Eliram Nof

I am a research fellow in the Mathematical Oncology Initiative, Memorial Sloan Kettering Research Center, New York City, hosted by Allen Tannenbaum and Joseph Deasy.

I received my Ph.D. from the Faculty of Biomedical Engineering at the Technion - Israel Institute of Technology in Haifa, Israel. Prior to that, I received a M.Sc. and B.Sc. in Mechanical Engineering at Ben-Gurion University of the Negev in an accelerated track (Meitar program).

I have worked on a diverse set of applied, high-impact problems relating to flow physics using a combination of experimental, computational, and theoretical tools:

Blastwave phenomena and hypersonic fluid-structure interactions for military and defense applications.

Laminar to low Reynolds turbulent flows in the human respiratory system for pharmacology and disease modeling, including airborne viral transmission.

More recently, I have been working on modeling flows in the tumor microenvironment of cancer patients for improved prediction, leveraging advanced image analysis tools and machine learning.

news

Apr 6, 2023	New paper out in PLOS Computational Biology!
Feb 21, 2022	Our paper, “Human multi-compartment airways-on-chip platform for emulating respiratory airborne transmission: from nose to pulmonary acini” is accepted to Frontiers in Physiology!
Jan 6, 2022	Our paper is out in Bioengineering & Translational Medicine, featured in the popular media by the Technion and the Jerusalem Post.
Apr 2, 2021	Moved to New York City!

selected publications

Ventilation-induced jet suggests biotrauma in reconstructed airways of the intubated neonate

Nof, E., Heller-Algazi, M., Coletti, F., Waisman, D., and Sznitman, J.

Journal of the Royal Society Interface 2020

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We investigate respiratory flow phenomena in a reconstructed upper airway model of an intubated neonate undergoing invasive mechanical ventilation, spanning conventional to high-frequency ventilation (HFV) modes. Using high-speed tomographic particle image velocimetry, we resolve transient, three-dimensional flow fields and observe a persistent jet flow exiting the endotracheal tube whose strength is directly modulated according to the ventilation protocol. We identify this synthetic jet as the dominating signature of convective flow under intubated ventilation. Concurrently, our in silico wall shear stress analysis reveals a hitherto overlooked source of ventilator-induced lung injury as a result of jet impingement on the tracheal carina, suggesting damage to the bronchial epithelium; this type of injury is known as biotrauma. We find HFV advantageous in mitigating the intensity of such impingement, which may contribute to its role as a lung protective method. Our findings may encourage the adoption of less invasive ventilation procedures currently used in neonatal intensive care units.
Ventilation-induced epithelial injury drives biological onset of lung trauma in vitro and is mitigated with anti-inflammatory therapeutics

Nof, E., Artzy-Schnirman, A., Bhardwaj, S., Sabatan, H., Waisman, D., Hochwald, O., Gruber, M., Borenstein-Levin, L., and Sznitman, J.

Bioengineering & Translational Medicine 2021

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Mortality rates among patients suffering from acute respiratory failure remain perplexingly high despite the maintenance of blood oxygen homeostasis during ventilatory support. The biotrauma hypothesis advocates that mechanical forces from invasive ventilation trigger immunological mediators that spread systemically. Yet, how these forces elicit an immune response remains unclear. Here, a biomimetic in vitro three-dimensional (3D) upper airways model allows to recapitulate lung injury and immune responses induced during invasive mechanical ventilation in neonates. Under such ventilatory support, flow-induced stresses injure the bronchial epithelium of the intubated airways model and directly modulate epithelial cell inflammatory cytokine secretion associated with pulmonary injury. Fluorescence microscopy and biochemical analyses reveal site-specific susceptibility to epithelial erosion in airways from jet-flow impaction and are linked to increases in cell apoptosis and modulated secretions of cytokines IL-6, -8, and -10. In an effort to mitigate the onset of biotrauma, prophylactic pharmacological treatment with Montelukast, a leukotriene receptor antagonist, reduces apoptosis and pro-inflammatory signaling during invasive ventilation of the in vitro model. This 3D airway platform points to a previously overlooked origin of lung injury and showcases translational opportunities in preclinical pulmonary research toward protective therapies and improved protocols for patient care.