Biology subjects

Montanino, A.

Publications and source records attributed to Montanino, A..

3 recordsLinked to original sources

bioRxiv2026

A coupled cerebro-ocular-CSF lumped-parameter model under gravitational and postural variations

Spaceflight-Associated Neuro-ocular Syndrome (SANS) involves complex interactions between intracranial pressure (ICP), intraocular pressure (IOP), and cerebrospinal fluid (CSF) dynamics within the optic nerve subarachnoid space (ONSAS). While existing computational models address specific aspects of these interactions, they lack a comprehensive, system-level representation. To bridge this gap, we present the HEAD (Hemodynamic Eye-brain Associated Dynamics) model. By consistently integrating several previously proposed physiological sub-models, HEAD provides a unified lumped-parameter framework that fully couples cerebrovascular autoregulation, multi-territory ocular hemodynamics, and compartmentalized craniospinal-ONSAS CSF circulation under gravitational loading. This formulation enables the simultaneous analysis of eye-brain-CSF dynamics within a single computational tool. Model predictions were validated against experimental data from supine (0{degrees}) to head-down tilt (HDT, -30{degrees}) postures, accurately reproducing posture-dependent IOP increases and achieving an excellent ICP match against clinical benchmarks at the -6{degrees} HDT standard bed-rest angle. The coupled system predicts bed-specific ocular hemodynamic responses, with retinal blood flow exhibiting the largest relative increase under HDT compared to the ciliary and choroidal circulations. Crucially, explicitly modeling the ONSAS as a distinct compartment reveals a posture-dependent pressure drop of 1.89-3.69 mmHg between the intracranial and perioptic spaces. This compartmentalization yields a translaminar pressure profile that remains positive (8.05-11.83 mmHg) across all simulated conditions but is chronically reduced under sustained HDT. Ultimately, the HEAD model elucidates the physiological mechanisms linking gravitational stress to translaminar mechanics, providing a robust computational foundation to investigate SANS and supply boundary conditions for structural models of the optic nerve head.

physiology↗

bioRxiv2025

A Computational Model for Retinal Hemodynamics Under Gravitational and Postural Variations

Understanding the effects of gravitational and postural variations on retinal circulation is crucial for both aerospace medicine and terrestrial health. This study presents a computational framework to analyze retinal hemodynamics under different gravitational conditions. A lumped-parameter model was developed to simulate blood flow, intraocular pressure, and vascular adaptations in response to changes in body posture and microgravity. Validation against experimental data demonstrated strong agreement in intraocular and ocular perfusion pressure variations across different tilt angles. Incorporating a simulated 4% constriction of the central retinal artery under microgravity conditions further model accuracy, highlighting the critical role of vascular remodeling. The simulation results indicate that posture significantly affects retinal circulation, leading to notable changes in vessel pressures, arterial velocities, and ocular perfusion. These findings emphasize the importance of fluid redistribution and vascular autoregulatory responses in conditions like Spaceflight-Associated Neuro-ocular Syndrome. This framework offers a powerful tool for developing countermeasures against vision-related risks in spaceflight and has potential applications in terrestrial ocular pathologies associated with altered intracranial pressures.

bioengineering↗

bioRxiv2019

Localized axolemma deformations suggest mechanoporation as axonal injury trigger

Traumatic brain injuries are a leading cause of morbidity and mortality worldwide. With almost 50% of traumatic brain injuries being related to axonal damage, understanding the nature of cellular level impairment is crucial. Experimental observations have so far led to the formulation of conflicting theories regarding the cellular primary injury mechanism. Disruption of the axolemma, or alternatively cytoskeletal damage has been suggested mainly as injury trigger. However, mechanoporation thresholds of generic membranes seem not to overlap with the axonal injury deformation range and microtubules appear too stiff and too weakly connected to undergo mechanical breaking. Here, we aim to shed a light on the mechanism of primary axonal injury, bridging finite element and molecular dynamics simulations. Despite the necessary level of approximation, our models can accurately describe the mechanical behavior of the unmyelinated axon and its membrane. More importantly, they give access to quantities that would be inaccessible with an experimental approach. We show that in a typical injury scenario, the axonal cortex sustains deformations large enough to entail pore formation in the adjoining lipid bilayer. The observed axonal deformation of 10-12% agree well with the thresholds proposed in the literature for axonal injury and, above all, allow us to provide quantitative evidences that do not exclude pore formation in the membrane as a result of trauma. Our findings bring to an increased knowledge of axonal injury mechanism that will have positive implications for the prevention and treatment of brain injuries.

bioengineering↗