arXiv subjects

Martin Garic

Publications and source records attributed to Martin Garic.

3 recordsLinked to original sources

arXiv2025

Intestinal villi and crypts density maximizing nutrient absorption

The villi and crypts of the gastrointestinal tract increase the effective surface area of the intestinal mucosa, potentially enhancing nutrient absorption. It is commonly assumed that this is their primary function, and that a higher villi density necessarily leads to improved absorption. However, when villi are packed too closely together, diffusion can be hindered, potentially offsetting this benefit. In this work, we investigate the relationship between the density of these structures and the overall efficiency of absorption. In three different simplified geometries, approximating crypts, leaf-like villi, and finger-like villi we calculate analytically the concentration profile and the absorption flux, assuming that there is only diffusion between these structures while the lumen is well mixed. When plotting the absorption flux per unit of gut length as a function of the structures' density, we observe that there is a density maximizing absorption. We study numerically this optimum. It depends weakly on the absorption properties of the given nutrient, so that a geometry optimal for one nutrient is close to optimum for another nutrient. Physiological data from various animal species align with this predicted optimal range and potentially reflect evolutionary selection for efficient nutrient uptake, supporting the model's validity.

q-bio.TO↗

arXiv2025

Hydrodynamics in a villi-patterned channel due to pendular-wave activity

Inspired by small intestine motility, we investigate the flow induced by a propagating pendular-wave along the walls of a channel lined with rigid, villi-like microstructures. The villi undergo harmonic axial oscillations with a phase lag relative to their neighbours, generating travelling patterns of intervillous contraction. Using two-dimensional lattice Boltzmann simulations, we resolve the flow within the villi zone and the lumen, sampling small to moderate Womersley numbers. We uncover a mixing boundary layer (MBL) just above the villi, composed of semi-vortical structures that travel with the imposed wave. In the lumen, an axial steady flow emerges, surprisingly oriented opposite to the wave propagation direction, contrary to canonical peristaltic flows. We attribute this flow reversal to the non-reciprocal trajectories of fluid trapped between adjacent villi, and derive a geometric scaling law that captures its magnitude in the Stokes regime. The MBL thickness is found to depend solely on the wave kinematics given by intervillous phase lag in the low-inertia limit. Above a critical threshold, oscillatory inertia induces dynamic confinement, limiting the radial extent of the MBL and leading to non-monotonic behaviour of the axial steady flux. We further develop an effective boundary condition at the villus tips, incorporating both steady and oscillatory components across relevant spatial scales. This framework enables coarse-grained simulations of intestinal flows without resolving individual villi. Our results shed light on the interplay between active microstructure, pendular-wave and finite inertia in biological flows, and suggests new avenues for flow control in biomimetic and microfluidic systems.

physics.flu-dyn↗

arXiv2024

How host mobility patterns shape antigenic escape during viral-immune co-evolution

Viruses like influenza have long coevolved with host immune systems, gradually shaping the evolutionary trajectory of these pathogens. Host immune systems develop immunity against circulating strains, which in turn avoid extinction by exploiting antigenic escape mutations that render new strains immune from existing antibodies in the host population. Infected hosts are also mobile, which can spread the virus to regions without developed host immunity, offering additional reservoirs for viral growth. While the effects of migration on long term stability have been investigated, we know little about how antigenic escape coupled with migration changes the survival and spread of emerging viruses. By considering the two processes on equal footing, we show that on short timescales an intermediate host mobility rate increases the survival probability of the virus through antigenic escape. We show that more strongly connected migratory networks decrease the survival probability of the virus. Using data from high traffic airports we argue that current human migration rates are beneficial for viral survival.

q-bio.PE↗