The Thermodynamics and Kinetics on the Solvent Sublation of Ni
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The removal of Ni ion from an aqueous solution was carried out by solvent sublation of Ni-diacetyldioxime-sodium dodecylbenzensulphonic (sublate) into isopentanol. The ratio of surfactant to Ni-diacetyldioxime complex at 20:1 was most effective for the removal, with over 90% Ni ion removed from the aqueous solution within 1 h. The effects of electrolytes (e.g. NaCl), non-hydrophobic organics (e.g. ethanol) and pH of the solution upon the process were well studied. The removal rate was enhanced by higher airflow rates but almost independent on the volume of the organic solvent floating on the top of the aqueous column. The process of solvent sublation followed first order kinetics. A characteristic parameter, the apparent activation energy of attachment of the sublate to bubbles, was estimated to be 8.99 kJ/mol. Furthermore, the simulation of a mathematical model with the experiment data on the solvent sublation of Ni-diacetyldioxime-SDS was proved to be validated.It is now widely recognized that surfactant replacement is a potential life-saving therapy in babies with severe respiratory distress syndrome. The most striking acute effects have been obtained with modified natural surfactant preparations containing both surface active lipids and the hydrophobic proteins, surfactant protein B and surfactant protein C. Clinical applications of exogenous surfactant have become increasingly important. Mechanisms of surfactant inactivation have also been studied extensively in recent years. Data from animal experiments as well as clinical pilot studies indicate that the inactivation of surfactant can be overcome by large doses of exogenous surfactant. The resistance of surfactant to inhibition seems to depend on the presence of surfactant protein A. Exogenous surfactants for treatment of patients with acute respiratory distress syndrome and similar conditions must therefore be carefully designed to resist inhibition.
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Summary Introduction It has been proposed that exogenous pulmonary surfactant can be used as a drug delivery system for immunosuppressive agents to the alveolar compartment of the lung while reducing the risk of systemic toxicity. Before using this combination, however, alterations in activity of both substances should be examined. Therefore, this study investigated whether the activity of a natural derived surfactant preparation is changed after it is mixed with cyclosporine A (CsA) or rapamycin (RPM). Methods A surfactant suspension was mixed with CsA or RPM and minimal surface tension of these mixtures was measured in vitro . Surfactant activity was evaluated in vivo by its capacity to restore gas exchange in an established model of surfactant deficiency in rats. CsA–surfactant, RPM–surfactant or surfactant alone was instilled intratracheally and blood gases were measured under standardized ventilatory conditions. Results Minimal surface tension of surfactant–CsA was comparable with that of surfactant alone, whereas minimal surface tension of the surfactant–RPM mixture was increased. In vivo partial arterial oxygen pressure levels increased immediately to prelavage values after instillation of CsA–surfactant, RPM–surfactant and surfactant only and were comparable during the entire study period. Conclusion The activity of a naturally derived surfactant was affected when mixed with RPM but not when mixed with CsA at the used concentrations.
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As birds have tubular lungs that do not contain alveoli, avian surfactant predominantly functions to maintain airflow in tubes rather than to prevent alveolar collapse. Consequently, we have evaluated structural, biochemical, and functional parameters of avian surfactant as a model for airway surfactant in the mammalian lung. Surfactant was isolated from duck, chicken, and pig lung lavage fluid by differential centrifugation. Electron microscopy revealed a uniform surfactant layer within the air capillaries of the bird lungs, and there was no tubular myelin in purified avian surfactants. Phosphatidylcholine molecular species of the various surfactants were measured by HPLC. Compared with pig surfactant, both bird surfactants were enriched in dipalmitoylphosphatidylcholine, the principle surface tension-lowering agent in surfactant, and depleted in palmitoylmyristoylphosphatidylcholine, the other disaturated phosphatidylcholine of mammalian surfactant. Surfactant protein (SP)-A was determined by immunoblot analysis, and SP-B and SP-C were determined by gel-filtration HPLC. Neither SP-A nor SP-C was detectable in either bird surfactant, but both preparations of surfactant contained SP-B. Surface tension function was determined using both the pulsating bubble surfactometer (PBS) and capillary surfactometer (CS). Under dynamic cycling conditions, where pig surfactant readily reached minimal surface tension values below 5 mN/m, neither avian surfactant reached values below 15 mN/m within 10 pulsations. However, maximal surface tension of avian surfactant was lower than that of porcine surfactant, and all surfactants were equally efficient in the CS. We conclude that a surfactant composed primarily of dipalmitoylphosphatidylcholine and SP-B is adequate to maintain patency of the air capillaries of the bird lung.
Dipalmitoylphosphatidylcholine
Lamellar granule
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Natural sheep surfactant, rabbit surfactant, human surfactant, and surfactant TA were compared for in vitro surface properties and for responses of preterm lambs to treatment. Equivalent amounts of sheep, rabbit, and human surfactants were needed to lower the surface tension to less than 10 dynes/cm, whereas four times less surfactant TA similarly lowered the surface tension. Surface-spreading rates were similar for the surfactants. The surface adsorption of the batch of human surfactant tested was much slower than was adsorption of the other surfactants. Ventilation was significantly improved in all surfactant-treated lambs relative to the control lambs, indicating the general efficacy of the surfactant treatments. Overall, surfactant TA had the best in vitro characteristics, yet the preterm lambs treated at birth with surfactant TA had lower PO2 values and higher ventilatory requirements than did the sheep surfactant-treated lambs. The in vivo responses to rabbit surfactant were intermediate between the responses to sheep surfactant and to surfactant TA. Human surfactant resulted in the least effective clinical response. More of the phosphatidylcholine associated with human surfactant and surfactant TA was lost from the alveoli and lung tissue after four hours of ventilation than was lost from sheep or rabbit surfactant-treated lambs. More intravascular radiolabeled albumin leaked into the alveoli of the surfactant TA-treated lambs than sheep or rabbit surfactant-treated lambs. The four surfactants also had different sensitivities to the effects on minimum surface tensions of the soluble proteins present in alveolar washes. The study demonstrates that the range of clinical responses was not predictable based on the in vitro surface properties that we measured.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wilhelmy plate
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Nano-sized particles (NSPs) have a diameter of less than 100 nm. When inhaled, they preferentially deposit in the deeper lung, where pulmonary surfactant covers the thin aqueous lining layer. Thus, pulmonary surfactant is the initial contact where NSPs impinge. This can lead to various consequences. For example, binding of NSPs to single surfactant components like phospholipids or surfactant proteins can occur, which might modulate toxic particle effects. Moreover, particle clearance can be modulated. Furthermore, the biophysical surfactant function itself can be disturbed by interaction with NSPs. In addition, surfactant displaces particles into the aqueous hypophase of the lining layer, where they can come into contact with type II pneumocytes. This interaction has been suggested to affect pulmonary surfactant metabolism. The potential interactions of nano-sized particles with the pulmonary surfactant system and the effects on biophysical surfactant function, surfactant metabolism, particle clearance, and on particle-induced toxicity are reviewed.
Particle (ecology)
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Close spacing bio-surfactant tertiary composite flooding pilot test indicated, compared to tertiary composite surfactant system without adding bio-surfactant, usage of sulphonate surfactant and cost of injected chemical decreased respectively by 1/2 and 30% for bio-surfactant tertiary composite system, which is formed by rhamnoilpid bio-surfactant and sulphonate surfactant. The ultra-low interface tension value between flooding system and crude oil reached 10-3mN/m, and recovery factor for central well site and that for overall area increased by 23. 24% and 16. 34% , respectively.
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In order to obtain the decomposition kinetics of MnO2,its decomposition processes were investigated by TG/DTA and XRD.The kinetics equation is(T625℃)and(T≥625℃)for 4MnO2=2Mn2O3+O2↑,and its activation energy is 90.239kJ/mol.The kinetics equation is for 6Mn2O3=4Mn3O4+O2↑,and its activation energy is 204.67kJ/mol.Two reactions were controlled by the nucleation and growth.
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The spreading rate of an exogenous surfactant monolayer due to surface tension gradients is examined by using our previously reported theoretical analysis, with particular attention given to the effects of endogenous surfactant. It is found that the presence of an endogenous surfactant reduces the spreading rate of exogenous surfactant and that, in certain circumstances, the spreading may be halted. A recently published paper (F. F. Espinosa, A. H. Shapiro, J. J. Fredberg, and R. D. Kamm. J. Appl. Physiol. 75: 2028–2039, 1993) reaches the opposite conclusion about the effect of endogenous surfactant, i.e., that the presence of an endogenous surfactant increases the spreading rate of the exogenous surfactant. This communication discusses the relevant issues associated with these different results and what the implications may be for surfactant replacement therapy. It is found that the endogenous surfactant, which is ahead of the advancing exogenous surfactant front, undergoes a concentration increase due to surface area compression of the air-liquid interface. Hence the spreading exogenous surfactant can raise surfactant concentrations in regions distal to its own location, and this is a previously unrecognized potential therapeutic mechanism of instilled surfactants. After initial instillations of intratracheal boluses of exogenous surfactant, additional surfactant may better reach the desired target site if delivered by aerosol. Predictions of surfactant and piggy-backed drug-delivery times through the lung are also discussed.
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