scholarly journals Tackling the Short-Lived Marangoni Motion Using a Supramolecular Strategy

CCS Chemistry ◽  
2019 ◽  
Vol 1 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Mengjiao Cheng ◽  
Dequn Zhang ◽  
Shu Zhang ◽  
Zuankai Wang ◽  
Feng Shi
Keyword(s):  
Surface Tension ◽  
Electricity Generation ◽  
Adsorption Equilibrium ◽  
Molecular Level ◽  
Surface Tension Gradient ◽  
Aggregation State ◽  
Physical Limit ◽  
Competitive Kinetics ◽  
Air Liquid Interface ◽  
Spontaneous Motion

Inspired by the intriguing capability of beetles to quickly slide on water, scientists have long translated this surface-tension-gradient–dominated Marangoni motion into various applications, for example, self-propulsion. However, this classical spontaneous motion is limited by a short lifetime due to the loss of the surface tension gradient. Indeed, the propellant of amphiphilic surfactants can rapidly reach an adsorption equilibrium and an excessive aggregation state at the air/liquid interface. Here, we demonstrate a supramolecular host–guest chemistry strategy that allows the breaking of the physical limit of the adsorption equilibrium and the simultaneous removal of surfactant molecules from the interface. By balancing the competitive kinetics between the two processes, we have prolonged the lifetime of the motion 40-fold. Our work presents an important advance in the query of long-lived self-propulsion transport through flexible interference at the molecular level and holds promise in electricity generation applications .

Tracing surfactant transformation from cellular release to insertion into an air-liquid interface

2004 ◽  
Vol 286 (5) ◽  
pp. L1009-L1015 ◽  
Author(s):  
T. Haller ◽  
P. Dietl ◽  
H. Stockner ◽  
M. Frick ◽  
N. Mair ◽  
...  
Keyword(s):  
Surface Tension ◽  
Cultured Cells ◽  
High Surface ◽  
Lamellar Body ◽  
Liquid Interface ◽  
Alveolar Type ◽  
Tensile Forces ◽  
Modify Surface ◽  
Fluorescence Imaging Microscopy ◽  
Air Liquid Interface

Pulmonary surfactant is secreted by alveolar type II cells as lipid-rich, densely packed lamellar body-like particles (LBPs). The particulate nature of released LBPs might be the result of structural and/or thermodynamic forces. Thus mechanisms must exist that promote their transformation into functional units. To further define these mechanisms, we developed methods to follow LBPs from their release by cultured cells to insertion in an air-liquid interface. When released, LBPs underwent structural transformation, but did not disperse, and typically preserved a spherical appearance for days. Nevertheless, they were able to modify surface tension and exhibited high surface activity when measured with a capillary surfactometer. When LBPs inserted in an air-liquid interface were analyzed by fluorescence imaging microscopy, they showed remarkable structural transformations. These events were instantaneous but came to a halt when the interface was already occupied by previously transformed material or when surface tension was already low. These results suggest that the driving force for LBP transformation is determined by cohesive and tensile forces acting on these particles. They further suggest that transformation of LBPs is a self-regulated interfacial process that most likely does not require structural intermediates or enzymatic activation.

A model for mechanical structure of the alveolar duct

1982 ◽  
Vol 52 (4) ◽  
pp. 1064-1070 ◽  
Author(s):  
T. A. Wilson ◽  
H. Bachofen
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Published Data ◽  
Scanning Electron Micrographs ◽  
Fiber System ◽  
Lung Capacity ◽  
Alveolar Duct ◽  
Tissue System ◽  
Line Elements ◽  
Air Liquid Interface

The appearance of the microstructure of the lung as revealed in transmission and scanning electron micrographs of perfusion-fixed air- and saline-filled lungs suggests the following model for the structure of the alveolar duct. There are two networks of force-bearing elements. The first is an interdependent part of the peripheral connective tissue system that starts from the pleura and extends into the interlobar and interlobular fissures. At the sublobular level, its geometry is not yet fully clear. This network is extended by changes in lung volume and is insensitive to surface tension. The second network is composed of the line elements that form the rims of the alveolar openings. This network is the terminal part of the axial fiber system that surrounds bronchi, bronchioli, and arteries. The line elements of this network are extended by the outward force of surface tension. The two-dimensional alveolar walls that form the alveoli are negligible mechanical components except as platforms for surface tension at the air-liquid interface. An analysis of the mechanics of this model yields relations among surface area, recoil pressure, lung volume, and surface tension that are consistent with published data for lung volumes below 80% of total lung capacity.

Breakdown of Evaporating Falling Films as a Function of Surface Tension Gradient

1996 ◽  
Vol 17 (4) ◽  
pp. 72-81 ◽  
Author(s):  
ALI G. BUDIMAN ◽  
C. FLORIJANTO ◽  
J. W. PALEN
Keyword(s):  
Surface Tension ◽  
Surface Tension Gradient ◽  
Falling Films

scholarly journals Effect of a surface tension gradient on the slip flow along a superhydrophobic air-water interface

2018 ◽  
Vol 3 (3) ◽  
Author(s):  
Dong Song ◽  
Baowei Song ◽  
Haibao Hu ◽  
Xiaosong Du ◽  
Peng Du ◽  
...  
Keyword(s):  
Surface Tension ◽  
Slip Flow ◽  
Surface Tension Gradient ◽  
Water Interface ◽  
Air Water Interface

Numerical Simulation of Oil-Droplet Cleavage by Surfactant

1996 ◽  
Vol 118 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Xiaoyi He ◽  
Micah Dembo
Keyword(s):  
Experimental Data ◽  
Numerical Simulation ◽  
Surface Tension ◽  
Large Deformation ◽  
Concentration Gradient ◽  
Surface Tension Gradient ◽  
Oil Droplets ◽  
Numerical Computations ◽  
Oil Droplet ◽  
Pure Surface

We present numerical computations of the deformation of an oil-droplet under the influence of a surface tension gradient generated by the surfactant released at the poles (the Greenspan experiment). We find this deformation to be very small under the pure surface tension gradient. To explain the large deformation of oil droplets observed in Greenspan’s experiments, we propose the existence of a phoretic force generated by the concentration gradient of the surfactant. We show that this hypothesis successfully explains the available experimental data and we propose some further tests.

Effects of surface tension and intraluminal fluid on mechanics of small airways

1997 ◽  
Vol 82 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Mark J. Hill ◽  
Theodore A. Wilson ◽  
Rodney K. Lambert
Keyword(s):  
Surface Tension ◽  
Bending Stiffness ◽  
Liquid Interface ◽  
Cross Sectional Area ◽  
Pressure Curve ◽  
Small Airways ◽  
Sectional Area ◽  
Cross Sectional ◽  
Inner Surface ◽  
Air Liquid Interface

Hill, Mark J., Theodore A. Wilson, and Rodney K. Lambert.Effects of surface tension and intraluminal fluid on the mechanics of small airways. J. Appl. Physiol.82(1): 233–239, 1997.—Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The muscosa has been modeled (R. K. Lambert. J. Appl. Physiol. 71: 666–673, 1991) as a thin elastic layer with a finite bending stiffness, and the contribution of its bending stiffness to airway elastance has been computed. In this study, we extend that work by including surface tension and intraluminal fluid in the model. With surface tension, the pressure on the inner surface of the elastic mucosa is modified by the pressure difference across the air-liquid interface. As folds form in the mucosa, intraluminal fluid collects in pools in the depressions formed by the folds, and the curvature of the air-liquid interface becomes nonuniform. If the amount of intraluminal fluid is small, <2% of luminal volume, the pools of intraluminal fluid are small, the air-liquid interface nearly coincides with the surface of the mucosa, and the area of the air-liquid interface remains constant as airway cross-sectional area decreases. In that case, surface energy is independent of airway area, and surface tension has no effect on airway mechanics. If the amount of intraluminal fluid is >2%, the area of the air-liquid interface decreases as airway cross-sectional area decreases, and surface tension contributes to airway compression. The model predicts that surface tension plus intraluminal fluid can cause an instability in the area-pressure curve of small airways. This instability provides a mechanism for abrupt airway closure and abrupt reopening at a higher opening pressure.

THE ALVEOLAR LINING LAYER

PEDIATRICS ◽  
1962 ◽  
Vol 30 (2) ◽  
pp. 324-330
Author(s):  
Mary Ellen Avery
Keyword(s):  
Surface Tension ◽  
Secretory Activity ◽  
Hyaline Membrane Disease ◽  
Normal Lung ◽  
Elastic Recoil ◽  
Alveolar Cells ◽  
Electron Microscopic ◽  
Hyaline Membrane ◽  
Surface Active ◽  
Air Liquid Interface

The alveoli of the normal lung are lined by a substance which exerts surface tension at the air-liquid interface. In the expanded lung the tension is high and operates to increase the elastic recoil of the lung. In the lung at low volumes the surface tension becomes extremely low. This confers stability on the airspaces and thus prevents atelectasis. This lining layer is a lipoprotein film, which is not found where alveoli are still lined by cuboidal epithelium. Its time of appearance coincides with the appearance of alveolar lining cells. Electron microscopic evidence of secretory activity in alveolar cells suggests that they may be the source of the surface-active film. The normal alveolar lining layer is not present in lungs of infants who die from profound atelectasis and hyaline membrane disease. Whether its absence is a failure of development or due to inactivation is not established.

Effect of surface tension on circulation in the excised lungs of dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 707-712 ◽  
Author(s):  
I. Bruderman ◽  
K. Somers ◽  
W. K. Hamilton ◽  
W. H. Tooley ◽  
J. Butler
Keyword(s):  
Surface Tension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Lung Volume ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Pressure ◽  
Pulmonary Arterial ◽  
Air Liquid Interface ◽  
Effect Of Surface

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963

Sign in / Sign up

Export Citation Format

Share Document