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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Surface Tension

 
 
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Disease relevance of Surface Tension

 

High impact information on Surface Tension

  • The possibility that the lipoprotein complex of lung surfactant functions in pulmonary host defense as well as lowering surface tension at the air-liquid interface has been the subject of renewed interest in light of the finding that surfactant proteins A and D (SP-A and SP-D) are members of a family of proteins known as collectins [6].
  • These data, together with findings that the SP-B-related peptides increase inter- and intramolecular order of the phospholipid layer, suggest that SP-B resists surface tension by increasing lateral stability of the phospholipid layer [7].
  • This value, when used in a simple geometric model for the curvature dependence of the hydrophobic effect, predicts a macroscopic alkane-water surface tension that is close to the macroscopic value [8].
  • We thus conclude that the amyloid-like fibrils of ChpD-H lower the water surface tension to allow aerial growth and cover aerial structures, rendering them hydrophobic [9].
  • The crude surfactant pellet was analyzed for total phospholipids (PL), individual phospholipids, SP-A, SP-B, and minimum surface tension (STmin) [10].
 

Biological context of Surface Tension

 

Anatomical context of Surface Tension

 

Associations of Surface Tension with chemical compounds

 

Gene context of Surface Tension

  • At lower concentrations, minimum surface tensions were higher for SP-A(-/-) mice [24].
  • Surfactant protein A (SP-A) is the major protein component of pulmonary surfactant, a material secreted by the alveolar type II cell that reduces surface tension at the alveolar air-liquid interface [25].
  • SP-C associates with surfactant lipids to reduce surface tension within the alveolus, maintaining lung volume at end expiration [26].
  • SP-C enhances surface tension lowering activity of surfactant phospholipids that is critical to the maintenance of alveolar volume at end expiration [27].
  • The surface tension measured with a Wilhelmy balance of the rSP-C surfactant was lower than the surface tension of natural sheep surfactant (containing SP-B and SP-C) [28].
 

Analytical, diagnostic and therapeutic context of Surface Tension

  • The Langmuir trough has been used to study monolayers of surfactant from beef lung extracts, dog lavage and the principal component (dipalmitoyl lecithin; DPL) in which surface tension has been simultaneously monitored on each film by the Wilhelmy method and the original Langmuir method whose readings are independent of contact angle [29].
  • Median minimal surface tension, measured by pulsating bubble surfactometer, was elevated (P < 0.01) in both infection (17.5 mN/m) and CF (17.1 mN/m) compared with the control group (1.5 mN/m) [30].
  • CONCLUSIONS: Exogenous surfactant preceding high peak inspiratory lung volumes prevents impairment of oxygenation, lung mechanics, and minimal surface tension of bronchoalveolar lavage fluid and reduces alveolar influx of Evans blue dye [31].
  • Dilute mixed solutions of non-surface active anionic polymers (polyacrylamide and polystyrene sulfonate, xanthan) and various surfactants have been studied with several methods: surface tension, ellipsometry, X-ray and neutron reflectivity, thin film balance, surface and bulk rheology [32].
  • Minimum surface tensions of alveolar washes fell from greater than 30 dynes/cm to 6.3 dynes/cm 10 min after treatment and again rose to 21.6 dynes/cm within 3 h [33].

References

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