolker, Jonathan Dushoff, and David Earn (McMaster University).

  • Seminars LMAH 2024

    Seminars LMAH 2020