Influence of surfactant on gas bubble stability

Gas-bubble stability is achieved either by a reduction in the Laplace pressure or by a reduction in the permeability of the gas-liquid interface. Although insoluble surfactants have been shown definitively in many studies to lower the permeability of the gas-liquid interface and hence increase the resistance to interfacial mass transfer, remarkably little work has been done on the effects of soluble surfactants. An experimental system was developed to measure the effect of the soluble surfactant dodecyl trimethylammonium bromide on the desorption and absorption of carbon dioxide gas through a quiescent planar interface. The desorption experiments conformed to the model of non-steady-state molecular diffusion. The absorption experiments, however, produced an unexpected mass transfer mechanism, with surface renewal, probably because of instability in the density gradient formed by the carbon dioxide. In general, the soluble surfactant produced no measurable reduction in the rate of interfacial mass transfer for desorption or absorption. This finding is consistent with the conclusion of Caskey and Barlage(30) that soluble surfactants produce a significantly lower resistance to interfacial mass transfer than do insoluble surfactants. The dynamic adsorption and desorption of the surfactant molecules at the gas-liquid interface creates short-term vacancies, which presumably permit the unrestricted transfer of the gas molecules through the interface. This surfactant exchange does not occur for insoluble surfactants. Gas bubbles formed in the presence of a high concentration of soluble surfactant were observed to dissolve completely, while those formed in the presence of the insoluble surfactant stearic acid did not dissolve easily, and persisted for very long periods. The interfacial concentration of stearic acid rises during bubble dissolution, as it is insoluble, and must eventually achieve full monolayer coverage and a state of compression, lowering the permeability of the interface. Thus, insoluble surfactants or hydrophobic impurities from solid surfaces may account for increased bubble stability

Complexities of Particulate Matter Measurement in Parenteral Formulations of Small-Molecule Amphiphilic Drugs

Reconstituted parenteral solutions of three surface-active anti-infective small-molecule drugs and solutions of sodium dodecyl sulfate (SDS, a model surfactant) were studied to quantify the impact of sample preparation and handling on particle counts. Turbidimetry and light obscuration profiles were recorded as a function of agitation and shearing with and without the introduction of foam into the solutions. SDS solutions at concentrations above the critical micelle concentration (CMC) show significantly greater sensitivity to shear and foam presence than SDS solution below the CMC: Values of >10 μm particles increased 8 fold over control (an unsheared sample) in the micellar solution vs. 4 fold particle count increase over control at a sub-micellar concentration. An even more significant increase in the ratio of particle count in sheared/unsheared solution is seen for >25 μm unit counts, due to the increased interference of foam with the measurement. Two commercial products, injection formulations of teicoplanin and cefotaxime sodium, as well as an investigational compound 1, showed an increase in scattering as a function of foam production. The impact of foaming was significant, resulting in an increase of turbidity and light obscuration measurements in all solutions. The results illustrate some of the challenges that are inherent to optically clear, homogeneous pharmaceutical injections containing compounds which have a tendency toward self-association and surfactant-like behavior

Identification of a disease-defining gene fusion in epithelioid hemangioendothelioma

Integrating transcriptomic sequencing with conventional cytogenetics, we identified WWTR1 (WW domain-containing transcription regulator 1) (3q25) and CAMTA1 (calmodulin-binding transcription activator 1) (1p36) as the two genes involved in the t(1;3)(p36;q25) chromosomal translocation that is characteristic of epithelioid hemangioendothelioma (EHE), a vascular sarcoma. This WWTR1/CAMTA1 gene fusion is under the transcriptional control of the WWTR1 promoter and encodes a putative chimeric transcription factor that joins the amino terminus of WWTR1, a protein that is highly expressed in endothelial cells, in-frame to the carboxyl terminus of CAMTA1, a protein that is normally expressed only in brain. Thus, CAMTA1 expression is activated inappropriately through a promoter-switch mechanism. The gene fusion is present in virtually all EHEs tested but is absent from all other vascular neoplasms, demonstrating it to be a disease-defining genetic alteration. A sensitive and specific break-apart fluorescence in situ hybridization assay was also developed to detect the translocation and will assist in the evaluation of this diagnostically challenging neoplasm. The chimeric WWTR1/CAMTA1 transcription factor may represent a therapeutic target for EHE and offers the opportunity to shed light on the functions of two poorly characterized proteins.status: publishe