Adsorption and Self-Assembly of Surfactants on Metal–Water Interfaces

Modifying properties of metal–water interfaces via adsorption of surfactants has applications in electrochemistry and catalysis. We report molecular simulations of adsorption of surfactant molecules on metal surfaces wherein we systematically vary the strength of hydrophobic interaction between surfactant tails, as well as the size of the surfactants’ polar head group. A surfactant molecule is represented by a linear, bead–spring model with a polar “head” bead and a chain of hydrophobic “tail” beads. A smooth surface, strongly attractive to the polar beads, represents the metal surface. Our main findings are that (1) hydrophobic interactions between adsorbed molecules promote adsorption and self-assembly and (2) the morphology of the adsorbed layer is governed by the geometry of the molecules. When the size of the polar bead is the same as that of the hydrophobic beads, an adsorbed self-assembled monolayer (SAM) is formed. When the polar bead is larger than the hydrophobic beads, cylindrical micelles are formed in the bulk and the adsorbed phase. For the adsorbed SAM, the layer is patchy, with a significant fraction of the molecules adsorbed with their polar beads pointing away from the surface. These results corroborate with experimental observations and provide new insights into the molecular nature of adsorbed layers

Adsorption Free Energies of Imidazolinium-Type Surfactants in Infinite Dilution and in Micellar State on Gold Surface

We report adsorption behavior of imidazolinium-type surfactant molecules in different aggregation states on metal–water interfaces studied using all-atom molecular dynamics simulations. Surfactant molecules with two different alkyl tail lengths, a 10-carbon and a 17-carbon tail (henceforth referred to as imid-10 and imid-17, respectively), have been considered. Six layers of face-centered cubic lattice of gold atoms submerged in water represent the metal–water interface. Our simulations reveal that, in infinite dilution, both types of surfactant molecules strongly adsorb onto the metal–water interface in a configuration with their alkyl tail lying parallel to the surface. This adsorption occurs through a barrierless transition with an adsorption free energy of ∼30 <i>k</i>_B<i>T</i> and is found to be enthalpically driven and entropically unfavorable. Surfactant micelles, on the other hand, experience a long-range repulsion from the metal surface at distances as large as 50–60 Å due to the presence of a large “corona” around the micelles that comprises counterions and their solvation layer. Surfactant micelles have an adsorption free energy barrier of ∼13–16 <i>k</i>_B<i>T</i>, which is associated with the removal of adsorbed water from the metal surface. Micelles are thermodynamically stable in the bulk aqueous phase, and the adsorbed micellar state is only metastable

Facet Selectivity of Cetyltrimethyl Ammonium Bromide Surfactants on Gold Nanoparticles Studied Using Molecular Simulations

We have studied facet selectivity of cetyltrimethyl ammonium bromide (CTAB) surfactants of varying alkyl tail lengths (C17TAB and C10TAB) during their adsorption on a spherical gold metal nanoparticle (MNP) using umbrella sampling and well-tempered metadynamics techniques in molecular simulations. We show that the surfactants strongly adsorb with their alkyl tails wrapped around the MNP. The adsorption morphologies are dictated by the strong preference of the polar head group of the surfactants to adsorb on to the atoms that lie between the facets of the MNP, that is, in the vicinity of low-coordinated gold atoms. The alkyl tails do not display any strong facet preference. Owing to the longer alkyl tails, C17TAB molecules pack together better than the C10TAB molecules in the adsorbed state on the MNP. These findings suggest that the regions near the edges of the facets and low-coordinated atoms are expected to be preferentially covered with the adsorbed surfactants

GII.4 detection rates worldwide among norovirus-positive children with sporadic acute gastroenteritis.

<p>Data were collected from 53 studies conducted in 31 different countries among children with sporadic acute gastroenteritis. Studies with samples collected after the year 2000 with sample collection done for a minimum of one year and based on genotyping of the capsid region are included. Due to lack of sufficient available data from Africa, studies conducted for less than one year have also been included for this region. The data shown are from a total of 6,283 genotyped samples from 28 different studies from Asia, 13 from Africa, five from South America, one from North America, and three each from Europe and Central America (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005385#ppat.1005385.s001" target="_blank">S1 Table</a>). The number (n) in the figure represents the number of genotyped samples, while the duration of sample collection for each region is mentioned within the parentheses. GII.NT represent non-typeables. Broken lines represent approximate percentages of secretors in the population.</p

Rotavirus and Serotonin Cross-Talk in Diarrhoea

<div><p>Rotavirus (RV) has been shown to infect and stimulate secretion of serotonin from human enterochromaffin (EC) cells and to infect EC cells in the small intestine of mice. It remains to identify which intracellularly expressed viral protein(s) is responsible for this novel property and to further establish the clinical role of serotonin in RV infection. First, we found that siRNA specifically silencing NSP4 (siRNA^NSP4) significantly attenuated secretion of serotonin from Rhesus rotavirus (RRV) infected EC tumor cells compared to siRNA^VP4, siRNA^VP6 and siRNA^VP7. Second, intracellular calcium mobilization and diarrhoeal capacity from virulent and avirulent porcine viruses correlated with the capacity to release serotonin from EC tumor cells. Third, following administration of serotonin, all (10/10) infants, but no (0/8) adult mice, responded with diarrhoea. Finally, blocking of serotonin receptors using Ondansetron significantly attenuated murine RV (strain EDIM) diarrhoea in infant mice (2.9 <i>vs</i> 4.5 days). Ondansetron-treated mice (n = 11) had significantly (p < 0.05) less diarrhoea, lower diarrhoea severity score and lower total diarrhoea output as compared to mock-treated mice (n = 9). Similarly, Ondansetron-treated mice had better weight gain than mock-treated animals (p < 0.05). A most surprising finding was that the serotonin receptor antagonist significantly (p < 0.05) also attenuated total viral shedding. In summary, we show that intracellularly expressed NSP4 stimulates release of serotonin from human EC tumor cells and that serotonin participates in RV diarrhoea, which can be attenuated by Ondansetron.</p></div

Rotavirus re-organizes serotonin appearance in EC tumor cells.

<p>(A) Infected and uninfected cells were co-stained for serotonin (green) and VP6 (red) expression. Infected cells displayed re-organization of serotonin from diffuse cytoplasmic and membrane-associated appearance in uninfected cells to an intense granular membrane-associated appearance in infected cells. (B) Illustration of an uninfected EC cell in close vicinity of an infected cell (red). Note the pronounced granular appearance of serotonin near the plasma membrane of the infected cell. (C) Fluorescent intensity (arbitar units, AU) (VP6) was calculated for each infected (n = 22) and uninfected (n = 13) cell and corresponding appearance (granular vs non-granular) taken into account. Data is presented as means ± SEM. *** = p < 0.001 with Mann-Whitney U test.</p

siRNA concentration, sequence and transfection incubation time-points in MA104 and EC tumor cells for NSP4, VP6, VP7 and VP4.

<p>siRNA concentration, sequence and transfection incubation time-points in MA104 and EC tumor cells for NSP4, VP6, VP7 and VP4.</p

Virulent OSU virus stimulates more release of serotonin from EC tumor cells than attenuated OSU virus.

<p>Following infection (MOI = 1) of EC tumor cells with attenuated OSU-a and virulent OSU-v virus for 1 and 7 h p.i, media was collected and the serotonin release determined with ELISA. Control: cell media from MA104 cells. Data is presented as mean ± SEM. *** = p ˂ 0.001 and ** = p ˂ 0.01 with Student’s t-test; n = 5.</p

Serotonin antagonist Ondansetron attenuates diarrhoea in rotavirus-infected mice.

<p>(A) Prevalence of diarrhoea over time in rotavirus (EDIM) infected mice. Mice infected with EDIM were compared with mice infected with EDIM and treated with Ondansetron (5 mg/kg). Mean values are presented. (B) Number of days with diarrhoea (NDD) in mice infected with EDIM or EDIM plus Ondansetron (5 mg/kg). Data is presented as mean ± SEM. * = p < 0.05 with Student’s t-test. (C) Daily diarrhoea score for each day between the groups of mock-treated infected mice and infected mice treated with Ondansetron. Mock-treated infected mice received significantly more severe diarrhoea after 48 and 72 h p.i. Data is presented as mean ± SEM. * = p < 0.05 and ** = p < 0.01 with Student’s t-test. (D) Total amount (mg) of diarrhoea per mouse up to 144 h p.i. Data is presented as mean +SEM.** = p < 0.01 with Student’s t-test. (E) Comparison of weight gain between treated and mock-treated mice over time. Treated infected mice had gained significantly more weight from 48 h p.i. in comparison to only those without treatment. Data is presented as mean ± SEM. *** = p < 0.001 with Student’s t-test. EDIM (n = 9), EDIM + Ondansetron (n = 11).</p

Intracellular expressed NSP4 stimulates serotonin release from human EC tumor cells.

<p>(A) EC tumor cells were transfected with siRNA^NSP4. At 24 h p.i cells were infected with RRV at a MOI of 0.5 and after 7 h p.i cells were harvested and stained for NSP4 by a rabbit anti- NSP4 and a rhodamine-conjugated goat anti-rabbit (red) conjugate. (B) Silencing effect on NSP4, VP4, VP6 and VP7 expression in EC tumor cells. Following transfection and infection, cells were lysed and viral protein expression analysed by western blotting. With every western blot analysis, the amount of loaded protein was adjusted by comparing protein content in Comassie Blue-stained gels. 28 kD = glycosylated form of NSP4, 20 kD = non-glycosylated form of NSP4. (C) EC tumor cells transfected with siRNA^NSP4 and infected. At 7 h p.i medium was changed and after 1 h supernatants were collected and analysed for serotonin. * = p ˂ 0.05 with Mann-Whitney U test; n = 4.</p