Skip to content

Mathematical Biophysics seminars

The NOLIN Lab together with professors from the mathematical department of the UPC interested on mathematical Biology organize regular informal seminars.  

The seminars take place usually in the room 0.6 of the EPSEB.

For more information please contact with:

 

NEXT SEMINARS

  • 26/10/2017 (12:00) Martí Català (phD Student UPC): The bubble model, a computational model for undestanding tuberculosis lesions dynamics in lungs.
Tuberculosis (TB) is an infectious bacterial disease caused by Mycobacterium tuberculosis (Mtb), which most commonly affects the lungs. In healthy people, an infection with Mtb often causes no symptoms, remaining controlled as a non-contagious latent tuberculosis infection. World Health Organization estimates that one third of the world population is already infected by this bacillus. From those, a 10% will probably develop an active disease the next decade. Nowadays, over 1 million people die annually because of an active TB.
The mechanisms that maintain a latent infection for a few years or that make it evolving towards an active disease are not fully understood, yet. In a previous work, the dynamics of TB lesions during an active disease in mice was described by an Agent-Based Model (ABM). This model accounted for the growth, coalescence and proliferation of lesions, showing that the most important mechanism for lesions’ growth during the active disease was coalescence. In a later work, the dynamics of lesions during a latent infection in minipigs was tackled by implementing a revised version of the previous ABM into a computational model of the bronchial tree. The model was fed with Computed Tomography scan data from latent infection in minipigs. In this case, the model showed that the proliferation of lesions through the bronchial tree was essential for maintaining the latent infection.
In this talk we propose a first approach on the evolution of a latent tuberculosis infection into an active disease. The parameter space will be explored trying to elucidate which is the role of each mechanism on the trigger for the disease.

 

PAST SEMINARS

  • 8/9/2017 (12:00) Francesc Font: Mathematical modeling of phase change at the nanoscale
  • 21/7/2017 (12:00) Pedro A. Arroyo: Discretization-dependent model for weakly connected excitable media
  • 14/7/2017 (15:00) Alexander V. Panfilov: Multiple mechanisms of cardiac arrhythmias studied using anatomically accurate modeling
  • 7/7/2017 (12:00) John Bush: Pilot-wave hydrodynamics
  • 9/6/2017 (12:00) Carsten Wiuf. Mathematical tools for analyzing systems of Ordinary Differential Equations
  • 7/6/2017 (12:00) Rodrigo Weber dos Santos. The multi-use of an optimization-based algorithm for the construction of biological networks: from arterial trees to cardiac Purkinje networks
  • 26/5/2017 (12:00) Enric Álvarez. Biological signaling networks. Robustness in cell decision  
  • 7/4/2017 (12:00) Gemma Huguet. Neuroprotective Role of Gap Junctions in a Neuron-Astrocyte Network Model
  • 10/3/2017 (12:00) Claudia Hawks. Connexin dynamics in cardiac tissue
  • 1/3/2017 (12:00) Sergio Alonso. Rheology of Living Cells: applications to active matter.
  • 8/2/2017 (11:30) Annette Witt. Custering and Correlation of Extreme Events.
  • 2/1/2017 (11:30) Toni Guillamon. Bifurcacions no locals bàsiques en sistemes d'equacions diferencials.
  • 1/12/2016 (12:15) Sergio Alonso. Stochastic computational methods: From microscopic algorithms to mesoscopic and macroscopic equations.
  • 10/11/2016 (12:15) Miquel Marchena. Development of a computational model of calcium signaling in cardiac cells at the submicron scale.