PubMed · 5922856
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J L de Gennes. 1966. [Hereditary hyperlipidemia].. https://pubmed.ncbi.nlm.nih.gov/5922856/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Glycerol monolaurate (GML) is a naturally occurring surfactant that has potential use as an additive to tampons and wound dressings to reduce the incidence of certain bacterial toxin-mediated illnesses. In vitro studies were undertaken to evaluate the effect of GML on the growth of and toxin production by potentially pathogenic bacteria. GML inhibited the growth of clinical isolates of group A, B, F, and G streptococci at concentrations of 10 to 20 micrograms/ml. Exotoxin production, including that of pyrogenic exotoxins and hemolysins, was reduced by concentrations of GML that were below those inhibitory for growth as well as growth inhibitory. The growth of Staphylococcus aureus strains from patients with toxic shock syndrome and scalded skin syndrome was inhibited or delayed in the presence of 100 to 300 micrograms of GML per ml. Growth inhibition by GML could be overcome by the production of lipase. S. aureus elaboration of hemolysin, toxic shock syndrome toxin 1, and exfoliative toxin A was inhibited at GML concentrations below those necessary to inhibit growth. Results similar to those for S. aureus were obtained in tests of S. hominis. Escherichia coli growth and Salmonella minnesota growth were unaffected by GML, but an S. minnesota Re mutant was susceptible to growth-inhibitory activity. Endotoxin release into the medium from E. coli cells was also unaffected by GML, but the release or activity of E. coli hemolysin was increased by GML. Streptococcal pyrogenic endotoxin A production by an E. coli clone was not affectd by GML. These studies indicate that GML is effective in blocking or delaying the production of exotoxins by pathogenic gram-positive bacteria.
Explore the source record for details and available documents.
In this paper we calculate surface conformation and deformation free energy associated with the incorporation of gramicidin channels into phospholipid bilayer membranes. Two types of membranes are considered. One is a relatively thin solvent-free membrane. The other is a thicker solvent-containing membrane. We follow the approach used for the thin membrane case by Huang (1986) in that we use smectic liquid crystal theory to evaluate the free energy associated with distorting the membrane to other than a flat configuration. Our approach is different from Huang, however, in two ways. One is that we include a term for surface tension, which Huang did not. The second is that one of our four boundary conditions for solving the fourth-order differential equation describing the free energy of the surface is different from Huang's. The details of the difference are described in the text. Our results confirm that for thin membranes Huang's neglect of surface tension is appropriate. However, the precise geometrical form that we calculate for the surface of the thin membrane in the region of the gramicidin channel is somewhat different from his. For thicker membranes that have to deform to a greater extent to accommodate the channel, we find that the contribution of surface tension to the total energy in the deformed surface is significant. Computed results for the shape of the deformed surface, the total energy in the deformed surface, and the contributions of different components to the total energy, are presented for the two types of membranes considered. These results may be significant for understanding the mechanisms of dimer formation and breakup, and the access resistance for ions entering gramicidin channels.