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Knowing the environmental spreading pathway of COVID-19 is crucial for improving safety practices, particularly for health care workers who are more susceptible to exposure. This paper focuses on the possible secondary transmission due to resuspension of virus-laden droplets from common surfaces, which several studies have shown to be possible under external disturbances. Such disturbances could be body motion during walking, running, clothes removal, or airflow in the environment. In this paper, a three-dimensional two-phase model is utilized to study respiratory droplet resuspension dynamics on various surfaces due to sudden agitation. The velocity range and variation during walking, surgical glove removal, and dropping an object are studied experimentally. A parametric study is performed to characterize the effects of droplet size and surface wettability on the minimum initial droplet velocity required for detachment from surfaces. The results are reported as average droplet velocity during the detachment process, total detachment time, and detached droplet volume. The obtained results indicate that respiratory droplets larger than 200 μm can detach from typical surfaces due to normal daily activities. Droplets are partially separated from hydrophilic surfaces with contact angle ≤ 90 ° , while the entire droplet is detached from hydrophobic surfaces with contact angle > --> 90 °. Furthermore, the minimum initial droplet velocity to induce the resuspension depends on the droplet size. Droplet velocity immediately after detachment is a function of droplet size, initial droplet velocity, and surface wettability. Bigger droplets have larger detached volume percentage as well as higher velocity after detachment compared to smaller droplets. Finally, a higher initial velocity is needed to separate droplets from hydrophilic surfaces as compared to hydrophobic surfaces. In accordance with the results, the droplet minimum initial velocity to cause detachment is 2 m s−1, while our experiments show that surface velocity can reach up to 3 m s−1 during normal human activities. We also develop an analytical model to predict the required kinetic energy to detach droplets from different surfaces, which is in good agreement with numerical results. The mechanism of droplet detachment is dictated by a competition between droplet kinetic energy induced by surface motion and surface energy due to droplet–surface interaction as well as droplet–vapor and surface–vapor interactions. We believe that the results of this fundamental study can potentially be used to suggest proper surface wettability and safe motion that reduce respiratory droplet resuspension from various surfaces. [ABSTRACT FROM AUTHOR]

Intracellular drug delivery by rapid squeezing is one of the most recent and simple cell membrane disruption-mediated drug encapsulation approaches. In this method, cell membranes are perforated in a microfluidic setup due to rapid cell deformation during squeezing through constricted channels. While squeezing-based drug loading has been successful in loading drug molecules into various cell types, such as immune cells, cancer cells, and other primary cells, there is so far no comprehensive understanding of the pore opening mechanism on the cell membrane and the systematic analysis on how different channel geometries and squeezing speed influence drug loading. This article aims to develop a three-dimensional computational model to study the intracellular delivery for compound cells squeezing through microfluidic channels. The Lattice Boltzmann method, as the flow solver, integrated with a spring-connected network via frictional coupling, is employed to capture compound capsule dynamics over fast squeezing. The pore size is proportional to the local areal strain of triangular patches on the compound cell through mathematical correlations derived from molecular dynamics and coarse-grained molecular dynamics simulations. We quantify the drug concentration inside the cell cytoplasm by introducing a new mathematical model for passive diffusion after squeezing. Compared to the existing models, the proposed model does not have any empirical parameters that depend on operating conditions and device geometry. Since the compound cell model is new, it is validated by simulating a nucleated cell under a simple shear flow at different capillary numbers and comparing the results with other numerical models reported in literature. The cell deformation during squeezing is also compared with the pattern found from our compound cell squeezing experiment. Afterward, compound cell squeezing is modeled for different cell squeezing velocities, constriction lengths, and constriction widths. We reported the instantaneous cell center velocity, variations of axial and vertical cell dimensions, cell porosity, and normalized drug concentration to shed light on the underlying physics in fast squeezing-based drug delivery. Consistent with experimental findings in the literature, the numerical results confirm that constriction width reduction, constriction length enlargement, and average cell velocity promote intracellular drug delivery. The results show that the existence of the nucleus increases cell porosity and loaded drug concentration after squeezing. Given geometrical parameters and cell average velocity, the maximum porosity is achieved at three different locations: constriction entrance, constriction middle part, and outside the constriction. Our numerical results provide reasonable justifications for experimental findings on the influences of constriction geometry and cell velocity on the performance of cell-squeezing delivery. We expect this model can help design and optimize squeezing-based cargo delivery. [ABSTRACT FROM AUTHOR]

Publisher's Note: "Respiratory droplet resuspension near surfaces: Modeling and analysis" [J. Appl. Phys. This article was originally published online on 8 July 2021 with the first author's name spelled incorrectly. All online versions of the article were corrected on 12 July 2021. [Extracted from the article]